Two More Countries Lift BSE-Related Bans On U.S. Beef
Apr 2, 2014
U.S. Meat Export Federation
U.S. beef exports gain access to the promising protein markets of Ecuador and Sri Lanka, but China, Australia, Argentina, Brazil, Uruguay, Morocco, Israel, South Africa and Saudi Arabia still retain BSE-related closures.
In March, two trading partners agreed to resume imports of U.S. beef for the first time since December 2003. Ecuador and Sri Lanka were among a handful of nations that had never reopened after the first U.S. case of BSE, but both are now accepting U.S. beef.
Ecuador offers strong potential for U.S. beef offal sales
Exports to Ecuador face very few restrictions, with muscle cuts and offal items from cattle of all ages now eligible.
“That’s a huge bonus in a market where we expect to export a significant volume of offal products,” says Cheyenne Dixon, U.S. Meat Export Federation (USMEF) technical services manager.
The only significant constraint involves beef derived from cattle imported from Canada, in which case the animal must be in the U.S. for 60 days prior to slaughter.
“We hope this restriction is temporary, and it is a point on which the U.S. and Ecuadorian governments continue to negotiate,” Dixon explains. “But products derived from all domestic cattle are eligible, as well as beef from cattle imported from Mexico.”
In addition to providing high-quality beef cuts for Ecuador’s hotel and restaurant sectors, USMEF expects U.S. exporters to find success with variety meat items such as beef tripe, livers and hearts. Two introductory seminars for Ecuadorian importers are planned later this month – one in the capital city of Quito and one in Ecuador’s largest city, Guayaquil.
According to the Global Trade Atlas, Ecuador imported 1,006 metric tons (mt) of beef last year at a value of $4.5 million – down about 10% from 2012. Chile was Ecuador’s leading beef supplier, followed by Uruguay.
Sri Lanka's tourism push offers potential for U.S. beef products
Located off the southeastern coast of India, Sri Lanka was plagued by civil war and ongoing political conflict until 2009. The country was also devastated by a deadly tsunami in 2004. But recently, Sri Lankans have enjoyed a much more peaceful existence, which has led to economic growth and a revitalized tourism sector.
“Sri Lanka has ambitious plans to make it onto the ‘A list’ of Asian tourist destinations, in line with Bali (Indonesia) and several locations in Thailand,” says Joel Haggard, USMEF senior vice president for the Asia Pacific.
Haggard also notes that the capital city of Colombo, which has a greater-metropolitan population of approximately 1.5 million people, has several modern supermarket chains that currently rely mostly on domestic products.
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“Sri Lanka’s retail sector is expanding rapidly and there are certainly growth opportunities there for U.S. beef,” Haggard says.
Recently a group of veterinary officials from Sri Lanka’s Central Department of Animal Production and Health received an in-depth look at the U.S. beef industry as part of the USDA Foreign Agriculture Service’s Cochran Fellowship Program. Tiskumarage Aruni Tiskumara, DVM, who headed the delegation, expressed confidence in the safety and quality of U.S. beef.
“We had good exposure to all of the systems the U.S. beef industry has adopted,” she explains. “We are quite satisfied with the processing regulations and with the biosecurity aspects as well.”
Tiskumara noted that the “negligible risk” designation for BSE from the World Organization for Animal Health, which the U.S. received in May 2013, was a key factor in Sri Lanka’s decision to reopen the market.
“Until the U.S. achieved negligible risk status, we were not interested in U.S. beef,” she said. “But now that you have the negligible risk designation, technically there is no reason why we should not import beef from the U.S.A.”
Sri Lanka is also open to U.S. beef from cattle of all ages. Last year, Sri Lanka imported 74 mt of beef – mostly from Australia – valued at about $400,000.
Markets that remain closed to U.S. beef due to BSE include China, Australia, Argentina, Brazil, Uruguay, Morocco, Israel and South Africa. Saudi Arabia reopened to U.S. beef in 2004, but suspended imports after a BSE case was detected in California in April 2012.
Joe Schuele is communications director for the U.S. Meat Export Federation.
