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

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



Update from USDA Regarding a Detection of Bovine Spongiform Encephalopathy (BSE) in the United States


USDA and FDA Continue to Assure Consumers That Existing Safeguards Protect Food Supply; Reiterates Safety of Consuming Beef and Dairy Products


WASHINGTON, April 26, 2012 – USDA’s Animal and Plant Health Inspection Service today released the following update on the BSE detection announced earlier this week:

On April 24, USDA confirmed the nation’s 4th case of Bovine Spongiform Encephalopathy (BSE) in an animal that was sampled for the disease at a rendering facility in central California. This animal was never presented for slaughter for human consumption, so at no time presented a risk to the food supply, or to human health in the United States. As the epidemiological investigation has progressed, USDA has continued to communicate findings in a timely and transparent manner.

As a result of USDA’s ongoing epidemiological investigation, more information about the history and age of the animal is now available.

The animal in question was 10 years and 7 months old and came from a dairy farm in Tulare County, Calif. The animal was humanely euthanized after it developed lameness and became recumbent. The animal’s carcass will be destroyed.

It is important to reiterate that this animal was never presented for slaughter for human consumption, did not enter food supply channels, and at no time presented any risk to human health.

USDA is continuing its epidemiological investigation and will provide additional information as it is available.

The positive animal was tested as part of targeted BSE surveillance at rendering facilities. Samples were sent to the California Animal Health and Food Safety Laboratory for testing and forwarded to the National Veterinary Services Laboratories (NVSL) on April 20th for confirmatory testing. APHIS announced the confirmed positive finding April 24th.

The United States has a longstanding system of three interlocking safeguards against BSE that protects public and animal health in the United States, the most important of which is the removal of specified risk materials – or the parts of an animal that would contain BSE should an animal have the disease – from all animals presented for slaughter in the United States. The second safeguard is a strong feed ban that protects cattle from the disease. The third safeguard—which led to this detection— is our ongoing BSE surveillance program that allows USDA to detect the disease if it exists at very low levels in the U.S. cattle population and provides assurances to consumers and our international trading partners that the interlocking system of safeguards in place to prevent BSE are working.


#


USDA is an equal opportunity provider and employer. To file a complaint of discrimination, write: USDA, Office of the Assistant Secretary for Civil Rights, Office of Adjudication, 1400 Independence Ave., SW, Washington, DC 20250-9410 or call (866) 632-9992 (Toll-free Customer Service), (800) 877-8339 (Local or Federal relay), (866) 377-8642 (Relay voice users).









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. partial and voluntary BSE mad cow feed ban of August 4, 1997 was nothing more than ink on paper, with as much as 10,000,000 LBS. of blood laced meat and bone meal MBM going out into commerce 10 years later in 2007. who knows since 2007 breach, fda et al stopped posting those warning letters. ARS said if atypical BSE was more virulent, SRM removal would have to change if tissue infectivity was found differently than c-BSE. it was. more virulent and infectivity was found in more tissues, including skeletal muscle. HOUSTON, WE HAVE A PROBLEM. ...






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.






please see ;






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...












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.














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










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 <http://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: <http://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. <http://www.prwatch.org/books/madcow.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...
















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 �� A different route of exposure or exposure at an older age �� A strain of Scrapie transmitted to cattle �� Sporadic or a spontaneous occurrence of BSE At his point in time, there is no evidence to conclude that any of the theories are or are not a possibility. There is considerable interest in the sporadic theory. If a form of BSE were to ocnaturally, this may suggest that certain control and prevention measure would have to remain in place indefinitely. Proving or disproving the occurrence of a relatively rare sporadic disease poses a significant challenge. It would require between 3 and 4.5 million tests performed on brain samples randomly taken from cattle over 7 years of age in a country with no evidencrisk from orally acquired BSE. It is unlikely that any country would have the will or resources to perform such a study. Lacking this type of evidence, systematic surveillance over a long time period may provide evidence about the nature of atypical BSE.




snip...see full text ;










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.












