Food Safety
California lists possible recipients of recalled Hallmark beef
By Janie Gabbett on 3/5/2008 for Meatingplace.com
It took the California Department of Public Health 120 pages to list nearly 3,000 restaurants and other businesses in the state that may have received some of the two years' worth of beef that Hallmark/Westland Meat Co. recalled last month.
The list, viewable on www.cdph.ca.gov, could be over the top, however. Some food distributors told Nation's Restaurant News they gave California officials their entire customer list rather than a roster of the restaurants that purchased the recalled beef.
The agency has also posted a list of products recalled by companies including ConAgra Foods, Kirkland, General Mills, Nestle and Richwood Meat because they could have contained meat involved in the recall.
No illnesses have been linked to the Class II recall that USDA prompted after videos shot by the Humane Society of the United States revealed animal handling of downer cows that were out of compliance with USDA's animal welfare rules.
Under current federal rules, retailers of recalled products are not revealed. California law, however, allows the state to reveal the names of businesses that may be selling the food in question. Some consumer groups and U.S. legislators have been calling for federal rule changes to allow such listings nationwide.
http://meatingplace.com/MembersOnly/webNews/details.aspx?item=19962
>>>No illnesses have been linked to the Class II recall that USDA prompted after videos shot by the Humane Society of the United States revealed animal handling of downer cows that were out of compliance with USDA's animal welfare rules. <<<
href="http://dhs.ca.gov/fdb/local/PDF/WestlandRecallRetailDistributionConsolidatedForWeb2-29-08.PDF">http://dhs.ca.gov/fdb/local/PDF/WestlandRecallRetailDistributionConsolidatedForWeb2-29-08.PDF
Additional Products Containing Westland Recalled Beef
http://dhs.ca.gov/fdb/local/PDF/AdditionalProductsContainingWestlandRecalledBeef2-29-08.PDF
IF the USDA and the FDA et al were not in bed with the industry so much, they would come clean with the rest of the states, and produce a list for the public from each state as was done in California. THAT'S just one state folks. nope, all the BSe about how No illnesses have been linked to the Class II recall that USDA prompted from BSE and or h-BASE or any other strain, is just that BS. the USDA knows PERFECTLY WELL that no one would get sick right off the bat from mad cow disease. Every parent out there should be demanding answers, not these same lies. THE USDA should follow every single child that consumed any of these products for the rest of there lives. there is no way out of it now. the product is gone, consumed, and these kids, the elderly, and most everybody in between have been exposed. non-ambulatory i.e. DOWNERS are the most likely to have a Transmissible Spongiform Encephalopathy. WE know it's here, we know why the USDA et al shut down the testing, they did not want to document any more. ...TSS
Science 23 November 2001: Vol. 294. no. 5547, pp. 1726 - 1728 DOI: 10.1126/science.1066838
Reports Estimation of Epidemic Size and Incubation Time Based on Age Characteristics of vCJD in the United Kingdom
Alain-Jacques Valleron,1 Pierre-Yves Boelle,1 Robert Will,2 Jean-Yves Cesbron3
SNIP...
The distribution of the vCJD incubation period that best fits the data within the framework of our model has a mean of 16.7 years, with a standard deviation of 2.6 years. The 95% upper percentile of this distribution is 21.4 years. The 95% confidence interval (CI) of the estimates of the mean and standard deviation is relatively narrow: The 95% CI for the estimate of the mean incubation period is 12.4 to 23.2 years, and the 95% CI of the standard deviation is 0.9 to 8 years (10). The decrease in susceptibility to infection in exposed subjects older than 15 years, as estimated from the parameter , was found to be very sharp: 16% per year of age (CI: 12 to 23%). This means that, under the best fitting hypothesis, an individual aged 20 years in 1981 had 55% less risk of becoming infected than a child aged 15 years (99.9% for an individual aged 70).
http://www.sciencemag.org/
NOW, the price of poker in the USA may be shorter, due to the fact the strain of mad cow disease in the USA is more virulent to humans, thus, the incubation period, for the same titre log of infectivity, via same route and source, might be faster. ...TSS
Communicated by: Terry S. Singeltary Sr.
