Hallmark/Westland Meat Packing Co., a Chino, Calif., establishment, is voluntarily recalling approximately 143,383,823 pounds of raw and frozen beef products that FSIS has determined to be unfit for human food because the cattle did not receive complete and proper inspection. Through evidence obtained by FSIS, the establishment did not consistently contact the FSIS public health veterinarian in situations in which cattle became non-ambulatory after passing ante-mortem inspection, which is not compliant with FSIS regulations.
Such circumstances require that an FSIS public health veterinarian reassess the non-ambulatory cattle which are either condemned and prohibited from the food supply, or tagged as suspect. Suspect cattle receive a more thorough inspection after slaughter than is customary.
This noncompliant activity occurred occasionally over the past two years and therefore all beef product produced during the period of time for which evidence indicates such activity occurred has been determined by FSIS to be unfit for human consumption, and is, therefore, adulterated.
This recall is designated as Class II due to the remote probability that the beef being recalled would cause adverse health effects if consumed. FSIS made this determination because the animals passed ante-mortem inspection but should have been identified as suspect requiring additional inspection after slaughter to determine if there is evidence of disease, injury, or other signs of abnormalities that may have occurred after ante-mortem inspection.
In July 2007, FSIS issued a final rule “Prohibition of the Use of Specified Risk Materials for Human Food and Requirements for the Disposition of Non-Ambulatory Disabled Cattle.” This rule requires that a case by case disposition must be made by an FSIS Public Health Veterinarian for every animal that becomes non-ambulatory disabled (“downer”) after passing ante-mortem inspection.
The prohibition of downer cattle from entering the food supply is only one measure in an interlocking system of controls the federal government has in place to protect the food supply. The government has multiple safeguards regarding BSE in place and the prevalence of the disease in the United States is extremely low. Other BSE security measures include the feed ban that prohibits feeding ruminant protein to other ruminants and an ongoing BSE surveillance program that began before the confirmation of the first BSE positive cow in the U.S. in 2003.
As another measure to reduce the risk of potential exposure to consumers, FSIS requires the removal of specified risk materials (SRM) so they do not enter the food supply. Several FSIS line inspectors are stationed at designated points along the production line where they are able to directly observe SRM removal activities.
The products subject to this recall were sent to wholesale distributors nationwide in bulk packages and are not available for direct purchase by consumers. All products subject to recall bear the establishment number “EST. 336” inside the USDA mark of inspection. The products were produced on various dates from Feb. 1, 2006 to Feb. 2, 2008. Companies are urged to check their inventories and hold the products until the recalling firm makes arrangements for final disposition of the products.
The following products are subject to recall: [View Labels]
http://www.fsis.usda.gov/images_recalls/005-2008_Labels.pdf
SEE FULL TEXT ;
http://www.fsis.usda.gov/PDF/Recall_005-2008_Release.pdf
Saturday, June 25, 2011
Transmissibility of BSE-L and Cattle-Adapted TME Prion Strain to Cynomolgus Macaque
"BSE-L in North America may have existed for decades"
http://transmissiblespongiformencephalopathy.blogspot.com/2011/06/transmissibility-of-bse-l-and-cattle.html
Wednesday, February 27, 2008
BEEF RECALL NATIONWIDE - SCHOOL LUNCH PROGRAM UPDATE
UNLIKE the typical uk bse strain, the last two mad cows _documented_ in the USA were h-BASE. IT is MORE VIRULENT TO HUMANS.
PLEASE, they keep saying that NO ONE HAS GOT SICK ???
for pete's sake with mad cow disease in humans, YOU CAN BE EXPOSED AND NOT KNOW IT, AND INCUBATE THE DISEASE FOR AS LONG AS UP TO 50 YEARS BEFORE GOING CLINICAL, and it could be much shorter too, BUT ONCE CLINICAL, CJD/TSEs ARE 100% FATAL!