BSE prions propagate as either variant CJD-like or sporadic CJD-like prion strains in transgenic mice expressing human prion protein
Variant Creutzfeldt–Jakob disease (vCJD) has been recognized to date only in individuals homozygous for methionine at PRNP codon 129. Here we show that transgenic mice expressing human PrP methionine 129, inoculated with either bovine spongiform encephalopathy (BSE) or variant CJD prions, may develop the neuropathological and molecular phenotype of vCJD, consistent with these diseases being caused by the same prion strain. Surprisingly, however, BSE transmission to these transgenic mice, in addition to producing a vCJD-like phenotype, can also result in a distinct molecular phenotype that is indistinguishable from that of sporadic CJD with PrPSc type 2. These data suggest that more than one BSE-derived prion strain might infect humans; it is therefore possible that some patients with a phenotype consistent with sporadic CJD may have a disease arising from BSE exposure.
-------- Original Message --------
Subject: re-BSE prions propagate as either variant CJD-like or sporadic CJD
Date: Thu, 28 Nov 2002 10:23:43 -0000
From: "Asante, Emmanuel A" firstname.lastname@example.org
To: "'email@example.com'" firstname.lastname@example.org
I have been asked by Professor Collinge to respond to your request. I am a Senior Scientist in the MRC Prion Unit and the lead author on the paper. I have attached a pdf copy of the paper for your attention.
Thank you for your interest in the paper.
In respect of your first question, the simple answer is, yes. As you will find in the paper, we have managed to associate the alternate phenotype to type 2 PrPSc, the commonest sporadic CJD. It is too early to be able to claim any further sub-classification in respect of Heidenhain variant CJD or Vicky Rimmer's version. It will take further studies, which are on-going, to establish if there are sub-types to our initial finding which we are now reporting. The main point of the paper is that, as well as leading to the expected new variant CJD phenotype, BSE transmission to the 129-methionine genotype can lead to an alternate phenotype which is indistinguishable from type 2 PrPSc.
I hope reading the paper will enlighten you more on the subject. If I can be of any further assistance please to not hesitate to ask. Best wishes.
Dr. Emmanuel A Asante MRC Prion Unit & Neurogenetics Dept. Imperial College School of Medicine (St. Mary's) Norfolk Place, LONDON W2 1PG Tel: +44 (0)20 7594 3794 Fax: +44 (0)20 7706 3272 email: email@example.com (until 9/12/02) New e-mail: firstname.lastname@example.org (active from now)
Thursday, August 12, 2010
Seven main threats for the future linked to prions
The TSE road map defining the evolution of European policy for protection against prion diseases is based on a certain numbers of hypotheses some of which may turn out to be erroneous. In particular, a form of BSE (called atypical Bovine Spongiform Encephalopathy), recently identified by systematic testing in aged cattle without clinical signs, may be the origin of classical BSE and thus potentially constitute a reservoir, which may be impossible to eradicate if a sporadic origin is confirmed.
***Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases constitute an unforeseen first threat that could sharply modify the European approach to prion diseases.
Monday, October 10, 2011
EFSA Journal 2011 The European Response to BSE: A Success Story
EFSA and the European Centre for Disease Prevention and Control (ECDC) recently delivered a scientific opinion on any possible epidemiological or molecular association between TSEs in animals and humans (EFSA Panel on Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical BSE prions as the only TSE agents demonstrated to be zoonotic so far
*** but the possibility that a small proportion of human cases so far classified as "sporadic" CJD are of zoonotic origin could not be excluded. Moreover, transmission experiments to non-human primates suggest that some TSE agents in addition to Classical BSE prions in cattle (namely L-type Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic wasting disease (CWD) agents) might have zoonotic potential.
To date the OIE/WAHO assumes that the human and animal health standards set out in the BSE chapter for classical BSE (C-Type) applies to all forms of BSE which include the H-type and L-type atypical forms. This assumption is scientifically not completely justified and accumulating evidence suggests that this may in fact not be the case. Molecular characterization and the spatial distribution pattern of histopathologic lesions and immunohistochemistry (IHC) signals are used to identify and characterize atypical BSE. Both the L-type and H-type atypical cases display significant differences in the conformation and spatial accumulation of the disease associated prion protein (PrPSc) in brains of afflicted cattle. Transmission studies in bovine transgenic and wild type mouse models support that the atypical BSE types might be unique strains because they have different incubation times and lesion profiles when compared to C-type BSE. When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE.
