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Obama Pushes Trade Deal With S. Korea

President Obama has directed the U.S. Trade Representative to launch new talks with the South Korean government to resolve issues holding up a bilateral free trade agreement.

Ron Kirk, U.S. Trade Representative, said in a news release that he has been directed to initiate discussions with the Korean Minister of Trade Kim Jong-hoon, and have those issues, including a disagreement over U.S. beef exports, settled by November, when the President will visit Seoul to attend the next G-20 meeting. The President would submit the Korea-US Free Trade Agreement to Congress following that meeting.

“We look forward to finalizing ways to address these concerns, level the playing field for U.S. workers and producers in the key sectors of autos and beef,” Kirk said.

The Korea-US Free Trade Agreement was concluded by the Bush Administration in June 2007 but has been held up under Democratic leadership in Congress and until now had not been top priority for the Obama Administration.

“It’s encouraging to see that this has been moved to the front burner,” Joe Schuele, spokesman for the U.S. Meat Export Federation, told Meatingplace.

The National Beef Cattlemen’s Association along with other industry groups, called the Korea-US Free Trade Agreement a “critical trade deal.”

The U.S. beef industry would reap $15 million in new tariff benefits in the first year alone, the association noted, with some $325 million in tariff reductions per year upon full implementation.  The deal would cut Korea’s current tariff from 40 percent to zero over 15 years. U.S. beef exports to South Korea totaled $815 million at its height. The the National Beef Cattlemen’s Association said the free trade agreement could push the value of the market to $1 billion.

South Korea is expected to hold new beef talks with Canada next month. Just last Friday China announced it is opening its borders to imports of Canadian beef.

Meatingplace reported that industry groups also have been pushing Congress to move forward on free trade pacts with Colombia and Panama.

“For each day Congress delays in approving the Colombia [Free Trade Agreement], American exporters overall pay $2 million in unnecessary tariffs,” the National Beef Cattlemen’s Association said.