OH, and about that mad cow ruminant to ruminant SRM feed ban, and other slaughter- houses letting sick and diseased cattle going to the food supply. they claim the feed ban is what the other safe guard is for downers. let's take a look, first at a few other plants allowing sick and diseased animals to enter the food supply, and then a few SRM warning letters and such ;
THESE are just a few examples for DISEASED cattle that likely entered the food supply.
On January 18, 2002, FDA's New Orleans District Office issued a Warning Letter to J. Randall Mayes, Pulaski, Tennessee, a dairy farmer. An FDA inspection conducted November 26 28, 2001, confirmed that the farmer sold a cow for use as human food containing gentamicin residues. USDA analysis of tissue samples from the cow sold by Mayes identified the presence of 7.12 ppm of gentamicin in the kidney tissue. There is no established tolerance for gentamicin in cattle. In addition, FDA's investigation found that the dairy farmer held animals under conditions which were so inadequate that diseased animals and/or medicated animals bearing potentially harmful drug residues were likely to enter the food supply.
http://www.fda.gov/ora/about/enf_story/archive/2002/ch5/cvm1.htm
The Warning Letter also noted that the owner holds animals under conditions which are so inadequate that diseased animals and/or medicated animals bearing potentially harmful drug residues are likely to enter the food supply.
http://www.fda.gov/ora/about/enf_story/archive/2001/ch5/default.htm
Mr. Sturm was found to hold animals on his farm under conditions that are so inadequate that diseased animals and/or medicated animals bearing potentially harmful drug residues are likely to enter the food supply. In addition, he failed to use the drug, Albon, containing sulfadimethoxine, in conformance with the labeling.
A warning letter was issued to the following firms for violations related to 21 CFR Part 589.2000—Animal Proteins Prohibited in Ruminant Feed. This regulation is intended to prevent the establishment and amplification of Bovine Spongiform Encephalopathy (BSE).
• Scott Nelson, Owner, Integra Fish Foods, Inc., Grand Junction, CO
• Bruce A. Burgett, General Manager, The Carrollton Farmers Exchange, Carrollton, OH
Violations included failure to label feeds that contain, or may contain, prohibited materials with the required cautionary statement "Do Not Feed to Cattle or Other Ruminants," insufficient customer records to track the distribution of products, and lack of written procedures for cleaning or flushing equipment after mixing feeds containing prohibited material.
http://www.fda.gov/cvm/Sep_Oct01.htm
Mr. Van Dam was found to hold animals under improper conditions whereby diseased animals and/or medicated animals bearing potentially harmful drug residues are likely to enter the food supply.
Ms. Silveira was found to be adulterating the drug Mutual Pharmaceutical brand of sulfamethoxazole and trimethoprim tablets, since she did not follow her veterinarian's prescribed withdrawal time of thirty days prior to slaughter.
Mr. Edwards did not properly identify treated animals to assure they are not sold for slaughter, did not maintain treatment records, and he did not follow labeling directions for medicated feed.
O & L Dairy was found to lack an adequate system for determining the medication status of animals offered for slaughter, and for assuring that animals which had been medicated had been withheld from slaughter for the appropriate periods of time to deplete potentially hazardous residues of drugs.
Mr. Sturm was found to hold animals on his farm under conditions that are so inadequate that diseased animals and/or medicated animals bearing potentially harmful drug residues are likely to enter the food supply. In addition, he failed to use the drug, Albon, containing sulfadimethoxine, in conformance with the labeling.
A warning letter was issued to the following firms for violations related to 21 CFR Part 589.2000—Animal Proteins Prohibited in Ruminant Feed. This regulation is intended to prevent the establishment and amplification of Bovine Spongiform Encephalopathy (BSE).