***In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.
LAST MAD COW IN USA, IN CALIFORNIA, WAS ATYPICAL L-TYPE BASE BSE TSE PRION DISEASE Thursday, February 20, 2014
Unnecessary precautions BSE MAD COW DISEASE Dr. William James FSIS VS Dr. Linda Detwiler 2014
From: Terry S. Singeltary Sr. [email@example.com]
Sent: Monday, July 24, 2006 1:09 PM
To: FSIS RegulationsComments
Subject: [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE) Page 1 of 98
FSIS, USDA, REPLY TO SINGELTARY
Sunday, August 09, 2009
Sunday, August 09, 2009
CJD...Straight talk with...James Ironside...and...Terry Singeltary... 2009
Tuesday, August 18, 2009
* BSE-The Untold Story - joe gibbs and singeltary 1999 - 2009
*** Because typical clinical signs of BSE cannot always be observed in nonambulatory disabled cattle, and because evidence has indicated these cattle are more likely to have BSE than apparently healthy cattle, FDA is designating material from nonambulatory disabled cattle as prohibited cattle materials.
Friday, March 21, 2014
Rancho Dead Stock Cancer Downers Recall Explained FSIS March 20 2014 ?
“As of March 20, 2014, FSIS has completed all checks (effectiveness checks and disposition verification checks) for recalls 002-2014 and 013-2014 regarding Rancho Feeding Corporation. FSIS has determined that based on the number of successful checks (see Directive 8080.1, Attachment 1, Table 3) where businesses were notified of the recall and removed affected products from commerce that the recall activities were effective.”
*** And Terry, I promised the editor you would respond so thanks for backing my prediction up. I have read your tripe before so did not reread the whole thing. but your point about the age of the cattle takes on the scientific regulatory bodies of every country but one that exports US beef. They all, but one, agree that meat from cattle under 30 months of age carries zero risk of BSE prions. 1 △ ▽ • Reply • Share ›
Terry S. Singeltary Sr. > doc raymond • a month ago
Dr. Richard Raymond Sir, I only reply when you are scientifically wrong. I commented today, because again, you were scientifically wrong, and I proved it again, with scientific facts to back it up. sorry if that upsets you. you can fool some of the folks some of the time, but not all of us all the time. you either blatantly lied in your editorial, or you are grossly uninformed, time and time again. I think the public can take their pick on that, and in both cases, and they would be correct in both cases, in my opinion. you have a nice day sir. ...kind regards, terry
kind regards, terry
What is a Downer Calf?
By Dr. Richard Raymond | February 21, 2014
see full text Dr. Richard Raymond vs Terry S. Singeltary Sr.
Monday, March 10, 2014
Investigators study silent variant of mad cow disease Galveston Daily News March 4, 2014
Saturday, August 4, 2012
Update from APHIS Regarding Release of the Final Report on the BSE Epidemiological Investigation
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)
I have been most interested to see IF the h-BSE (h-BSE or g-h-BSEalabama???), but i have been most interested to see if in fact this atypical h-BSE is more virulent than c-BSE, as is the L-BSE (Italian strain) has been documented to be. We know from the studies of Kong et al that h-BSE will transmit to TG human mice;
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.
HOWEVER, as to the virulance of it one way or the other compared to c-BSE and or L-BSE, i don't think no one has said yet or not? interesting this debate of the h-BSE TEXAS (2nd mad cow finally confirmed 7 months after the fact, and an act of Congress), compared to the g-h-BSEalabama strain documented in Alabama, that is identicle to the new human CJD in the USA that is killing the young and old, with clinical long duration, and different symptoms in some cases too, but not related to this ??? ALSO, this IBNC BSE, might this be the g-h-BSEalabama strain?
THE last two mad cows documented in the USA were in Alabama and Texas, both of which were atypical h-BSE.