[In submitting these data, Terry S. Singeltary Sr. draws attention to the steady increase in the "type unknown" category, which, according to their definition, comprises cases in which vCJD could be excluded. The total of 26 cases for the current year (2007) is disturbing, possibly symptomatic of the circulation of novel agents.
Characterization of these agents should be given a high priority. - Mod.CP]
[see also:
snip...
************************************************************ Become a ProMED-mail Premium Subscriber at
************************************************************ Visit ProMED-mail's web site at .
http://pro-med.blogspot.com/2007/11/proahedr-prion-disease-update-2007-07.html
SEE STEADY INCREASE IN SPORADIC CJD IN THE USA FROM 1997 TO 2006. SPORADIC CJD CASES TRIPLED, with phenotype of 'UNKNOWN' strain growing. ...
http://www.cjdsurveillance.com/resources-casereport.html
There is a growing number of human CJD cases, and they were presented last week in San Francisco by Luigi Gambatti(?) from his CJD surveillance collection.
He estimates that it may be up to 14 or 15 persons which display selectively SPRPSC and practically no detected RPRPSC proteins.
http://www.fda.gov/ohrms/dockets/ac/06/transcripts/1006-4240t1.htm
http://www.fda.gov/ohrms/dockets/ac/06/transcripts/2006-4240t1.pdf
PLEASE SEE !
P02.35 Molecular Features of the Protease-resistant Prion Protein (PrPres) in H- type BSE
Biacabe, A-G1; Jacobs, JG2; Gavier-Widén, D3; Vulin, J1; Langeveld, JPM2; Baron, TGM1 1AFSSA, France; 2CIDC-Lelystad, Netherlands; 3SVA, Sweden
Western blot analyses of PrPres accumulating in the brain of BSE- infected cattle have demonstrated 3 different molecular phenotypes regarding to the apparent molecular masses and glycoform ratios of PrPres bands. We initially described isolates (H-type BSE) essentially characterized by higher PrPres molecular mass and decreased levels of the diglycosylated PrPres band, in contrast to the classical type of BSE. This type is also distinct from another BSE phenotype named L-type BSE, or also BASE (for Bovine Amyloid Spongiform Encephalopathy), mainly characterized by a low representation of the diglycosylated PrPres band as well as a lower PrPres molecular mass. Retrospective molecular studies in France of all available BSE cases older than 8 years old and of part of the other cases identified since the beginning of the exhaustive surveillance of the disease in 20001 allowed to identify 7 H- type BSE cases, among 594 BSE cases that could be classified as classical, L- or H-type BSE. By Western blot analysis of H-type PrPres, we described a remarkable specific feature with antibodies raised against the C-terminal region of PrP that demonstrated the existence of a more C-terminal cleaved form of PrPres (named PrPres#2 ), in addition to the usual PrPres form (PrPres #1). In the unglycosylated form, PrPres #2 migrates at about 14 kDa, compared to 20 kDa for PrPres #1. The proportion of the PrPres#2 in cattle seems to by higher compared to the PrPres#1. Furthermore another PK–resistant fragment at about 7 kDa was detected by some more N-terminal antibodies and presumed to be the result of cleavages of both N- and C- terminal parts of PrP. These singular features were maintained after transmission of the disease to C57Bl/6 mice. The identification of these two additional PrPres fragments (PrPres #2 and 7kDa band) *** reminds features reported respectively in sporadic Creutzfeldt-Jakob disease and in Gerstmann-Sträussler-Scheinker (GSS) syndrome in humans.