BY the way, ammonia treated beef DOES NOT KILL MAD COW DISEASE !!!






Tuesday, April 24, 2012




MAD COW DISEASE USA 4TH CASE DOCUMENTED ATYPICAL BSE CALIFORNIA










Wednesday, April 25, 2012




4th MAD COW DISEASE U.S.A. CALIFORNIA ATYPICAL L-TYPE BSE 2012












Wednesday, April 25, 2012




ACTUALITY - USDA Chief Veterinary Officer On Surveillance And Milk Safety and BSE aka MAD COW DISEASE












Thursday, April 26, 2012




Maternal Transmission of the BSE and Birth Cohorts












Harvard Risk Assessment of Bovine Spongiform Encephalopathy Update, October 31, 2005 INTRODUCTION The United States Department of Agriculture’s Food Safety and Inspection Service (FSIS) held a public meeting on July 25, 2006 in Washington, D.C. to present findings from the Harvard Risk Assessment of Bovine Spongiform Encephalopathy Update, October 31, 2005 (report and model located on the FSIS website:










Comments on technical aspects of the risk assessment were then submitted to FSIS.




Comments were received from Food and Water Watch, Food Animal Concerns Trust (FACT), Farm Sanctuary, R-CALF USA, Linda A Detwiler, and Terry S. Singeltary.




This document provides itemized replies to the public comments received on the 2005 updated Harvard BSE risk assessment. Please bear the following points in mind:












Owens, Julie From: Terry S. Singeltary Sr. [mailto:flounder9%40verizon.net]




Sent: Monday, July 24, 2006 1:09 PM




To: FSIS RegulationsComments




Subject: [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE) Page 1 of 98












Sunday, November 13, 2011




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












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






don’t forget the children...






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




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




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








SCHOOL LUNCH PROGRAM FROM DOWNER CATTLE UPDATE














DID YOUR CHILD CONSUME SOME OF THESE DEAD STOCK DOWNER COWS, THE MOST HIGH RISK FOR MAD COW DISEASE ???




you can check and see here ;














ATYPICAL L-TYPE BASE BSE AND TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TME, is there a link ???








4.6.1. Epidemiology TME is a disease that affected mink ranches, decimating the herds, in the frame of five to eleven isolated outbreaks, from 1947 to 1985, mainly in USA (Wisconsin was the main affected State since it is where mink ranches where mainly located) (Robinson et al., 1994). Moreover, eastern European countries (East Germany, Finland and USSR) also reported outbreaks in the mid-sixties.




According to its rare occurrence associated with a massive rate of infection, and in the absence of probing horizontal or vertical transmission, the hypothesis of a food-borne infection is the most convincing explanation. This theory is enforced by the fact that three of those outbreaks occurred in large mink production facilities that prepared on-site feed involving the use of non-ambulatory (i.e. animal unable to stand alone) cattle (Hartsoug and Burger, 1965; Marsh et al.,


1991).








SNIP...














IS THERE A SCRAPIE-LIKE DISEASE IN CATTLE ?




In April of 1985, a mink rancher in Wisconsin reported a debilitating neurologic disease in his herd which we diagnosed as TME by histopathologic findings confirmed by experimental transmission to mink and squirrel monkeys. The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle and a few horses. She had never been fed.




We believe that these findings may indicate the presence of a previously unrecognized scrapie-like disease in cattle and wish to alert dairy practitioners to this possibility.




snip...