• Scott Nelson, Owner, Integra Fish Foods, Inc., Grand Junction, CO
• Bruce A. Burgett, General Manager, The Carrollton Farmers Exchange, Carrollton, OH
Violations included failure to label feeds that contain, or may contain, prohibited materials with the required cautionary statement "Do Not Feed to Cattle or Other Ruminants," insufficient customer records to track the distribution of products, and lack of written procedures for cleaning or flushing equipment after mixing feeds containing prohibited material.
http://www.fda.gov/cvm/Sep_Oct.htm
Our investigation also found that you hold animals on your farm under conditions that are so inadequate that diseased animals and/or medicated animals bearing potentially harmful drug residues are likely to enter the food supply. For example, you failed to maintain treatment records for bull calves fed medicated milk replacer, lack a system for assuring that the milk replacer is used in a manner not contrary to label instructions, and lack a system for assuring the medicated animals have been withheld from slaughter for appropriate periods of time to permit depletion of potentially hazardous drug residues from edible tissues. Foods from animals held under such conditions are adulterated under Section 402(a)(4) of the Act [21 U.S.C. Section 342(a)(4)].
http://www.fda.gov/foi/warning_letters/archive/awl2.htm
Our investigation also found that you hold animals on your farm under conditions that are so inadequate that diseased animals and lormedicated animals bearing potentially harmful drug residues are likely to enter the food supply. For example, you lack a system for assuring that drugs are used in a manner not contrary to label instructions, and for assuring animals medicated on your farrn have been withheld from slaughter for appropriate periods of time to permit depletion of potentially hazardous drug residues from edible tissues. Foods from animals held under such conditions are adulterated under Section 402(a)(4) of the Act.
http://www.fda.gov/foi/warning_letters/archive/awl6.htm
Our investigation also found that you hold animals which are ultimately offered for slaughter as food, under conditions which are so inadequate that diseased animals and/or medicated animals bearing potentially harmful drug residues are likely to enter the food supply.
John Weststeyn 2 T & J Dairy
http://www.fda.gov/foi/warning_letters/archive/awl130.pdf
FOR IMMEDIATE RELEASE Statement May 4, 2004 Media Inquiries: 301-827-6242 Consumer Inquiries: 888-INFO-FDA
Statement on Texas Cow With Central Nervous System Symptoms On Friday, April 30 th , the Food and Drug Administration learned that a cow with central nervous system symptoms had been killed and shipped to a processor for rendering into animal protein for use in animal feed.
FDA, which is responsible for the safety of animal feed, immediately began an investigation. On Friday and throughout the weekend, FDA investigators inspected the slaughterhouse, the rendering facility, the farm where the animal came from, and the processor that initially received the cow from the slaughterhouse.
FDA's investigation showed that the animal in question had already been rendered into "meat and bone meal" (a type of protein animal feed). Over the weekend FDA was able to track down all the implicated material. That material is being held by the firm, which is cooperating fully with FDA.
Cattle with central nervous system symptoms are of particular interest because cattle with bovine spongiform encephalopathy or BSE, also known as "mad cow disease," can exhibit such symptoms. In this case, there is no way now to test for BSE. But even if the cow had BSE, FDA's animal feed rule would prohibit the feeding of its rendered protein to other ruminant animals (e.g., cows, goats, sheep, bison).
FDA is sending a letter to the firm summarizing its findings and informing the firm that FDA will not object to use of this material in swine feed only. If it is not used in swine feed, this material will be destroyed. Pigs have been shown not to be susceptible to BSE. If the firm agrees to use the material for swine feed only, FDA will track the material all the way through the supply chain from the processor to the farm to ensure that the feed is properly monitored and used only as feed for pigs.
http://www.fda.gov/bbs/topics/news/2004/NEW01061.html
daaa, then the pigs are fed back to cattle. not too brilliant. the TSE agent survives the digestional track. ...tss
From: Terry S. Singeltary Sr. [flounder9@verizon.net] Sent: Thursday, September 08, 2005 6:17 PM To: mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000384/!x-usc:mailto:fsis.regulationscomments@fsis.usda.gov
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
SRM SPECIFIED RISK MATERIALS
RUMINANT TO RUMINANT ANIMAL PROTEIN IN COMMERCE 2006-2007
snip...
If only a proportion of infected cattle can be detected, does testing provide significant consumer protection?
The extent to which testing increases consumer protection is still open to question, especially if other protective measures are in place (see below).