SINGE then, the surveillance for TSE in cattle in the USA has been reduced to a number of which detecting any TSE would almost impossible.
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
Thursday, December 04, 2008 2:37 PM
"we have found that H-BSE can infect humans."
personal communication with Professor Kong. ...TSS
TEXAS ATYPICAL H-BSE MAD COW CASE
On June 24, 2005, the USDA announced receipt of final results from The Veterinary Laboratories Agency in Weybridge, England, confirming BSE in a cow that had conflicting test results in 2004. This cow was from Texas, died at approximately 12 years of age, and represented the first endemic case of BSE in the United States. (see Texas BSE Investigation, Final Epidemiology Report, August 2005 External Web Site Policy PDF Document Icon (PDF – 83 KB))
ALABAMA ATYPICAL H-TYPE GENETIC BSE
On March 15, 2006, the USDA announced the confirmation of BSE in a cow in Alabama. The case was identified in a non-ambulatory (downer) cow on a farm in Alabama. The animal was euthanized by a local veterinarian and buried on the farm. The age of the cow was estimated by examination of the dentition as 10-years-old. It had no ear tags or distinctive marks; the herd of origin could not be identified despite an intense investigation (see second featured item above and Alabama BSE Investigation, Final Epidemiology Report, May 2006 External Web Site PolicyPDF Document Icon (PDF – 104 KB)).
In August 2008, several ARS investigators reported that a rare, genetic abnormality that may persist within the cattle population "is considered to have caused" BSE in this atypical (H-type) BSE animal from Alabama. (See Identification of a Heritable Polymorphism in Bovine PRNP Associated with Genetic Transmissible Spongiform Encephalopathy: Evidence of Heritable BSE External Web Site Policy. Also see BSE Case Associated with Prion Protein Gene Mutation External Web Site Policy.)
On December 23, 2003, the U.S. Department of Agriculture (USDA) announced a presumptive diagnosis of the first known case of BSE in the United States. It was in an adult Holstein cow from Washington State. This diagnosis was confirmed by an international reference laboratory in Weybridge, England, on December 25. Trace-back based on an ear-tag identification number and subsequent genetic testing confirmed that the BSE-infected cow was imported into the United States from Canada in August 2001. Because the animal was non-ambulatory (a "downer cow") at slaughter, brain tissue samples were taken by USDA's Animal and Plant Health Inspection Service as part of its targeted surveillance for BSE. However the animal's condition was attributed to complications from calving. After the animal was examined by a USDA Food Safety and Inspection Service (FSIS) veterinary medical officer both before and after slaughter, the carcass was released for use as food for human consumption. During slaughter, the tissues considered to be at high risk for the transmission of the BSE agent were removed. On December 24, 2003, FSIS recalled beef from cattle slaughtered in the same plant on the same day as the BSE positive cow. (see Bovine Spongiform Encephalopathy in a Dairy Cow - Washington State, 2003.)
Tuesday, August 22, 2006
BSE ATYPICAL TEXAS AND ALABAMA UPDATE JANUARY 20, 2007
ABOUT THAT USDA INC FDA TRIPLE MAD COW FIREWALL ...HA, HA, HA, jokes you, it was nothing but ink on paper...
*** FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE DECEMBER 2013 UPDATE ***
OAI (Official Action Indicated) when inspectors find significant objectionable conditions or practices and believe that regulatory sanctions are warranted to address the establishment’s lack of compliance with the regulation.
*** An example of an OAI classification would be findings of manufacturing procedures insufficient to ensure that ruminant feed is not co...ntaminated with prohibited material.
Inspectors will promptly re-inspect facilities classified OAI after regulatory sanctions have been applied to determine whether the corrective actions are adequate to address the objectionable conditions.