PROCEEDINGS OF THE SEVENTH ANNUAL WESTERN CONFERENCE FOR FOOD ANIMAL VETERINARY MEDICINE, University of Arizona, March 17-19, 1986




















Saturday, December 01, 2007




Phenotypic Similarity of Transmissible Mink Encephalopathy in Cattle and L-type Bovine Spongiform Encephalopathy in a Mouse Model




Volume 13, Number 12–December 2007 Research




Phenotypic Similarity of Transmissible Mink Encephalopathy in Cattle and L-type Bovine Spongiform Encephalopathy in a Mouse Model




Thierry Baron,* Anna Bencsik,* Anne-Gaëlle Biacabe,* Eric Morignat,* andRichard A. Bessen†*Agence Française de Sécurité Sanitaire des Aliments–Lyon, Lyon, France; and†Montana State University, Bozeman, Montana, USA




Abstract




Transmissible mink encepholapathy (TME) is a foodborne transmissible spongiform encephalopathy (TSE) of ranch-raised mink; infection with a ruminant TSE has been proposed as the cause, but the precise origin of TME is unknown. To compare the phenotypes of each TSE, bovine-passaged TME isolate and 3 distinct natural bovine spongiform encephalopathy (BSE) agents (typical BSE, H-type BSE, and L-type BSE) were inoculated into an ovine transgenic mouse line (TgOvPrP4). Transgenic mice were susceptible to infection with bovine-passaged TME, typical BSE, and L-type BSE but not to H-type BSE. Based on survival periods, brain lesions profiles, disease-associated prion protein brain distribution, and biochemical properties of protease-resistant prion protein, typical BSE had a distint phenotype in ovine transgenic mice compared to L-type BSE and bovine TME.The similar phenotypic properties of L-type BSE and bovine TME in TgOvPrP4 mice suggest that L-type BSE is a much more likely candidate for the origin of TME than is typical BSE.




snip...




Conclusion




These studies provide experimental evidence that the Stetsonville TME agent is distinct from typical BSE but has phenotypic similarities to L-type BSE in TgOvPrP4 mice. Our conclusion is that L-type BSE is a more likely candidate for a bovine source of TME infection than typical BSE. In the scenario that a ruminant TSE is the source for TME infection in mink, this would be a second example of transmission of a TSE from ruminants to non-ruminants under natural conditions or farming practices in addition to transmission of typical BSE to humans, domestic cats, and exotic zoo animals(37). The potential importance of this finding is relevant to L-type BSE, which based on experimental transmission into humanized PrP transgenic mice and macaques, suggests that L-type BSE is more pathogenic for humans than typical BSE (24,38).
























Emmanuel Comoy,1,† Valérie Durand,1 Evelyne Correia,1 Sophie Freire,1 Jürgen Richt,2 Justin Greenlee,3 Juan-Maria Torres,4 Paul Brown,1 Bob Hills5 and Jean-Philippe Deslys1


1Atomic Energy Commission; Fontenay-aux-Roses, France; 2Kansas State University; Manhattan, KS USA; 3USDA; Ames, IA USA; 4INIA; Madrid, Spain; 5Health Canada; Ottawa, ON Canada†Presenting author; Email: emmanuel.comoy@cea.fr


The epidemiology of Transmissible mink encephalopathy (TME) indicates an alimentary origin. Several inter-species transmission experiments have not succeeded in establishing with certainty any natural reservoir of this prion strain, although both ovine and bovine sources have been suspected. Cattle exposed to TME develop a spongiform encephalopathy that is distinct from classical Bovine Spongiform Encephalopathy (c-BSE).


Inoculation of c-BSE to cynomolgus macaque provided early evidence of a possible risk to humans, and remains an important model to define the risk of both primary (oral transmission from cattle to primate) and secondary (intravenous intra-species transmission) exposures. We have also evaluated the transmissibility of other cattle prion strains to macaques, including L- and H- atypical forms of BSE, namely BSE-L and BSE-H, and cattle-adapted TME.


BSE-L induced a neurological disease distinct from c-BSE. Peripheral exposures demonstrate the transmissibility of BSE-L by oral, intravenous, and intra-cerebral routes, with incubation periods similar to c-BSE. Cattle-adapted TME also induced a rapid disease in cynomolgus macaque. The clinical features, lesion profile, and biochemical signature of the induced disease was similar to the features observed in animals exposed to BSE-L, suggesting a link between the two prion strains. Secondary transmissions to a common host (transgenic mouse overexpressing bovine PrP) of cattle-TME and BSE-L before or after passage in primates induced diseases with similar incubation periods: like the c-BSE strain, these cattle strains maintained their distinctive features regardless of the donor species and passages.