It is conceivable that tissues not previously recognised as infected may still be found as research continues. Infectivity levels are expected to be extremely low, and undetectable with the tools used so far. If these tissues were otherwise consumed then the destruction of the carcase would afford the consumer a greater degree of protection. If the tissues are not sufficiently infectious to pose a health risk, and/or are not consumed, then the additional protection provided may be nil.
Recent results from Japan and Germany confirm this point(2,11,12,14), with positivity or infectivity being detected in some peripheral nerves that would not normally be removed as SRM. The amount of infectivity present is low, and considered be up to 1000-fold lower than the brain. Unpublished evidence suggests that these become positive only after the brain and spinal cord. This therefore confirms that testing and removal of positive animals does provide some additional, as yet unquantifiable, protection to consumers over and above that provided by removal of SRM. Given that detection of positivity or infectivity in some peripheral nerves coincides with the onset of clinical signs, it is probable that such animals would be detected before slaughter, and therefore excluded from the food chain.
http://www.tafsforum.org/position_papers/TAFS_POSITION_PAPER_ON_TESTING_OF_CATTLE_FOR_BSE_070516.pdf
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. MBM IN COMMERCE USA 2007
Date: March 21, 2007 at 2:27 pm PST
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II
___________________________________
PRODUCT
Bulk cattle feed made with recalled Darling’s 85% Blood Meal, Flash Dried, Recall # V-024-2007
CODE
Cattle feed delivered between 01/12/2007 and 01/26/2007
RECALLING FIRM/MANUFACTURER
Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.
Firm initiated recall is ongoing.
REASON
Blood meal used to make cattle feed was recalled because it was cross-contaminated with prohibited bovine meat and bone meal that had been manufactured on common equipment and labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
42,090 lbs.
DISTRIBUTION
WI
___________________________________
PRODUCT
Custom dairy premix products: MNM ALL PURPOSE Pellet, HILLSIDE/CDL Prot-Buffer Meal, LEE, M.-CLOSE UP PX Pellet, HIGH DESERT/ GHC LACT Meal, TATARKA, M CUST PROT Meal, SUNRIDGE/CDL PROTEIN Blend, LOURENZO, K PVM DAIRY Meal, DOUBLE B DAIRY/GHC LAC Mineral, WEST PIONT/GHC CLOSEUP Mineral, WEST POINT/GHC LACT Meal, JENKS, J/COMPASS PROTEIN Meal, COPPINI – 8# SPECIAL DAIRY Mix, GULICK, L-LACT Meal (Bulk), TRIPLE J – PROTEIN/LACTATION, ROCK CREEK/GHC MILK Mineral, BETTENCOURT/GHC S.SIDE MK-MN, BETTENCOURT #1/GHC MILK MINR, V&C DAIRY/GHC LACT Meal, VEENSTRA, F/GHC LACT Meal, SMUTNY, A-BYPASS ML W/SMARTA, Recall # V-025-2007
CODE
The firm does not utilize a code - only shipping documentation with commodity and weights identified.
RECALLING FIRM/MANUFACTURER
Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete.
REASON
Products manufactured from bulk feed containing blood meal that was cross contaminated with prohibited meat and bone meal and the labeling did not bear cautionary BSE statement.
VOLUME OF PRODUCT IN COMMERCE
9,997,976 lbs.
DISTRIBUTION
ID and NV
END OF ENFORCEMENT REPORT FOR MARCH 21, 2007
http://www.fda.gov/Safety/Recalls/EnforcementReports/2007/ucm120446.htm
Subject: MAD COW FEED RECALL USA SEPT 6, 2006 1961.72 TONS IN COMMERCE AL, TN, AND WV
Date: September 6, 2006 at 7:58 am PST
PRODUCT
a) EVSRC Custom dairy feed, Recall # V-130-6;
snip...
PLEASE SEE FULL TEXT AND LONG LAUNDRY LIST OF MAD COW PROTEIN AND SRM ''IN COMMERCE'' ;
snip...