FC5.5.1 BASE Transmitted to Primates and MV2 sCJD Subtype Share PrP27-30 and PrPSc C-terminal Truncated Fragments
Zanusso, G1; Commoy, E2; Fasoli, E3; Fiorini, M3; Lescoutra, N4; Ruchoux, MM4; Casalone, C5; Caramelli, M5; Ferrari, S3; Lasmezas, C6; Deslys, J-P4; Monaco, S3 1University of Verona, of Neurological and Visual Sciences, Italy; 2CEA, IMETI/SEPIA, France; 3University of Verona, Neurological and Visual Sciences, Italy; 4IMETI/SEPIA, France; 5IZSPLVA, Italy; 6The Scripps Research Insitute, USA
The etiology of sporadic Creutzfeldt-Jakob disease (sCJD), the most frequent human prion disease, remains still unknown. The marked disease phenotype heterogeneity observed in sCJD is thought to be influenced by the type of proteinase K- resistant prion protein, or PrPSc (type 1 or type 2 according to the electrophoretic mobility of the unglycosylated backbone), and by the host polymorphic Methionine/Valine (M/V) codon 129 of the PRNP. By using a two-dimensional gel electrophoresis (2D-PAGE) and imunoblotting we previously showed that in sCJD, in addition to the PrPSc type, distinct PrPSc C-terminal truncated fragments (CTFs) correlated with different sCJD subtypes. Based on the combination of CTFs and PrPSc type, we distinguished three PrPSc patterns: (i) the first was observed in sCJD with PrPSc type 1 of all genotypes,;
(ii) the second was found in M/M-2 (cortical form); (iii) the third in amyloidogenic M/V- 2 and V/V-2 subtypes (Zanusso et al., JBC 2004) . Recently, we showed that sCJD subtype M/V-2 shared molecular and pathological features with an atypical form of BSE, named BASE, thus suggesting a potential link between the two conditions. This connection was further confirmed after 2D-PAGE analysis, which showed an identical PrPSc signature, including the biochemical pattern of CTFs. To pursue this issue, we obtained brain homogenates from Cynomolgus macaques intracerebrally inoculated with brain homogenates from BASE. Samples were separated by using a twodimensional electrophoresis (2D-PAGE) followed by immunoblotting. We here show that the PrPSc pattern obtained in infected primates is identical to BASE and sCJD MV-2 subtype. *** These data strongly support the link, or at least a common ancestry, between a sCJD subtype and BASE.
This work was supported by Neuroprion (FOOD-CT-2004-506579)
************************************************** *****
USA MAD COW CASES IN ALABAMA AND TEXAS
***PLEASE NOTE***
USA BASE CASE, (ATYPICAL BSE), AND OR TSE (whatever they are calling it today), please note that both the ALABAMA COW, AND THE TEXAS COW,both were ''H-TYPE'', personal communication Detwiler et al Wednesday, August 22, 2007 11:52 PM. ...TSS
http://lists.iatp.org/listarchive/archive.cfm?listID=147&startrow=1081
Tuesday, November 17, 2009
SEAC NEW RESULTS ON IDIOPATHIC BRAINSTEM NEURONAL CHROMATOLYSIS (IBNC) FROM THE VETERINARY LABORATORIES AGENCY (VLA) SEAC 103/1
http://bse-atypical.blogspot.com/2009/11/seac-new-results-on-idiopathic.html
2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006
http://bse-atypical.blogspot.com/2006/08/bse-atypical-texas-and-alabama-update.html
Monday, October 19, 2009
Atypical BSE, BSE, and other human and animal TSE in North America Update October 2009
http://bse-atypical.blogspot.com/2009/10/atypical-bse-bse-and-other-human-and.html
Tuesday, November 10, 2009
Surveillance On the Bovine Spongiform Encephalopathy and rabies in Taiwan and USA
http://usdavskorea.blogspot.com/2009/11/surveillance-on-bovine-spongiform.html
**************************************************
FC5.5.2 Transmission of Italian BSE and BASE Isolates in Cattle Results into a Typical BSE Phenotype and a Muscle Wasting Disease
Zanusso, G1; Lombardi, G2; Casalone, C3; D’Angelo, A4; Gelmetti, D2; Torcoli, G2; Barbieri, I2; Corona, C3; Fasoli, E1; Farinazzo, A1; Fiorini, M1; Gelati, M1; Iulini, B3; Tagliavini, F5; Ferrari, S1; Monaco, S1; Caramelli, M3; Capucci, L2 1University of Verona, Neurological and Visual Sciences, Italy; 2IZSLER, Italy; 3IZSPLVA, Italy; 4University of Turin, Animal Pathology, Italy; 5Isituto Carlo Besta, Italy