If the link between TME and BSE-L is confirmed, our results would suggest that BSE-L in North America may have existed for decades, and highlight a possible preferential transmission of animal prion strains to primates after passage in cattle.




=====================end...tss====================






link url not available, please see PRION 2011 ;


















In Confidence - Perceptions of unconventional slow virus diseases of animals in the USA - APRIL-MAY 1989 - G A H Wells




snip...






PAGE 31




Appendix I




VISIT TO USA - DR A E WRATHALL - INFO ON BSE AND SCRAPIE




1. Dr Clark lately of the Scrapie Research Unit, Mission Texas has successfully transmitted ovine and caprine scrapie to cattle. The experimental results have not been published but there are plans to do this. This work was initiated in 1978. A summary of it is:-




Expt A 6 Her x Jer calves born in 1978 were inoculated as follows with a 2nd Suffolk scrapie passage:-




i/c 1ml i/m, 5ml; s/c 5ml; oral 30ml.




1/6 went down after 48 months with a scrapie/BSE-like disease.




Expt B 6 Her or Jer or HxJ calves were inoculated with angora Goat virus 2/6 went down similarly after 36 months.




Expt C Mice inoculated from brains of calves/cattle in expts A & B were resistant, only 1/20 going down with scrapie and this was the reason given for not publishing.




Diagnosis in A, B, C was by histopath. No reports on SAF were given.




Dr Warren Foote indicated success so far in eliminating scrapie in offspring from experimentally- (and naturally) infected sheep by ET. He had found difficulty in obtaining emhryos from naturally infected sheep (cf SPA).




3. Prof. A Robertson gave a brief account of BSE. The US approach was to




PAGE 32




accord it a very low profile indeed. Dr A Thiermann showed the picture in the "Independent" with cattle being incinerated and thought this was a fanatical incident to be avoided in the US at all costs. BSE was not reported in USA.




4. Scrapie incidents (ie affected flocks) have shown a dramatic increase since 1978. In 1953 when the National Control Scheme was started there were 10-14 incidents, in 1978 - 1 and in 1988 so far 60.




5. Scrapie agent was reported to have been isolated from a solitary fetus.




6. A western blotting diagnostic technique (? on PrP} shows some promise.




7. Results of a questionnaire sent to 33 states on the subject of the national sheep scrapie programme survey indicated;




17/33 wished to drop it 6/33 wished to develop it 8/33 had few sheep and were neutral




Information obtained from Dr Wrathall's notes of a meeting of the U.S. Animal Health Association at Little Rock, Arkansas Nov. 1988.






please see ;






In Confidence - Perceptions of unconventional slow virus diseases of animals in the USA - APRIL-MAY 1989 - G A H Wells














Thursday, March 29, 2012




atypical Nor-98 Scrapie has spread from coast to coast in the USA 2012




NIAA Annual Conference April 11-14, 2011San Antonio, Texas












*** Chronic Wasting Disease CWD CDC REPORT MARCH 2012 ***






Saturday, February 18, 2012




Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease




CDC Volume 18, Number 3—March 2012




SNIP...




Long-term effects of CWD on cervid populations and ecosystems remain unclear as the disease continues to spread and prevalence increases. In captive herds, CWD might persist at high levels and lead to complete herd destruction in the absence of human culling. Epidemiologic modeling suggests the disease could have severe effects on free-ranging deer populations, depending on hunting policies and environmental persistence (8,9). CWD has been associated with large decreases in free-ranging mule deer populations in an area of high CWD prevalence (Boulder, Colorado, USA) (5).




SNIP...