ATL-DO 1035703 Newberry Feed & Farm Ctr, Inc. 2431 Vincent St. Newberry SC 29108-0714 OPR DR, FL, FR, TH HP 9/9/2013 OAI Y
DET-DO 1824979 Hubbard Feeds, Inc. 135 Main, P.O. Box 156 Shipshewana IN 46565-0156 OPR DR, FL, OF DP 8/29/2013 OAI Y
ATL-DO 3001460882 Talley Farms Feed Mill Inc 6309 Talley Rd Stanfield NC 28163-7617 OPR FL, TH NP 7/17/2013 OAI N
NYK-DO 3010260624 Sherry Sammons 612 Stoner Trail Rd Fonda NY 12068-5007 OPR FR, OF NP 7/16/2013 OAI Y
DEN-DO 3008575486 Rocky Ford Pet Foods 21693 Highway 50 East Rocky Ford CO 81067 OPR RE, TH HP 2/27/2013 OAI N
CHI-DO 3007091297 Rancho Cantera 2866 N Sunnyside Rd Kent IL 61044-9605 OPR FR, OF HP 11/26/2012 OAI Y
DEN-DO 1713202 Weld County Bi Products, Inc. 1138 N 11th Ave Greeley CO 80631-9501 OPR RE, TH HP 10/12/2012 OAI N
Ruminant Feed Inspections Firms Inventory (excel format)
PLEASE NOTE, the VAI violations were so numerous, and unorganized in dates posted, as in numerical order, you will have to sift through them for yourselves. ...tss
snip...see full text ;
Sunday, December 15, 2013
FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED VIOLATIONS OFFICIAL ACTION INDICATED OIA UPDATE DECEMBER 2013 UPDATE
ONE SUCH INCIDENT CAN CAUSE 10,000,000 MILLION POUNDS OF SUSPECT BANNED MAD COW PROTEIN GOING INTO COMMERCE TO BE FED OUT ;
10,000,000+ LBS. of PROHIBITED BANNED MAD COW FEED I.E. BLOOD LACED MBM IN COMMERCE USA 2007
Date: March 21, 2007 at 2:27 pm PST
RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINES -- CLASS II
Bulk cattle feed made with recalled Darling's 85% Blood Meal, Flash Dried, Recall # V-024-2007
Cattle feed delivered between 01/12/2007 and 01/26/2007
Pfeiffer, Arno, Inc, Greenbush, WI. by conversation on February 5, 2007.
Firm initiated recall is ongoing.
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
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
The firm does not utilize a code - only shipping documentation with commodity and weights identified.
Rangen, Inc, Buhl, ID, by letters on February 13 and 14, 2007. Firm initiated recall is complete.
*** 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
ID and NV
END OF ENFORCEMENT REPORT FOR MARCH 21, 2007
Saturday, August 4, 2012
*** Final Feed Investigation Summary - California atypical L-TYPE BASE BSE Case - July 2012
The accumulation of PrPSc in the hamster tongue following i.c. inoculation of two hamster-adapted TME strains and four hamster-adapted scrapie strains indicates that the spread of prions to the tongue may be a common event in prion diseases. The detection of PrPSc in axons of the tongue after i.c. inoculation suggests that one possible route involved in the establishment of tongue infection is axonal transport of HY TME from the brain to the tongue. In this case, TME transport may be via the motor efferent or sensory afferent pathways of the tongue. Prion infection of the XII nucleus, the spinal trigeminal nucleus, or the nucleus of the solitary tract would be necessary for prions to have access to and be transported within the tongue-associated cranial nerves. In cases of both natural and experimental oral infection of ruminants with scrapie and BSE, as well as in infection of deer with the CWD agent, there is evidence for the infection of the tongue-associated brain stem nuclei (27, 48, 56, 57).
The findings of the present study, and the ability of BSE to target brain stem regions that are synaptically connected to the tongue, indicate that the Specified Risk Material Regulations (15), which do not completely exclude tongue from human consumption, need to be reevaluated in order to minimize human exposure to BSE and other prion diseases through ingestion of food products containing tongue.
Exposure of the tongue to the prion agent during oral ingestion makes it a potential site of agent entry and neuroinvasion, especially if lesions have disrupted the mucosal epithelium (4). Although there are no epidemiological data that indicate this is a common route of prion agent entry, the tongue is a highly innervated peripheral tissue that may be a relevant site of neuroinvasion for a subset of prion diseases of livestock in which evidence for LRS infection is lacking.