The clinical phenotype of bovine spongiform encephalopathy has been extensively reported in early accounts of the disorder. Following the introduction of statutory active surveillance, almost all BSE cases have been diagnosed on a pathological/molecular basis, in a pre-symptomatic clinical stage. In recent years, the active surveillance system has uncovered atypical BSE cases, which are characterized by distinct conformers of the PrPSc, named high-type (BSE-H) and low-type (BSE-L), whose clinicopathological phenotypes remain unknown. We recently reported two Italian atypical cases with a PrPSc type similar to BSE-L, pathologically characterized by PrP amyloid plaques. Experimental transmission to TgBov mice has recently disclosed that BASE is caused by a distinct prion strain which is extremely virulent. A major limitation of transmission studies to mice is the lack of reliable information on clinical phenotype of BASE in its natural host. In the present study, we experimentally infected Fresian/Holstein and Alpine/Brown cattle with Italian BSE and BASE isolates by i.c. route. BASE infected cattle showed survival times significantly shorter than BSE, a finding more readily evident in Fresian/Holstein, and in keeping with previous observations in TgBov mice. Clinically, BSE-infected cattle developed a disease phenotype highly comparable with that described in field BSE cases and in experimentally challenged cattle. On the contrary, BASE-inoculated cattle developed an amyotrophic disorder accompanied by mental dullness. The molecular and neuropathological profiles, including PrP deposition pattern, closely matched those observed in the original cases. This study further confirms that BASE is caused by a distinct prion isolate and discloses a novel disease phenotype in cattle, closely resembling the phenotype previous reported in scrapie-inoculated cattle *** and in some subtypes of inherited and sporadic Creutzfeldt-Jakob disease.
Oral Abstracts 14
snip...
P04.27
Experimental BSE Infection of Non-human Primates: Efficacy of the Oral Route
Holznagel, E1; Yutzy, B1; Deslys, J-P2; Lasmézas, C2; Pocchiari, M3; Ingrosso, L3; Bierke, P4; Schulz-Schaeffer, W5; Motzkus, D6; Hunsmann, G6; Löwer, J1 1Paul-Ehrlich-Institut, Germany; 2Commissariat à l´Energie Atomique, France; 3Instituto Superiore di Sanità, Italy; 4Swedish Institute for Infectious Disease control, Sweden; 5Georg August University, Germany; 6German Primate Center, Germany
Background:
In 2001, a study was initiated in primates to assess the risk for humans to contract BSE through contaminated food. For this purpose, BSE brain was titrated in cynomolgus monkeys.
Aims:
The primary objective is the determination of the minimal infectious dose (MID50) for oral exposure to BSE in a simian model, and, by in doing this, to assess the risk for humans. Secondly, we aimed at examining the course of the disease to identify possible biomarkers.
Methods:
Groups with six monkeys each were orally dosed with lowering amounts of BSE brain: 16g, 5g, 0.5g, 0.05g, and 0.005g. In a second titration study, animals were intracerebrally (i.c.) dosed (50, 5, 0.5, 0.05, and 0.005 mg).
Results:
In an ongoing study, a considerable number of high-dosed macaques already developed simian vCJD upon oral or intracerebral exposure or are at the onset of the clinical phase. However, there are differences in the clinical course between orally and intracerebrally infected animals that may influence the detection of biomarkers.
Conclusions:
Simian vCJD can be easily triggered in cynomolgus monkeys on the oral route using less than 5 g BSE brain homogenate. The difference in the incubation period between 5 g oral and 5 mg i.c. is only 1 year (5 years versus 4 years). However, there are rapid progressors among orally dosed monkeys that develop simian v CJD as fast as intracerebrally inoculated animals.
