From Gate to Plate, BSE, USDA, NAIS, AND TRACEABILITY
Traceability: From Gate to Plate
Wyatt Bechtel August 9, 2018 05:50 AM Print
Kansas pilot project aims at improving cattle traceability. ( Wyatt Bechtel ) Traceability in the U.S. beef industry lags behind other global competitors. Australia launched its National Livestock Identification System in 1999, helping the island country gain a foothold in the European Union and Asian markets. Uruguay and New Zealand are a few other major beef exporters who have started cattle traceability systems in the past decade. Those countries all began traceability in their cattle herds to help monitor diseases in an effort to reduce the risk of an outbreak.
Meanwhile, adoption of traceability systems for cattle in the U.S. haven’t been taken on nationally or even at the state level, but producers do have an interest in securing the beef supply. A recent study conducted by World Perspectives, Inc. surveying more than 600 beef industry members found that 57% of producers support animal identification at the ranch of origin. The study also revealed 62% of producers support the idea that information generated by an animal identification and traceability system should be made available to government entities in the event of a disease outbreak.
Cattle traceability may soon have a framework in the U.S. thanks to a pilot project that is being led in Kanas. A public-private partnership called Cattle Trace has the aim to test and develop a cattle disease traceability infrastructure in Kansas that can be used as an example nationally.
“We have the opportunity to develop a cattle disease traceability system on our terms. The capabilities of Cattle Trace will enable us to do the right thing for animal health and biosecurity, and for the entire U.S. beef cattle industry,” says Brandon Depenbusch, vice president of cattle operations for Innovative Livestock Services (ILS), a cattle feeding group with nine yards in Kansas and Nebraska.
Ultra-high frequency technologies will be utilized in Cattle Trace to collect the minimal data necessary, including an individual animal identification number, a GPS location, and date and time, in order to track animals in the event of a disease outbreak.
At least ten feedlots plan to participate in the pilot project along with ILS. The project will also include participation from livestock markets, cow-calf ranches and beef processors who will have tag readers to monitor cattle movement. Beginning in fall 2018, movement data will be collected and the project plans to continue for approximately two years.
“We know for a traceability system to be effective, it needs to be simple, fast, and affordable to make its adoption within the industry as seamless as possible,” says Brad White, director of the Beef Cattle Institute at Kansas State University. “We are working to build a system to test today and one that will serve the U.S. beef cattle industry in the future.”
CattleTrace is a collaborative partnership between Kansas State University, the Kansas Livestock Association (KLA), the Kansas Department of Agriculture (KDA), USDA and individual producers. Funding is coming both from the public and private sector.
“KLA members have long recognized the importance of traceability for animal disease purposes to help protect their livelihoods and the industry,” says Matt Teagarden, Chief Executive Officer of KLA. “We are excited to be part of this effort to move traceability forward for Kansas producers and ultimately the entire U.S. livestock sector.”
In 2017, KLA members amended policy to support mandatory cattle disease traceability for all ages of cattle.
“The development of CattleTrace is a direct result of proactive leaders in the Kansas beef industry recognizing an opportunity to develop a traceability system that works for producers,” says Kansas Secretary of Agriculture Jackie McClaskey. “We have seen tremendous leadership from industry partners ready to step up and take an active role on this critical issue.”
“We are proud that the Kansas beef industry has taken the lead in this important project that will enhance our ability to protect cattle health here and across the nation,” says Governor Jeff Colyer.