(PLEASE NOTE, .005 grams of TSE tainted mad cow feed is lethal enough to kill a cow. ...tss)
http://madcowspontaneousnot.blogspot.com/2008/02/specified-risk-materials-srm.html
USDA CERTIFIED H-BASE MAD COW SCHOOL LUNCH PROGRAM
http://cjdmadcowbaseoct2007.blogspot.com/2008/02/usda-certified-h-base-mad-cow-school.html
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
Release No. 0046.08
Contact:
USDA Press Office (202) 720-4623
http://cjdmadcowbaseoct2007.blogspot.com/2008/02/release-no-004608-statement-by.html
Thursday, February 21, 2008
TRANSCRIPT: Technical Briefing - Hallmark/Westland Meat Packing Company - (02/21/08)
Release No. 0054.08
http://downercattle.blogspot.com/
http://downercattle.blogspot.com/2008/02/transcript-technical-briefing.html
Geographical BSE Risk (GBR) assessments covering 2000-2006
Date : 01.08.2006
http://www.efsa.europa.eu/EFSA/Scientific_Document/GBR_assessments_table_Overview_assessed_countries_2002-2006.pdf
In this context, a word is in order about the US testing program. After the discovery of the first (imported) cow in 2003, the magnitude of testing was much increased, reaching a level of >400,000 tests in 2005 (Figure 4). Neither of the 2 more recently indigenously infected older animals with nonspecific clinical features would have been detected without such testing, and neither would have been identified as atypical without confirmatory Western blots. Despite these facts, surveillance has now been decimated to 40,000 annual tests (USDA news release no. 0255.06, July 20, 2006) and invites the accusation that the United States will never know the true status of its involvement with BSE.
http://www.cdc.gov/ncidod/EID/vol12no12/06-0965.htm
CDC DR. PAUL BROWN TSE EXPERT COMMENTS 2006
The U.S. Department of Agriculture was quick to assure the public earlier this week that the third case of mad cow disease did not pose a risk to them, but what federal officials have not acknowledged is that this latest case indicates the deadly disease has been circulating in U.S. herds for at least a decade.
The second case, which was detected last year in a Texas cow and which USDA officials were reluctant to verify, was approximately 12 years old.
These two cases (the latest was detected in an Alabama cow) present a picture of the disease having been here for 10 years or so, since it is thought that cows usually contract the disease from contaminated feed they consume as calves. The concern is that humans can contract a fatal, incurable, brain-wasting illness from consuming beef products contaminated with the mad cow pathogen.
"The fact the Texas cow showed up fairly clearly implied the existence of other undetected cases," Dr. Paul Brown, former medical director of the National Institutes of Health's Laboratory for Central Nervous System Studies and an expert on mad cow-like diseases, told United Press International. "The question was, 'How many?' and we still can't answer that."
Brown, who is preparing a scientific paper based on the latest two mad cow cases to estimate the maximum number of infected cows that occurred in the United States, said he has "absolutely no confidence in USDA tests before one year ago" because of the agency's reluctance to retest the Texas cow that initially tested positive.
USDA officials finally retested the cow and confirmed it was infected seven months later, but only at the insistence of the agency's inspector general.
"Everything they did on the Texas cow makes everything USDA did before 2005 suspect," Brown said. ...snip...end
http://www.upi.com/ConsumerHealthDaily/view.php?StoryID=20060315-055557-1284r
CDC - Bovine Spongiform Encephalopathy and Variant Creutzfeldt ... Dr. Paul Brown is Senior Research Scientist in the Laboratory of Central Nervous System ... Address for correspondence: Paul Brown, Building 36, Room 4A-05, ...
http://www.cdc.gov/ncidod/eid/vol7no1/brown.htm
PAUL BROWN COMMENT TO ME ON THIS ISSUE
Tuesday, September 12, 2006 11:10 AM
"Actually, Terry, I have been critical of the USDA handling of the mad cow issue for some years, and with Linda Detwiler and others sent lengthy detailed critiques and recommendations to both the USDA and the Canadian Food Agency."
http://lists.iatp.org/listarchive/archive.cfm?listID=147&startrow=1081
Volume 12, Number 12–December 2006
PERSPECTIVE
On the Question of Sporadic
or Atypical Bovine SpongiformEncephalopathy and
Creutzfeldt-Jakob Disease
Paul Brown,* Lisa M. McShane,† Gianluigi Zanusso,‡ and Linda Detwiler§
A link between BSE and
sporadic CJD has been suggested on the basis of laboratory
studies but is unsupported by epidemiologic observation.