The work referenced was performed in partial fulfilment of the study “BSE in primates“ supported by the EU (QLK1-2002-01096).
http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf
Subject: Aspects of the Cerebellar Neuropathology in Nor98
Date: September 26, 2007 at 4:06 pm PST
P03.141
Aspects of the Cerebellar Neuropathology in Nor98
Gavier-Widén, D1; Benestad, SL2; Ottander, L1; Westergren, E1 1National Veterinary Insitute, Sweden; 2National Veterinary Institute, Norway
Nor98 is a prion disease of old sheep and goats. This atypical form of scrapie was first described in Norway in 1998. Several features of Nor98 were shown to be different from classical scrapie including the distribution of disease associated prion protein (PrPd) accumulation in the brain. The cerebellum is generally the most affected brain area in Nor98. The study here presented aimed at adding information on the neuropathology in the cerebellum of Nor98 naturally affected sheep of various genotypes in Sweden and Norway. A panel of histochemical and immunohistochemical (IHC) stainings such as IHC for PrPd, synaptophysin, glial fibrillary acidic protein, amyloid, and cell markers for phagocytic cells were conducted. The type of histological lesions and tissue reactions were evaluated. The types of PrPd deposition were characterized. The cerebellar cortex was regularly affected, even though there was a variation in the severity of the lesions from case to case. Neuropil vacuolation was more marked in the molecular layer, but affected also the granular cell layer. There was a loss of granule cells. Punctate deposition of PrPd was characteristic. It was morphologically and in distribution identical with that of synaptophysin, suggesting that PrPd accumulates in the synaptic structures. PrPd was also observed in the granule cell layer and in the white matter. *** The pathology features of Nor98 in the cerebellum of the affected sheep showed similarities with those of sporadic Creutzfeldt-Jakob disease in humans.
http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf
Wednesday, July 1, 2009
Nor98 scrapie identified in the United States J Vet Diagn Invest 21:454-463 (2009)
http://nor-98.blogspot.com/2009/07/nor98-scrapie-identified-in-united.html
full text ;
ATYPICAL NOR-98 SCRAPIE LOCATION UPDATE ON 5 DOCUMENTED CASES THIS YEAR ;
The flocks of origin are WY, CO, CA, IN, and MN.
personal communication USDA et al. ...TSS
http://nor-98.blogspot.com/
ANIMAL HEALTH REPORT 2006 (BSE h-BASE EVENT IN ALABAMA, Scrapie, and CWD)
http://animalhealthreport2006.blogspot.com/
CREUTZFELDT JAKOB DISEASE MAD COW BASE UPDATE USA
http://cjdmadcowbaseoct2007.blogspot.com/
CREUTZFELDT JAKOB DISEASE MAD COW BASE UPDATE USA
http://cjdmadcowbaseoct2007.blogspot.com/2008/02/evaluation-of-human-transmission-risk.html
Friday, February 8, 2008
Creutzfeldt Jakob Disease Delaware UPDATE
http://cjdmadcowbaseoct2007.blogspot.com/2008/02/creutzfeldt-jakob-disease-delaware.html
CJD TEXAS
http://cjdtexas.blogspot.com/
Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States
http://cjdusa.blogspot.com/
Creutzfeldt Jakob Disease
http://creutzfeldt-jakob-disease.blogspot.com/
Creutzfeldt-Jakob Disease, Prion Protein Gene Codon 129VV, and a Novel PrPSc Type in a Young British Woman
http://creutzfeldt-jakob-disease.blogspot.com/2008/01/creutzfeldt-jakob-disease-prion-protein.html
Friday, January 11, 2008
CJD HUMAN TSE REPORT UK, USA, CANADA, and Mexico JANUARY 2008
http://cjdmadcowbaseoct2007.blogspot.com/2008/01/cjd-human-tse-report-uk-usa-canada-and.html
Sunday, December 16, 2007
Risk factors for sporadic Creutzfeldt-Jakob disease
Published Online: 11 Dec 2007
http://creutzfeldt-jakob-disease.blogspot.com/2007/12/risk-factors-for-sporadic-creutzfeldt.html
http://creutzfeldt-jakob-disease.blogspot.com/2008/01/risk-factors-for-sporadic-creutzfeldt.html
Monday, December 31, 2007
Risk Assessment of Transmission of Sporadic Creutzfeldt-Jakob Disease in Endodontic Practice in Absence of Adequate Prion Inactivation
http://creutzfeldt-jakob-disease.blogspot.com/2007/12/risk-assessment-of-transmission-of.html
Friday, January 25, 2008
January 2008 Update on Feed Enforcement Activities to Limit the Spread of BSE