Progress 12/01/08 to 11/30/09
Therefore, saliva may be one source of prions that is shed from a host and can infect a naive host through direct or indirect contact. The spread of prions into skeletal muscle cells via nerve fibers suggest that muscle tissue, and not just nerves that transverse muscle, are a potential source of prion exposure upon ingestion of food products containing meat.
Progress 12/01/05 to 11/30/09
To determine if the prion agent can directly infect epithelial cells at the tongue mucosa we analyzed the keratin layer of the stratified squamous epithelium (SSE). PrP-res was detected in both the keratin layer of the SSE and the SSE of filiform papillae. PrP-res did not always colocalize with markers for nerve fibers in these locations suggesting infection was present in epithelial cells. These studies strongly suggest that epithelial cells in the oral mucosa can support prion infection and shedding of the mucosa may be a source of prion infection in saliva. We investigated infection of tongue and nasal turbinates in over 80 ruminants infected with prion diseases. In prion-infected sheep, deer, and elk greater than 85% of tongue and nasal turbinates were PrP-res positive. Tongue and nasal turbinates from CWD or TME-infected cattle were examined from over 25 animals, but we were unable to detect PrP-res in any of these samples. These findings indicate that prion infection is present in mucosal tissues in ruminant species in which there is horizontal transmission of prions, but not in cattle in which there is not an endemic prion infection.
Impacts The implication from these findings is that the prion agent can spread away from the brain into mucosa tissues in the head, specifically the tongue and nasal cavity. Since these tissues have a mucosal surface, it may be possible that the prion agent is shed from the tongue or nasal cavity. In the tongue, the epithelium is continually undergoing terminal differentiation and shedding, and is then sloughed into saliva. In the nasal mucosa, olfactory neurons continually mature and turnover during adult life and prions may be shed from this mucosa into nasal secretions. Therefore, saliva and nasal secretions may be a potential source of prions that are shed from a host and can infect a naive host through direct or indirect contact. Another implication of these findings is that prion infection of ruminant muscle is a potential threat to animal and human food safety. The head of ruminants is banned for human or ruminant consumption with the exception of the tongue. Our findings indicate that prions undergo centrifugal spread from the brainstem to the tongue and can enter skeletal muscle cells via the neuromuscular junction and further replicate in muscle cells. These studies suggest that tongue should also be included in the specified risk materials in order to minimize exposure to tongue products containing prion agent.
Class I Recall 013-2014 Health Risk: High Feb 8, 2014
30- and 60-lb. boxes of “Beef Tongue”
*** Bovine spongiform encephalopathy: the effect of oral exposure dose on attack rate and incubation period in cattle -- an update 5 December 2012
Saturday, December 21, 2013
**** Complementary studies detecting classical bovine spongiform encephalopathy infectivity in jejunum, ileum and ileocaecal junction in incubating cattle ****
Saturday, November 10, 2012
Wisconsin Firm Recalls Beef Tongues That May Contain Specified Risk Materials
Nov 9, 2012 WI Firm Recalls Beef Tongues
Saturday, July 23, 2011
CATTLE HEADS WITH TONSILS, BEEF TONGUES, SPINAL CORD, SPECIFIED RISK MATERIALS (SRM's) AND PRIONS, AKA MAD COW DISEASE
Friday, October 15, 2010
BSE infectivity in the absence of detectable PrPSc accumulation in the tongue and nasal mucosa of terminally diseased cattle
Sunday, October 18, 2009
Wisconsin Firm Recalls Beef Tongues That Contain Prohibited Materials SRM WASHINGTON, October 17, 2009
Thursday, October 15, 2009
Nebraska Firm Recalls Beef Tongues That Contain Prohibited Materials SRM WASHINGTON, Oct 15, 2009