Related Topics: Kansas BEEF Animal health Cattle Feedyard Fed Cattle feeder
i have a problem with this part;
''The study also revealed 62% of producers support the idea that information generated by an animal identification and traceibility system should be made available to government entities in the event of a disease outbreak.'' ...end
my opinion, the public needs to have this information as well. we are the one's buying and consuming your product. IF you will not be truthful, the consumer will stop buying your product.
the trace out and trace in of BSE exposed was seriously flawed with the cases of mad cow disease in the USA, and the surveillance and any potential disease outbreak of critical demise and transmission to other animals and species is exactly what we need, but to suppress this information to the public will only bring forth great suspicion to the public, when the information does get out, and i assure you, it will. to think that mad cow disease has gone away is laughable. it's here, it's mutating, and it is spreading. if you don't test, you don't find, but the problem is not solved, because it will eventually find you. the USA mad cow feed ban is a recipe for disaster with the recent findings that cwd and scrapie spreads to pigs by the oral route. you have feed now that has all kinds of tse prion mixed in, and if and when, if it has not already, some of this TSE Prion that transmits vertically and/or horizontally in cattle as it does in cervid and Caprinae, you keep rolling the dice, you crap out eventually, and that price of tse prion poker just keeps going up...and up$$$ tracing of cattle that was exposed to the madcow in Texas back in 2005 was a joke. need to fix this...
***> NEW TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION DISEASE (MAD CAMEL DISEASE) IN A NEW SPECIES <***
NEW OUTBREAK OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHY TSE PRION DISEASE IN A NEW SPECIES
Subject: Prion Disease in Dromedary Camels, Algeria
Our identification of this prion disease in a geographically widespread livestock species requires urgent enforcement of surveillance and assessment of the potential risks to human and animal health.
Wednesday, May 30, 2018
Dromedary camels in northern Africa have a neurodegenerative prion disease that may have originated decades ago
***> IMPORTS AND EXPORTS <***
SEE MASSIVE AMOUNTS OF BANNED ANIMAL PROTEIN AKA MAD COW FEED IN COMMERCE USA DECADES AFTER POST BAN
TUESDAY, AUGUST 07, 2018
Cervid Health Operational Plan Fiscal Year 2018 Animal and Plant Health Inspection Services Veterinary Services
TUESDAY, AUGUST 07, 2018
Passage of scrapie to deer results in a new phenotype upon return passage to sheep
WEDNESDAY, JULY 11, 2018
CONFIDENTIAL IN CONFIDENCE SPONGIFORM ENCEPHALOPATHY OF PIGS FDA EMERGENCY REQUEST FOR RULE CHANGE USA Section 21 C.F.R. 589.2000
TUESDAY, JULY 10, 2018
CONFIDENTIAL IN CONFIDENCE SPONGIFORM ENCEPHALOPATHY OF PIGS
*** ''but feeding of other ruminant protein, including scrapie-infected sheep, can continue to pigs.''
CONFIDENTIAL SPONGIFORM ENCEPHALOPATHY OF PIGS
*** Singeltary reply ; Molecular, Biochemical and Genetic Characteristics of BSE in Canada Singeltary reply ;
>>> The occurrence of atypical cases of BSE in countries such as Canada with low BSE prevalence and transmission risk argues for the occurrence of sporadic forms of BSE worldwide. <<<
In my opinion ;
THE statement above is about as non-scientific as a statement can be. There is no proof what-so-ever that any of the atypical BSE cases or atypical scrapie cases anywhere on the globe was a spontaneous case without any route and source of the TSE agent. This is a myth. The USDA and the OIE are trying to make the atypical BSE cases and they have already made the atypical Scrapie cases a legal trading commodity, without any transmission studies first confirming that in fact these atypical TSE will not transmit via feed. I suppose it is a human transmission study in progress. IT's like what happened in England with c-BSE and the transmission to humans via nvCJD never happened to the OIE and the USDA. Canada does not have a low prevalence of BSE either, they have a high prevalence. WHO knows about North America ? it's just that the U.S.A. try's much harder at concealing cases of mad cow disease. THIS was proven with the first