http://madcowspontaneousnot.blogspot.com/2008/01/january-2008-update-on-feed-enforcement.html
http://madcowspontaneousnot.blogspot.com/
BSE BASE MAD COW TESTING TEXAS, USA, AND CANADA
http://madcowtesting.blogspot.com/
Sunday, February 17, 2008 Release No. 0046.08
Statement by Secretary of Agriculture Ed Schafer Regarding Hallmark/Westland Meat Packing Company Two Year Product Recall
USDA Press Office (202) 720-4623
http://cjdmadcowbaseoct2007.blogspot.com/2008/02/release-no-004608-statement-by.html
NON-AMBULATORY (DOWNER) COW
http://downercattle.blogspot.com/
Wednesday, February 27, 2008
BEEF RECALL NATIONWIDE - SCHOOL LUNCH PROGRAM UPDATE
http://downercattle.blogspot.com/2008/02/beef-recall-nationwide-school-lunch.html
CJD QUESTIONNAIRE
http://cjdquestionnaire.blogspot.com/
Specified Risk Material SRM
http://madcowspontaneousnot.blogspot.com/2008/02/specified-risk-materials-srm.html
Subject: [Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk Materials for Human Food and Requirements for the Disposition of Non-Ambulatory Disabled Cattle
Greetings FSIS,
I would kindly like to submit the following to [Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk Materials for Human Food and Requirements for the Disposition of Non-Ambulatory Disabled Cattle
THE BSE/TSE SUB CLINICAL
Non-Ambulatory Disabled Cattle Broken bones and such may be the first signs of a sub clinical BSE/TSE Non-Ambulatory Disabled Cattle ;
SUB CLINICAL PRION INFECTION MRC-43-00 Issued: Monday, 28 August 2000
NEW EVIDENCE OF SUB-CLINICAL PRION INFECTION: IMPORTANT RESEARCH FINDINGS RELEVANT TO CJD AND BSE
A team of researchers led by Professor John Collinge at the Medical Research Council Prion Unit1 report today in the Proceedings of the National Academy of Sciences, on new evidence for the existence of a ?sub-clinical? form of BSE in mice which was unknown until now. The scientists took a closer look at what is known as the ?species barrier? - the main protective factor which
limits the ability of prions2 to jump from one species to infect another. They found the mice had a ?sub-clinical? form of disease where they carried high levels of infectivity but did not develop the clinical disease during their normal lifespan. The idea that individuals can carry a disease and show no clinical symptoms is not new. It is commonly seen in conventional infectious diseases. Researchers tried to infect laboratory mice with hamster prions3 called Sc237 and found that the mice showed no apparent signs of disease. However, on closer inspection they found that the mice had high levels of mouse prions in their brains. This was surprising because it has always been assumed that hamster prions could not cause the disease in mice, even when injected directly into the brain. In addition the researchers showed that this new sub-clinical infection could be easily passed on when injected into healthy mice and hamsters. The height of the species barrier varies widely between different combinations of animals and also varies with the type or strain of prions. While some barriers are quite small (for instance BSE easily infects mice), other combinations of strain and species show a seemingly impenetrable barrier. Traditionally, the particular barrier studied here was assumed to be robust. Professor John Collinge said: "These results have a number of important implications. They suggest that we should re-think how we measure species barriers in the laboratory, and that we should not assume that just because one species appears resistant to a strain of prions they have been exposed to, that they do not silently carry the infection.
This research raises the possibility, which has been mentioned before, that apparently healthy cattle could harbour, but never show signs of, BSE. "This is a timely and unexpected result, increasing what we know about prion disease. These new findings have important implications for those researching prion disease, those responsible for preventing infected material getting into the food chain and for those considering how best to safeguard health and reduce the risk that theoretically, prion disease could be contracted through medical and surgical procedures."