© Food Safety News
  • Canada and the USA have been swapping cattle and cattle by-products, and cattle feed, like two lovers swapping spit, and they have done this for years, decades. Mad Cow disease is more prevalent that both Governments would have you believe, in fact, they have no idea how bad it is. There only goal is trade. South Korea and other Nations know this, and that is why they do not want beef that has not been tested, where they know mad cow exist. IT”S like Australia and Taiwan, they don’t want our beef, and IF people would look at the facts, they would see why they don’t want it. …
    ****************PLEASE READ THE FOLLOWING CAREFULLY************
    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.
    14th International Congress on Infectious Diseases H-type and L-type Atypical BSE January 2010 (special pre-congress edition)
    18.173 page 189
    Experimental Challenge of Cattle with H-type and L-type Atypical BSE
    A. Buschmann1, U. Ziegler1, M. Keller1, R. Rogers2, B. Hills3, M.H. Groschup1. 1Friedrich-Loeffler-Institut, Greifswald-Insel Riems, Germany, 2Health Canada, Bureau of Microbial Hazards, Health Products & Food Branch, Ottawa, Canada, 3Health Canada, Transmissible Spongiform Encephalopathy Secretariat, Ottawa, Canada
    Background: After the detection of two novel BSE forms designated H-type and L-type atypical BSE the question of the pathogenesis and the agent distribution of these two types in cattle was fully open. From initial studies of the brain pathology, it was already known that the anatomical distribution of L-type BSE differs from that of the classical type where the obex region in the brainstem always displays the highest PrPSc concentrations. In contrast in L-type BSE cases, the thalamus and frontal cortex regions showed the highest levels of the pathological prion protein, while the obex region was only weakly involved.
    Methods:We performed intracranial inoculations of cattle (five and six per group) using 10%brainstemhomogenates of the two German H- and L-type atypical BSE isolates. The animals were inoculated under narcosis and then kept in a free-ranging stable under appropriate biosafety conditions.At least one animal per group was killed and sectioned in the preclinical stage and the remaining animals were kept until they developed clinical symptoms. The animals were examined for behavioural changes every four weeks throughout the experiment following a protocol that had been established during earlier BSE pathogenesis studies with classical BSE.
    Results and Discussion: All animals of both groups developed clinical symptoms and had to be euthanized within 16 months. The clinical picture differed from that of classical BSE, as the earliest signs of illness were loss of body weight and depression. However, the animals later developed hind limb ataxia and hyperesthesia predominantly and the head. Analysis of brain samples from these animals confirmed the BSE infection and the atypical Western blot profile was maintained in all animals. Samples from these animals are now being examined in order to be able to describe the pathogenesis and agent distribution for these novel BSE types. Conclusions: A pilot study using a commercially avaialble BSE rapid test ELISA revealed an essential restriction of PrPSc to the central nervous system for both atypical BSE forms. A much more detailed analysis for PrPSc and infectivity is still ongoing.
    14th ICID International Scientific Exchange Brochure –
    Final Abstract Number: ISE.114
    Session: International Scientific Exchange
    Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America
    update October 2009
    T. Singeltary
    Bacliff, TX, USA
    An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie’s, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and fed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.
    12 years independent research of available data
    I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.
    I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena’s. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.
    see page 114 ;
    International Society for Infectious Diseases Web: http://www.isid.org
    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 ;
    ”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
    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.
    Wednesday, March 31, 2010
    Atypical BSE in Cattle
    Thursday, June 24, 2010
    Accumulation of L-type Bovine Prions in Peripheral Nerve Tissues
    Volume 16, Number 7–July 2010
    Saturday, June 12, 2010
    PUBLICATION REQUEST AND FOIA REQUEST Project Number: 3625-32000-086-05 Study of Atypical Bse
    Archive Number 20100405.1091 Published Date 05-APR-2010
    Subject PRO/AH/EDR> Prion disease update 1010 (04)
    [Terry S. Singeltary Sr. has added the following comment:
    “According to the World Health Organisation, the future public health threat of vCJD in the UK and Europe and potentially the rest of the world is of concern and currently unquantifiable. However, the possibility of a significant and geographically diverse vCJD epidemic occurring over the next few decades cannot be dismissed
    The key word here is diverse. What does diverse mean? If USA scrapie transmitted to USA bovine does not produce pathology as the UK c-BSE, then why would CJD from there look like UK vCJD?”
    > Up until about 6 years ago, the pt worked at Tyson foods where she
    > worked on the assembly line, slaughtering cattle and preparing them for
    > packaging. She was exposed to brain and spinal cord matter when she
    > would euthanize the cattle.
    Monday, April 5, 2010
    Tuesday, June 1, 2010
    USA cases of dpCJD rising with 24 cases so far in 2010
    Wednesday, June 16, 2010
    Defining sporadic Creutzfeldt-Jakob disease strains and their transmission properties
    Tuesday, March 2, 2010
    Animal Proteins Prohibited in Ruminant Feed/Adulterated/Misbranded Rangen Inc 2/11/10 USA