stumbling and staggering mad cow in Texas, that was Wisk away to be rendered without any test at all. Then, you had the second case of mad cow disease that the USDA et al was almost as successful with as the first one, but the O.I.G. stepped in and demanded testing over seas, this after many scientist around the globe spoke out. Finally, after an act of Congress, the second case of mad cow disease in Texas was confirmed. all this was done for a reason, and that reason was the OIE USDA BSE MRR policy. Again, This study reeks of TRADE policy wrangling. There is NO proof that the atypical TSE are spontaneous. please show me these transmission studies ? on the other hand, we now know that the L-type atypical BSE is much more virulent than the typical C-BSE, and we now know that the H-type atypical BSE will transmit to humans. WHY can it not be that these atypical cases are simply from feed that had different strains of TSE ? WHY is it that no one will comment on the studies that was suppose to show infectivity of tissues from atypical BSE ? WHY is it I had to file a FOIA on that issue? L-type atypical BSE (BASE) is more virulent than classical BSE, has a lymphotropic phenotype, and displays a modest transmission barrier in our humanized mice. BSE-H is also transmissible in our humanized Tg mice. SEE
*** It also suggests a similar cause or source for atypical BSE in these countries. ***
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. ***
see page 176 of 201 pages...tss
SATURDAY, JULY 21, 2018
Chronic Wasting Disease: new experience in Europe
TUESDAY, JULY 03, 2018
Chronic Wasting Disease CWD TSE Prion Global Report Update, USA, CANADA, KOREA, NORWAY, FINLAND, Game Farms and Fake news
SUNDAY, APRIL 8, 2018
Transmissible Spongiform Encephalopathy TSE Prion Disease Global Pandemic Urgent Update April 9, 2018
TUESDAY, AUGUST 7, 2018
Unexpected prion phenotypes in experimentally transfused animals: predictive models for humans?
TUESDAY, JULY 31, 2018
USA CJD TSE Tables of Cases Examined National Prion Disease Pathology Surveillance Center Cases Examined May 1, 2018
BSE, USDA, NAIS, AND TRACEABILITY
Let's look at how the USDA et al trace BSE aka mad cow cases, birth, and index herd cattle in the past (or rather how they could not trace them).
TEXAS MAD COW (h-BSE), that was finally tested and documented 7+ months after an act of Congress, and Scientist from all over the Globe questioning the testing methods and negative findings of this Texas mad cow. ...
TEXAS h-BSE MAD COW CASE THAT WAS FINALLY DOCUMENTED
***> The animal of interest traced to this herd was classified as untraceable because all leads were exhausted.
this seemed to be the excuse of the day on countless trace efforts of this madcow outbreak in Texas...terry see;
PRION 2018 CONFERENCE ABSTRACT;
READING OVER THE Prion 2018 Book of Absracts, seems they found that;
O10 Zoonotic potential of atypical BSE prions: a systematic evaluation
Marín-Moreno A (1), Espinosa JC (1), Douet JY (2), Aguilar-Calvo P (1), Píquer J (1), Lorenzo P (1), Lacroux C (2), Huor A (2), Lugan S (2), Tillier C (2), Andreoletti O (2) and Juan María Torres (1)
Our results confirm that L-BSE transmits to TgMet129 even better than epidemic BSE. However, atypical L-BSE agent was unable to infect TgVal129 or TgMet/Val129 mice, even after passage in TgMet129. No transmission was observed with H-BSE in any mice model inoculated, irrespectively of the 129 polymorphism.
***>After passage in sheep PrP expressing host, the properties of both H and LBSE including their capacity to cross the human species barrier were dramatically affected, emerging prion strains features that resemble those of sporadic Creutzfeldt-Jakob disease (sCJD). To date, this is the more extensive and complete analysis of the zoonotic potential of atypical BSE prions.
***>These results advise not to ignore the zoonotic potential of these agents.
also, another study;
P77 In vitro approach to estimate the human transmission risk of prions
Iwamaru Y (1) Imamura M (2) Matsuura Y (1) Kohtaro Miyazawa (1) Takashi Yokoyama (3) (1 ) National Institute of Animal Health, Prion Disease Unit, Ibaraki, Japan (2) University of Miyazaki, Division of Microbiology, Miyazaki, Japan (3) National Institute of Animal Health, Department of Planning and General Administration, Ibaraki, Japan.
snip...