ISSUED FRIDAY 25 AUGUST UNDER EMBARGO. PLEASE NOTE THAT THE EMBARGO IS SET BY THE JOURNAL.
http://www.mrc.ac.uk/index/public_interest/public-press_office/public-press_releases_2000/public-mrc-43-00.htm
SNIP...
https://web01.aphis.usda.gov/regpublic.nsf/0/eff9eff1f7c5cf2b87256ecf000df08d?OpenDocument
PNAS August 29, 2000 vol. 97 no. 18 10248-10253 Neurobiology
Species-barrier-independent prion replication in apparentlyresistant species
Andrew F. Hill*, Susan Joiner*, Jackie Linehan*, Melanie Desbruslais*, Peter L. Lantos , and John Collinge*,
SEE FULL TEXT 17 pages ;
http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
CJD QUESTIONNAIRE
http://cjdquestionnaire.blogspot.com/
Specified Risk Material SRM
http://madcowspontaneousnot.blogspot.com/2008/02/specified-risk-materials-srm.html
TSS
Wednesday, February 27, 2008
BEEF RECALL NATIONWIDE - SCHOOL LUNCH PROGRAM UPDATE
http://downercattle.blogspot.com/2008/02/beef-recall-nationwide-school-lunch.html
Beef - Westland/Hallmark Recall OF BEEF WITH DEADSTOCK DOWNER COWS, THE MOST HIGH RISK CATTLE FOR BSE/TSE AKA MAD COW DISEASE
Additional Products Listing 5-20-08
http://www.cdph.ca.gov/pubsforms/Documents/fdb%20eru%20Hmrk%20Addl%20Prod052008.pdf
http://www.cdph.ca.gov/HEALTHINFO/Pages/FDB%20Beef-WestlandHallmarkRecall.aspx
TOTAL DISTRIBUTION LIST
http://www.cdph.ca.gov/pubsforms/Documents/fdb%20eru%20Hmrk%20All%20Dist042008.pdf
ADDITIONAL PRODUCTS CONTAINING RECALLED BEEF
http://www.cdph.ca.gov/pubsforms/Documents/fdb%20eru%20Hmrk%20Addl%20Prod052008.pdf
SEE FULL LIST OF ALL RECALLED SUSPECT DEAD STOCK DOWNER COW PRODUCTS HERE ;
http://www.cdph.ca.gov/HEALTHINFO/Pages/FDB%20Beef-WestlandHallmarkRecall.aspx
Beef - Westland/Hallmark Recall OF BEEF WITH DEADSTOCK DOWNER COWS, THE MOST HIGH RISK CATTLE FOR BSE/TSE AKA MAD COW DISEASE
Additional Products Listing 5-20-08
http://www.cdph.ca.gov/pubsforms/Documents/fdb%20eru%20Hmrk%20Addl%20Prod052008.pdf
http://www.cdph.ca.gov/HEALTHINFO/Pages/FDB%20Beef-WestlandHallmarkRecall.aspx
TOTAL DISTRIBUTION LIST
http://www.cdph.ca.gov/pubsforms/Documents/fdb%20eru%20Hmrk%20All%20Dist042008.pdf
ADDITIONAL PRODUCTS CONTAINING RECALLED BEEF
http://www.cdph.ca.gov/pubsforms/Documents/fdb%20eru%20Hmrk%20Addl%20Prod052008.pdf
SEE FULL LIST OF ALL RECALLED SUSPECT DEAD STOCK DOWNER COW PRODUCTS HERE ;
http://www.cdph.ca.gov/HEALTHINFO/Pages/FDB%20Beef-WestlandHallmarkRecall.aspx
>>>In the papers, the government alleges the meatpacking plant slaughtered and processed downer cows for nearly four years — from January 2004 to September 2007 — <<<
95%) downer or dead dairy cattle and a few horses. Sheep 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
http://web.archive.org/web/20030331063559/http://www.bseinquiry.gov.uk/files/mb/m09a/tab01.pdf
http://web.archive.org/web/20030516051623/http://www.bseinquiry.gov.uk/files/mb/m09/tab05.pdf
IN CONFIDENCE
PERCEPTIONS OF UNCONVENTIONAL SLOW VIRUS DISEASES OF ANIMALS IN THE USA
http://collections.europarchive.org/tna/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf
TSS
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