Such a link might yet be established by the discovery
of a specific molecular marker or of particular combinations
of trends over time of typical and atypical BSE and various
subtypes of sporadic CJD, as their numbers are influenced
by a continuation of current public health measures that
exclude high-risk bovine tissues from the animal and
human food chains.
SNIP...
Sporadic CJD
The possibility that at least some cases of apparently sporadic CJD might be due to infection by sporadic cases of BSE cannot be dismissed outright. Screening programs needed to identify sporadic BSE have yet to be implemented, and we know from already extant testing programs that at least a proportion of infected animals have no symptoms and thus would never be identified in the absence of systematic testing. Thus, sporadic BSE (or for that matter, sporadic disease in any mammalian species) might be occurring on a regular basis at perhaps the same annual frequency as sporadic CJD in humans, that is, in the range of 1 case per million animals.
Whether humans might be more susceptible to atypical forms of BSE cannot be answered at this time. Experimentally transmitted BASE shows shorter incubation periods than BSE in at least 1 breed of cattle, bovinized transgenic mice, and Cynomolgus monkeys (12,13). In humanized transgenic mice, BASE transmitted, whereas typical BSE did not transmit (13). Paradoxically, the other major phenotype (H) showed an unusually long incubation period in bovinized transgenic mice (12).
The limited experimental evidence bearing on a possible relationship between BSE and sporadic CJD is difficult to interpret. The original atypical BASE strain of BSE had a molecular protein signature very similar to that of 1 subtype (type 2 M/V) of sporadic CJD in humans (5). In another study, a strain of typical BSE injected into humanized mice encoding valine at codon 129 showed a glycopattern indistinguishable from the same subtype of sporadic CJD (15). In a third study, the glycopatterns of both the H and L strains of atypical BSE evidently did not resemble any of the known sporadic CJD subtypes (12).
To these molecular biology observations can be added the epidemiologic data accumulated during the past 30 years. The hypothesis that at least some cases of apparently sporadic CJD are due to unrecognized BSE infections cannot be formally refuted, but if correct, we might expect by now to have some epidemiologic evidence linking BSE to at least 1 cluster of apparently sporadic cases of CJD. Although only a few clusters have been found (and still fewer published), every proposed cluster that has been investigated has failed to show any common exposure to bovines. For that matter, no common exposure has been shown to any environmental vehicles of infection, including the consumption of foodstuffs from bovine, ovine, and porcine sources, the 3 livestock species known to be susceptible to transmissible spongiform encephalopathies. Additional negative evidence comes from several large case-control studies in which no statistically significant dietary differences were observed between patients with sporadic CJD and controls (16,17).
On the other hand, the difficulty of establishing a link between BSE and CJD may be compounded by our ignorance of the infectious parameters of a sporadic form of BSE (e.g., host range, tissue distribution of infectivity, route of transmission, minimum infectious dose for humans, whether single or multiple). Presumably, these parameters would resemble those of variant CJD; that is, high infectivity central nervous system and lymphoreticular tissues of an infected cow find their way into products consumed by humans. Transmissions that might have occurred in the past would be difficult to detect because meat products are generally not distributed in a way that results in detectable geographic clusters.
Barring the discovery of a specific molecular signature (as in variant CJD), the most convincing clue to an association will come from the observation of trends over time of the incidence of typical and atypical BSE and of sporadic and variant CJD. With 4 diseases, each of which could have increasing, unchanging, or decreasing trends, there could be 81 (34) possible different combinations. However, it is highly likely that the trends for typical BSE and variant CJD will both decrease in parallel as feed bans continue to interrupt recycled contamination. The remaining combinations are thus reduced to 9 (32), and some of them could be highly informative.