In attempt to develop the more time- and cost-saving method for assessment of the human transmission risk of prions, we performed experiments using protein misfolding cyclic amplification (PMCA) technique to investigate whether PMCA can be compatible with bioassay. Using brain homogenates of Tg expressing bovine PrP as the PrP substrate, we optimized the versatile PMCA condition that could amplify PrPSc from cattle affected with C-, H- or L-BSE.
***>We measured the 50% PMCA seeding activity dose and the 50% lethal dose in 1 g equivalent of C-, H- or L-BSE cattle brain tissue by using PMCA or bioassay, respectively, and assessed the correlations between these doses.
and also this study;
P98 The agent of H-type bovine spongiform encephalopathy associated with E211K prion protein polymorphism transmits after oronasal challenge
Greenlee JJ (1), Moore SJ (1), and West Greenlee MH (2)
This study demonstrates that the H-type BSE agent is transmissible by the oronasal route. These results reinforce the need for ongoing surveillance for classical and atypical BSE to minimize the risk of potentially infectious tissues entering the animal or human food chains.
Sunday, February 25, 2018
PRION ROUND TABLE CONFERENCE 2018 MAY, 22-25 A REVIEW
sadly, i remember trying to tell them this long ago;
2009 UPDATE ON ALABAMA AND TEXAS MAD COWS 2005 and 2006
LET'S take a closer look at this new prionpathy or prionopathy, and then let's look at the g-h-BSEalabama mad cow.
This new prionopathy in humans?
the genetic makeup is IDENTICAL to the g-h-BSEalabama mad cow, the only _documented_ mad cow in the world to date like this, ......
wait, it get's better. this new prionpathy is killing young and old humans, with LONG DURATION from onset of symptoms to death, and the symptoms are very similar to nvCJD victims, OH, and the plaques are very similar in some cases too, bbbut, it's not related to the g-h-BSEalabama cow,
WAIT NOW, it gets even better, the new human prionpathy that they claim is a genetic TSE, has no relation to any gene mutation in that family. daaa, ya think it could be related to that mad cow with the same genetic make-up ???
there were literally tons and tons of banned mad cow protein in Alabama in commerce, and none of it transmitted to cows, and the cows to humans there from ??? r i g h t $$$
ALABAMA MAD COW g-h-BSEalabama
In this study, we identified a novel mutation in the bovine prion protein gene (Prnp), called E211K, of a confirmed BSE positive cow from Alabama, United States of America.
This mutation is identical to the E200K pathogenic mutation found in humans with a genetic form of CJD.
This finding represents the first report of a confirmed case of BSE with a potential pathogenic mutation within the bovine Prnp gene.
We hypothesize that the bovine Prnp E211K mutation most likely has caused BSE in "the approximately 10-year-old cow" carrying the E221K mutation.