Thursday, June 26, 2008
Texas Firm Recalls Cattle Heads That Contain Prohibited Materials
Tuesday, July 1, 2008
Missouri Firm Recalls Cattle Heads That Contain Prohibited Materials SRMs
Friday, August 8, 2008
Texas Firm Recalls Cattle Heads That Contain Prohibited Materials SRMs 941,271 pounds with tonsils not completely removed
Saturday, April 5, 2008
SRM MAD COW RECALL 406 THOUSAND POUNDS CATTLE HEADS WITH TONSILS KANSAS
Wednesday, April 30, 2008
Consumption of beef tongue: Human BSE risk associated with exposure to lymphoid tissue in bovine tongue in consideration of new research findings
Monday, March 3, 2014
*** Gov. C.L. "Butch" Otter of Idaho signs bill that will force consumers to eat dead stock downers and whatever else the industry decides
see updated Rancho CLASS 1 HIGH RISK dead stock cancer downer recall for IDAHO
Prion 6:1, 52-61; January/February/March 2012; © 2012 Landes Bioscience
Salivary prions in sheep and deer
Experiments in prion-infected rodents have shown that the oral and nasal mucosa, including the papillae in the tongue, can harbor prions and may act as potential sources for the horizontal transmission of animal prion diseases since these tissues may release prions during their normal turnover. 34,35 Equally, the tongue, and the oral and nasal mucosa can also act as routes for neuroinvasion.36-39 Although prions were reported previously in the saliva of CWD-infected mule deer,10 the titers were not determined. A pooled and concentrated (10- fold) saliva sample from five white-tailed deer with CWD was reported to transmit prion disease to 8 of 9 Tg(CerPrP+/-)1536 mice in 342 ± 102 dpi.11 Based on published titration results with a pooled elk CWD inoculum in Tg(CerPrP+/-)1536 mice,40 we estimated the equivalent titer for this pooled CWD saliva sample to be -0.7 log ID50 U, which is similar to our value of -0.9 log ID50 U for scrapie saliva sample 444 based on 30 μl of 10% saliva preparations (Table 1).
Our results indicate a similar magnitude of salivary prion shedding between sheep and deer. Although salivary prion titers are much lower in comparison to those measured in brain, spleen and lymph nodes of affected animals, the number of prions secreted in saliva over the incubation period may approach that found in the brains of terminally ill animals, assuming that, similar to fecal prion shedding, salivary prion shedding is not restricted to terminally sick animals (Table 4). Also, possible differences between prion strains and animal species used in titration studies may affect the estimated titers. Whether these assumptions are accurate requires additional studies. It remains to be determined at what quantities scrapie prions are shed in urine and feces of scrapie-infected sheep (Table 4) as well as when and to what level this shedding may occur in presymptomatic animals. Whether prions shed in saliva have different strain characteristics from prions shed in feces is also unknown. In light of the similarities in peripheral prion distribution patterns and shedding of infectious prions by small ruminants and cervids, it will be important to determine whether patients with variant Creutzfeldt-Jakob disease (vCJD) who harbor prions in their lymphoreticular tissues,43,44 also shed vCJD prions in saliva, urine or feces.
Sunday, March 23, 2014
APHIS USDA National Scrapie Eradication Program February 2014 Monthly Report Fiscal Year 2014
Thursday, November 21, 2013
*** Assessing the susceptibility of transgenic mice over-expressing deer prion protein to bovine spongiform encephalopathy
The present study was designed to assess the susceptibility of the prototypic mouse line, Tg(CerPrP)1536+/- to bovine spongiform encephalopathy (BSE) prions, which have the ability to overcome species barriers. Tg(CerPrP)1536+/- mice challenged with red deer-adapted BSE resulted in a 90-100% attack rates, BSE from cattle failed to transmit, indicating agent adaptation in the deer.