Reasons for Caution There are several reasons for caution with respect to zoonotic and interspecies CWD transmission. First, there is strong evidence that distinct CWD strains exist (36). Prion strains are distinguished by varied incubation periods, clinical symptoms, PrPSc conformations, and CNS PrPSc depositions (3,32). Strains have been identified in other natural prion diseases, including scrapie, BSE, and CJD (3). Intraspecies and interspecies transmission of prions from CWD-positive deer and elk isolates resulted in identification of >2 strains of CWD in rodent models (36), indicating that CWD strains likely exist in cervids. However, nothing is currently known about natural distribution and prevalence of CWD strains. Currently, host range and pathogenicity vary with prion strain (28,37). Therefore, zoonotic potential of CWD may also vary with CWD strain. In addition, diversity in host (cervid) and target (e.g., human) genotypes further complicates definitive findings of zoonotic and interspecies transmission potentials of CWD. Intraspecies and interspecies passage of the CWD agent may also increase the risk for zoonotic CWD transmission. The CWD prion agent is undergoing serial passage naturally as the disease continues to emerge. In vitro and in vivo intraspecies transmission of the CWD agent yields PrPSc with an increased capacity to convert human PrPc to PrPSc (30). Interspecies prion transmission can alter CWD host range (38) and yield multiple novel prion strains (3,28). The potential for interspecies CWD transmission (by cohabitating mammals) will only increase as the disease spreads and CWD prions continue to be shed into the environment. This environmental passage itself may alter CWD prions or exert selective pressures on CWD strain mixtures by interactions with soil, which are known to vary with prion strain (25), or exposure to environmental or gut degradation. Given that prion disease in humans can be difficult to diagnose and the asymptomatic incubation period can last decades, continued research, epidemiologic surveillance, and caution in handling risky material remain prudent as CWD continues to spread and the opportunity for interspecies transmission increases. Otherwise, similar to what occurred in the United Kingdom after detection of variant CJD and its subsequent link to BSE, years of prevention could be lost if zoonotic transmission of CWD is subsequently identified, SNIP...SEE FULL TEXT ;




*** Chronic Wasting Disease CWD CDC REPORT MARCH 2012 ***




Saturday, February 18, 2012




Occurrence, Transmission, and Zoonotic Potential of Chronic Wasting Disease




CDC Volume 18, Number 3—March 2012










see much more here ;












Sunday, January 22, 2012




Chronic Wasting Disease CWD cervids interspecies transmission












Thursday, January 26, 2012




The Risk of Prion Zoonoses




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












Thursday, January 26, 2012




Facilitated Cross-Species Transmission of Prions in Extraneural Tissue




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












CJD9/10022




October 1994




Mr R.N. Elmhirst Chairman British Deer Farmers Association Holly Lodge Spencers Lane BerksWell Coventry CV7 7BZ




Dear Mr Elmhirst,




CREUTZFELDT-JAKOB DISEASE (CJD) SURVEILLANCE UNIT REPORT




Thank you for your recent letter concerning the publication of the third annual report from the CJD Surveillance Unit. I am sorry that you are dissatisfied with the way in which this report was published.




The Surveillance Unit is a completely independant outside body and the Department of Health is committed to publishing their reports as soon as they become available. In the circumstances it is not the practice to circulate the report for comment since the findings of the report would not be amended. In future we can ensure that the British Deer Farmers Association receives a copy of the report in advance of publication.




The Chief Medical Officer has undertaken to keep the public fully informed of the results of any research in respect of CJD. This report was entirely the work of the unit and was produced completely independantly of the the Department.




The statistical results reqarding the consumption of venison was put into perspective in the body of the report and was not mentioned at all in the press release. Media attention regarding this report was low key but gave a realistic presentation of the statistical findings of the Unit. This approach to publication was successful in that consumption of venison was highlighted only once by the media ie. in the News at one television proqramme.