Saturday, August 14, 2010
BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY (see mad cow feed in COMMERCE IN ALABAMA...TSS)
her healthy calf also carried the mutation (J. A. Richt and S. M. Hall PLoS Pathog. 4, e1000156; 2008). This raises the possibility that the disease could occasionally be genetic in origin. Indeed, the report of the UK BSE Inquiry in 2000 suggested that the UK epidemic had most likely originated from such a mutation and argued against the scrapierelated assumption. Such rare potential pathogenic PRNP mutations could occur in countries at present considered to be free of BSE, such as Australia and New Zealand. So it is important to maintain strict surveillance for BSE in cattle, with rigorous enforcement of the ruminant feed ban (many countries still feed ruminant proteins to pigs). Removal of specified risk material, such as brain and spinal cord, from cattle at slaughter prevents infected material from entering the human food chain. Routine genetic screening of cattle for PRNP mutations, which is now available, could provide additional data on the risk to the public. Because the point mutation identified in the Alabama animals is identical to that responsible for the commonest type of familial (genetic) CJD in humans, it is possible that the resulting infective prion protein might cross the bovine-human species barrier more easily. Patients with vCJD continue to be identified. The fact that this is happening less often should not lead to relaxation of the controls necessary to prevent future outbreaks. Malcolm A. Ferguson-Smith Cambridge University Department of Veterinary Medicine, Madingley Road, Cambridge CB3 0ES, UK e-mail: maf12@cam.ac.uk Jürgen A. Richt College of Veterinary Medicine, Kansas State University, K224B Mosier Hall, Manhattan, Kansas 66506-5601, USA NATURE|Vol 457|26 February 2009
Thursday, July 24, 2014
*** Protocol for further laboratory investigations into the distribution of infectivity of Atypical BSE SCIENTIFIC REPORT OF EFSA New protocol for Atypical BSE investigations
snip...see full text ;
Saturday, August 14, 2010
BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY
UPDATE
I ask Professor Kong ; Thursday, December 04, 2008 3:37 PM
Subject: RE: re--Chronic Wating Disease (CWD) and Bovine Spongiform Encephalopathies (BSE): Public Health Risk Assessment
''IS the h-BSE more virulent than typical BSE as well, or the same as cBSE, or less virulent than cBSE? just curious.....''
Professor Kong reply ;
.....snip
''As to the H-BSE, we do not have sufficient data to say one way or another, but we have found that H-BSE can infect humans. I hope we could publish these data once the study is complete. Thanks for your interest.''
Best regards, Qingzhong Kong, PhD Associate Professor Department of Pathology Case Western Reserve University Cleveland, OH 44106 USA END...TSS
Thursday, December 04, 2008 2:37 PM
"we have found that H-BSE can infect humans."
personal communication with Professor Kong. ...TSS
BSE-H is also transmissible in our humanized Tg mice. The possibility of more than two atypical BSE strains will be discussed.
Supported by NINDS NS052319, NIA AG14359, and NIH AI 77774.
please see below from PRION2013 ;
** This study imply the possibility that the novel BSE prions with high virulence in cattle will be emerged during intraspecies transmission.
AD.56: The emergence of novel BSE prions by serial passages of H-type BSE in bovinized mice
Kentaro Masujin, Naoko Tabeta, Ritsuko Miwa, Kohtaro Miyazawa, Hiroyuki Okada, Shirou Mohri and Takashi Yokoyama National Institute of Animal Health; Tsukuba, Japan
H-type bovine spongiform encephalopathy (BSE) is an atypical form of BSE, and has been detected in several European countries, and North America. Transmission studies of H-type BSE led to the emergence of the classical BSE (C-BSE) phenotypes during passages in inbred wild type and bovinized PrP-overexpressing transgenic mice. In this study, we conducted serial passages of Canadian H-type BSE isolate in bovinized PrP-overexpressing transgenic mice (TgBoPrP). H-type BSE isolate was transmitted to TgBoPrP with incubation periods of 320 ± 12.2 d at primary passage. The incubation period of 2nd and 3rd passage were constant (~= 220 d), no clear differences were observed in their biological and biochemical properties. However, at the forth passage, 2 different BSE phenotypes were confirmed; one is shorter survival times (109 ± 4 d) and the other is longer survival times. TgBoPrP mice with longer incubation period showed the H-type phenotype of PrPsc profile and pathology. However, those of shorter incubation period were different phenotypes from previously existed BSE prions (C-BSE, L-type BSE, and H-type BSE).
*** This study imply the possibility that the novel BSE prions with high virulence in cattle will be emerged during intraspecies transmission.
www.landesbioscience.com
please see ;
Thursday, August 15, 2013
The emergence of novel BSE prions by serial passages of H-type BSE in bovinized mice
SUNDAY, JUNE 3, 2018
Clinical, pathological, and molecular features of classical and L-type atypical-BSE in goats
Terry S. Singeltary Sr.
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