Friday, November 22, 2013
Wasting disease is threat to the entire UK deer population CWD TSE Prion disease Singeltary submission to Scottish Parliament
Saturday, March 15, 2014
Potential role of soil properties in the spread of CWD in western Canada
Saturday, March 29, 2014
Game Farm, CWD Concerns Rise at Boone and Crockett Club
this just out cdc...tss
Sunday, March 30, 2014
*** Chronic Wasting Disease Agents in Nonhuman Primates ***
Monday, August 6, 2012
TAFS BSE in USA August 6, 2012
BSE in USA
Saturday, November 2, 2013
Exploring the risks of a putative transmission of BSE to new species
Sunday, November 13, 2011
California BSE mad cow beef recall, QFC, CJD, and dead stock downer livestock
Saturday, May 2, 2009
APHIS AND WHO PLAN TO EXEMPT THE ATYPICAL SCRAPIE NOR-98 FROM REGULATIONS AT MEETING THIS MONTH
Monday, November 30, 2009
USDA AND OIE COLLABORATE TO EXCLUDE ATYPICAL SCRAPIE NOR-98 ANIMAL HEALTH CODE
Thursday, December 20, 2012
OIE GROUP RECOMMENDS THAT SCRAPE PRION DISEASE BE DELISTED AND SAME OLD BSe WITH BOVINE MAD COW DISEASE
Tuesday, July 2, 2013
APHIS USDA Administrator Message to Stakeholders: Agency Vision and Goals Eliminating ALL remaining BSE barriers to export market
I lost my mother to the Heidenhain Variant of Creutzfeldt Jakob Disease DOD 12/14/97 ‘confirmed’, and never could except the science that the USDA et al brought forth to date i.e. the UKBSEnvCJD only theory. I simply made a promise to mom, NEVER FORGET, and so soon you all FORGOT $
Seems none of the officials remember, that went through the mad cow debacle, or mad cow follies as I have termed them, and they are ongoing, for anyone who thinks mad cow disease is gone, they are only fooling themselves, and at the same time, making fools out of everyone that goes along with this TSE prion mad cow junk science that the OIE has brought to every country around the globe, and we will ALL pay the price in the years and decades to come. ...
IT is of my opinion, that the OIE and the USDA et al, are the soul reason, and responsible parties, for Transmissible Spongiform Encephalopathy TSE prion diseases, including typical and atypical BSE, typical and atypical Scrapie, and all strains of CWD, and human TSE there from, spreading around the globe.
I have lost all confidence of this organization as a regulatory authority on animal disease, and consider it nothing more than a National Trading Brokerage for all strains of animal TSE, just to satisfy there commodity. AS i said before, OIE should hang up there jock strap now, since it appears they will buckle every time a country makes some political hay about trade protocol, commodities and futures. IF they are not going to be science based, they should do everyone a favor and dissolve there organization.
JUST because of low documented human body count with nvCJD and the long incubation periods, the lack of sound science being replaced by political and corporate science in relations with the fact that science has now linked some sporadic CJD with atypical BSE and atypical scrapie, and the very real threat of CWD being zoonosis, I believed the O.I.E. has failed terribly and again, I call for this organization to be dissolved. ...
IN A NUT SHELL ;
(Adopted by the International Committee of the OIE on 23 May 2006)
11. Information published by the OIE is derived from appropriate declarations made by the official Veterinary Services of Member Countries. The OIE is not responsible for inaccurate publication of country disease status based on inaccurate information or changes in epidemiological status or other significant events that were not promptly reported to the Central Bureau,
Thursday, May 30, 2013
World Organization for Animal Health (OIE) has upgraded the United States' risk classification for mad cow disease to "negligible" from "controlled", and risk further exposing the globe to the TSE prion mad cow type disease
U.S. gets top mad-cow rating from international group and risk further exposing the globe to the TSE prion mad cow type disease
Creutzfeldt-Jakob Disease CJD cases rising North America updated report August 2013
*** Creutzfeldt-Jakob Disease CJD cases rising North America with Canada seeing an extreme increase of 48% between 2008 and 2010 ***
Sunday, October 13, 2013
*** CJD TSE Prion Disease Cases in Texas by Year, 2003-2012
*** When people talk about 1 per million, often they interpret that as thinking it is incredibly rare. They think they have a 1-in-a-million chance of developing this disease. You haven’t. You’ve got about a 1-in-30,000 chance of developing it.
Tuesday, April 01, 2014
*** Questions linger in U.S. CJD cases 2005, and still do in 2014 ***
Wednesday, April 2, 2014
Do prions cause Parkinson disease?: The evidence accumulates (pages 331–333)
kind regards, ......terry