For example, if the incidence of atypical BSE declines in parallel with that of typical BSE, its candidacy as a sporadic form of disease would be eliminated (because sporadic disease would not be influenced by current measures to prevent oral infection). If, on the other hand, atypical BSE continues to occur as typical BSE disappears, this would be a strong indication that it is indeed sporadic, and if in addition at least 1 form of what is presently considered as sporadic CJD (such as the type 2 M/V subtype shown to have a Western blot signature like BASE) were to increase, this would suggest (although not prove) a causal relationship (Figure 5).
Recognition of the different forms of BSE and CJD depends upon continuing systematic testing for both bovines and humans, but bovine testing will be vulnerable to heavy pressure from industry to dismantle the program as the commercial impact of declining BSE cases ceases to be an issue. Industry should be aware, however, of the implications of sporadic BSE. Its occurrence would necessitate the indefinite retention of all of the public health measures that exclude high-risk bovine tissues from the animal and human food chains, whereas its nonoccurrence would permit tissues that are now destroyed to be used as before, once orally acquired BSE has disappeared.
SNIP...
PLEASE READ FULL TEXT ;
http://www.cdc.gov/ncidod/EID/vol12no12/06-0965.htm?s_cid=eid06_0965_e
THE SEVEN SCIENTIST REPORT ***
http://www.fda.gov/ohrms/dockets/dockets/02n0273/02n-0273-EC244-Attach-1.pdf
full text ;
http://bse-atypical.blogspot.com/2006/08/bse-atypical-texas-and-alabama-update.html
Thursday, January 31, 2008
Evaluation of the Human Transmission Risk of an Atypical Bovine Spongiform Encephalopathy Prion Strain
J. Virol. doi:10.1128/JVI.02561-07 Copyright (c) 2008, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.
Thursday, January 31, 2008 Evaluation of the Human Transmission Risk of an Atypical Bovine Spongiform Encephalopathy Prion Strain J. Virol. doi:10.1128/JVI.02561-07 Copyright (c) 2008, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.
Evaluation of the Human Transmission Risk of an Atypical Bovine Spongiform Encephalopathy Prion Strain
Qingzhong Kong*, Mengjie Zheng, Cristina Casalone, Liuting Qing, Shenghai Huang, Bikram Chakraborty, Ping Wang, Fusong Chen, Ignazio Cali, Cristiano Corona, Francesca Martucci, Barbara Iulini, Pierluigi Acutis, Lan Wang, Jingjing Liang, Meiling Wang, Xinyi Li, Salvatore Monaco, Gianluigi Zanusso, Wen-Quan Zou, Maria Caramelli, and Pierluigi Gambetti* Department of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA; CEA, Istituto Zooprofilattico Sperimentale, 10154 Torino, Italy; Department of Neurological and Visual Sciences, University of Verona, 37134 Verona, Italy
* To whom correspondence should be addressed. Email: mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000384/!x-usc:mailto:qxk2@case.edu. mhtml:%7B33B38F65-8D2E-434D-8F9B-8BDCD77D3066%7Dmid://00000384/!x-usc:mailto:pxg13@case.edu.
Abstract
Bovine spongiform encephalopathy (BSE), the prion disease in cattle, was widely believed to have only one strain (BSE-C). BSE-C causes the fatal prion disease named new variant Creutzfeldt-Jacob disease in humans. Two atypical BSE strains, BASE (or BSE-L) and BSE-H, have been discovered in several countries since 2004; their transmissibility and phenotypes in humans are unknown. We investigated the infectivity and human phenotype of BASE by inoculating transgenic (Tg) mice expressing the human prion protein with brain homogenates from two BASE-affected cattle. Sixty percent of the inoculated Tg mice became infected after 20-22 months incubation, a transmission rate higher than those reported for BSE-C. A quarter of BASE-infected Tg mice, but none of the Tg mice infected with a sporadic human prion disease, showed presence of pathogenic prion protein isoforms in the spleen, indicating that the BASE prion is intrinsically lymphotropic. The pathological prion protein isoforms in BASE-infected humanized Tg mouse brains are different from those of the original cattle BASE or sporadic human prion disease. Minimal brain spongiosis and long incubation time are observed in the BASE-infected Tg mice. These results suggest that, in humans, BASE is a more virulent BSE strain and likely lymphotropic.