I believe that a further statement about the report, or indeed statistical links between CJD and consumption of venison, would increase, and quite possibly give damaging credence, to the whole issue. From the low key media reports of which I am aware it seems unlikely that venison consumption will suffer adversely, if at all.












THIRD CJD REPORT UK 1994




snip...




Consumption of venison and veal was much less widespread among both cases and controls. For both of these meats, there was evidence of a trend with increasing frequency of consumption being associated with increasing risk of CJD. These associations were largely unchanged when attention was restricted to pairs with data obtained from relatives. ...












Wednesday, March 14, 2012




PINK SLIME, MRM’s, BSE AKA MAD COW DISEASE, AND THE USDA NSLP












Saturday, March 5, 2011




MAD COW ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE RISE IN NORTH AMERICA












Sunday, February 12, 2012




National Prion Disease Pathology Surveillance Center Cases Examined1 (August 19, 2011) including Texas












Wednesday, March 28, 2012




VARIABLY PROTEASE-SENSITVE PRIONOPATHY IS TRANSMISSIBLE, price of prion poker goes up again $












Monday, August 9, 2010




Variably protease-sensitive prionopathy: A new sporadic disease of the prion protein or just more PRIONBALONEY ?




snip...see full text ;
















O.K. let's compare some recent cases of this prionpathy in other countries besides Gambetti's first 10 recently, that he claims is a spontaneous event, from a genetic disorder, that is not genetic, but sporadic, that is related to no animal TSE in North America, or the world. ...














Wednesday, October 27, 2010




A novel variant of human disease with a protease-sensitive prion protein and heterozygosity methionine/valine at codon 129: Case report












Wednesday, March 28, 2012




CJD FOUNDATION CWRU GAMBETTI FAMILIAL FAMILY AFFAIR CONFERENCE 2012












Thursday, April 12, 2012




Health professions and risk of sporadic Creutzfeldt–Jakob disease, 1965 to 2010




Eurosurveillance, Volume 17, Issue 15, 12 April 2012




Research articles












Tuesday, November 08, 2011






Can Mortality Data Provide Reliable Indicators for Creutzfeldt-Jakob Disease Surveillance? A Study in France from 2000 to 2008 Vol. 37, No. 3-4, 2011 Original Paper




Conclusions:These findings raise doubt about the possibility of a reliable CJD surveillance only based on mortality data.












Terry S. Singeltary Sr. on the Creutzfeldt-Jakob Disease Public Health Crisis
























full text with source references ;
















PLEASE REMEMBER ;






The Akron, Ohio-based CJD Foundation said the Center for Disease Control revised that number in October of 2004 to about one in 9,000 CJD cases per year in the population group age 55 and older.




HAVE YOU GOT YOUR CJD QUESTIONNAIRE ASKING REAL QUESTIONS PERTAINING TO ROUTE AND SOURCE OF THE TSE AGENT THAT KILLED YOUR LOVED ONE ???




if not, why not...






Friday, November 30, 2007




CJD QUESTIONNAIRE USA CWRU AND CJD FOUNDATION




















Monday, April 16, 2012




Continuing Enhanced National Surveillance for Prion Diseases in the United States












Wednesday, April 25, 2012




USA MAD COW DISEASE AND CJD THERE FROM SINGELTARY ET AL 1999 - 2012










U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001










Information released on 2 February  2005



Summary of information requested



What statistics are available on cattle less than 30 months of age found to have BSE?



Information released


VLA has recorded approximately 100 cases of BSE in cattle of 30 months of age or under during the entire period of the BSE epidemic (1986 - 2005). The figure is approximate as for 51 of these the age is only estimated. This is because farmers did not have accurate documentation to confirm birth date. This was not a requirement at the time.



We can confirm that of the 100 cases, 49 were under 30 months of age, of these the youngest case was 20 months old.



http://vla.defra.gov.uk/vla/vla_ati_020205.htm





http://bseyoungestage.blogspot.com/2008/05/bse-youngest-age-statistics-under-30.html









layperson




Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518 flounder9@verizon.net


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