http://jvi.asm.org/cgi/content/abstract/JVI.02561-07v1?papetoc
for those interested, further into this study, it gets very interesting ;
http://cjdmadcowbaseoct2007.blogspot.com/2008/02/evaluation-of-human-transmission-risk.html
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)
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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
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
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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
SEE FULL TEXT ;
Creutzfeldt Jakob Disease Delaware UPDATE
http://cjdmadcowbaseoct2007.blogspot.com/2008/02/creutzfeldt-jakob-disease-delaware.html
Creutzfeldt Jakob Disease Texas
http://cjdtexas.blogspot.com/
FSIS STATES ;
Bovine Spongiform Encephalopathy - "Mad Cow Disease"
In addition, on December 30, 2003, Agriculture Secretary Ann Veneman announced new policies that would further strengthen an existing solid food safety system against BSE. On that date, an immediate ban was enacted to prevent all non-ambulatory disabled cattle from being used in the human food supply. This group contains the HIGHEST risk population of cattle that could possibly have BSE. However, even before this ban, FSIS inspectors at slaughterhouses were condemning all cattle they suspected of showing central nervous system disorders.
snip...
Are meats used in the National School Lunch Program safe?
Yes. USDA's Agricultural Marketing Service (AMS), by specification, does not allow beef that is mechanically separated from bone with automatic deboning systems, advanced lean (meat) recovery (AMR) systems, or powered knives for any commodity programs. USDA procurement specifications for beef specifically prohibit the use of meat from downer animals - animals too sick or injured to walk.
http://www.fsis.usda.gov/Fact_Sheets/Bovine_Spongiform_Encephalopathy_Mad_Cow_Disease/index.asp
Audit Report
Animal and Plant Health Inspection Service
Bovine Spongiform Encephalopathy (BSE) Surveillance Program - Phase II
and
Food Safety and Inspection Service
Controls Over BSE Sampling, Specified Risk Materials, and Advanced Meat Recovery Products - Phase III
Report No. 50601-10-KC January 2006
Finding 2 Inherent Challenges in Identifying and Testing High-Risk Cattle Still Remain
Our prior report identified a number of inherent problems in identifying and testing high-risk cattle. We reported that the challenges in identifying the universe of high-risk cattle, as well as the need to design procedures to obtain an appropriate representation of samples, was critical to the success of the BSE surveillance program. The surveillance program was designed to target nonambulatory cattle, cattle showing signs of CNS disease (including cattle testing negative for rabies), cattle showing signs not inconsistent with BSE, and dead cattle. Although APHIS designed procedures to ensure FSIS condemned cattle were sampled and made a concerted effort for outreach to obtain targeted samples, industry practices not considered in the design of the surveillance program reduced assurance that targeted animals were tested for BSE.
USDA/OIG-A/50601-10-KC Page 27
observe these animals ante mortem when possible to assure the animals from the target population are ultimately sampled and the clinical signs evaluated.
snip...
http://www.usda.gov/oig/webdocs/50601-10-KC.pdf
>>>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.
PLEASE SEE ;
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
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
Friday, September 4, 2009
FOIA REQUEST ON FEED RECALL PRODUCT 429,128 lbs. feed for ruminant animals may have been contaminated with prohibited material Recall # V-258-2009
http://madcowfeed.blogspot.com/2009/09/foia-request-on-feed-recall-product.html
Saturday, August 29, 2009
FOIA REQUEST FEED RECALL 2009 Product may have contained prohibited materials Bulk Whole Barley, Recall # V-256-2009
http://madcowfeed.blogspot.com/2009/08/foia-request-feed-recall-2009-product.html
----- Original Message ----- From: "Terry S. Singeltary Sr."
http://madcowfeed.blogspot.com/2009/11/re-foia-request-on-feed-recall-product.html
Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518
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