    Monday, March 1, 2010
    Terry S. Singeltary Sr. (Submitted question): Monday, April 5, 2010
    Update on Feed Enforcement Activities to Limit the Spread of BSE April 5, 2010
    Can you say TOYOTA. IT is a sad day when trade trumps human and animal health. as the case with the BSE MRR policy. Behind closed doors, the BSe spin machine is working i.e. Vilsack saying that ‘The U.S. has had no cases in the last three years, and only three in two decades.’ i can tell you with absolute certainty, that is only part of the story. i can tell you that in fact, the USDA BSE surveillance and testing have failed the consumer here in the USA, and abroad, and that we have been exposed to the TSE agent, i.e. USA atypical BSE, which laboratory studies show is more virulent. i can tell you with absolute certainty they infamous June 2004 enhanced BSE surveillance program, where some 800,000+ cattle were tested over many years of testing, was fraught with fraud, and in short, a failed program, and proven to be so by the GAO and the OIG, where it was proven that some of the testing program was using perfectly healthy cattle in their BSE testing program. Where some 9,200+ BSE test on suspect questionable cattle, only the IHC test were used. THE IHC is the least likely test to find BSE. IT only tells you if that part of the tissue sample is in fact infected or not, but it does not tell you about the rest of the brain. By only using the IHC, you miss many cases (Detwiler et al 2003 BSE ROUNDTABLE). i can tell you with absolute certainty, that when pressed, the USDA et al will say that even if we are missing cases of BSE, that the BSE mad cow feed ban of August 4, 1997, will stop BSE, but the ban was nothing more than ink on paper. This mad cow feed ban was only partial and voluntary. i can tell you with absolute certainty that in 2010, since 8/4/97, banned mad cow feed is in commerce here in the USA, BY THE TONS. i can tell you with absolute certainty, that when the BSE MRR policy was put in place, that this exposed everyone around the globe with the TSE agent, either by consumption and or friendly fire there from, and that decision was based NOT on science, but on trade. i can tell you with absolute certainty, that SINCE the USDA and the NSLP did in fact expose our children across the Nation with BSE via the NSLP USDA DEAD STOCK DOWNER COW SCHOOL LUNCH PROGRAM, that if they are capable of this, they are capable of exposing any person, in any country with the BSE TSE agent. North America has documented the so called typical c-BSE, l-BSE, and h-BSE. typical scrapie strains are rampant in the USA in sheep and goats, and the atypical Nor-98 scrapie is spreading, and CWD in deer and elk is spreading, with now documented a 2nd strain, and two strains of TME in mink. all this over the years have been fed back to food producing animals for animals and humans. Confucius ask, IF USA sheep Scrapie transmitted to USA cattle does not produce the same pathology as the U.K. c-BSE, why then would human CJD there from look like the U.K. nvCJD ??? what the USA has done defies all science and logic i.e. NO MAD COW DISEASE and or any human TSE there from. Either the BSE Mad Cow outbreak and human infection nvCJD there from, that happened in the U.K. was totally false, or the same thing is happening in the USA as we speak. sCJD of unknown phenotypes are rising in the USA. sporadic CJD is not a single strain, but multiple strains of unknown routes and sources of the TSE agent. IF the federal government can lie for almost a century about asbestos, and or tobacco, just to protect those two industry giants, i can guarantee you that they are doing it with mad cow type disease i.e. Transmissible Spongiform Encephalopathy. or just ask the Indians. …TSS
    full text ;
    Saturday, April 10, 2010
    When the OIE and the USDA et al collaborated to make legal the trading of Transmissible Spongiform Encephalopathy, when they did away with the BSE GBR risk assessments, where the USA, Canada, and Mexico were categorized as BSE GBR III. please see ;
    EFSA concludes that the current GBR level of USA is III, i.e. it is likely but not confirmed that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent. As long as there are no significant changes in rendering or feeding, the stability remains extremely/very unstable. Thus, the probability of cattle to be (pre-clinically or clinically) infected with the BSE-agent persistently increases.
    Annex to the EFSA Scientific Report (2004) 3, 1-17 on the Assessment of the Geographical BSE Risk of USA
    please see full text ;
    YET, in 2010, tons and tons of banned mad cow protein are still in commerce here in the USA, scientific studies are being misconstrued and manipulated by ARS USDA, which are still going by TSE science that is decades old, while refusing to acknowledge new scientific studies, and FOIA requests are still being held up by the USDA et al on these urgent matters (see source related materials below). CJD of unknown phenotype, in victims that are getting younger, with longer clinical course from first onset of symptoms to death are occurring, in fact, sporadic CJD is still rising, where the TSEs in the different species are mutating here in the USA, and we still have this same dog and pony show by the OIE and USDA et al. IF you go back and look at the Countries that went by these OIE BSE guidelines, most all came down with BSE. I have said it before, I was say it again now, 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. …TSS
    Saturday, June 19, 2010
    see full text and reasons why here ;
    Wednesday, August 20, 2008
    Bovine Spongiform Encephalopathy Mad Cow Disease typical and atypical strains, was there a cover-up ? August 20, 2008
    sadly, the USDA and the NSLP, they fed our children all across the country dead stock downer cows, the most high risk cattle for mad cow disease and other deadly disease, they did this for over 4 years. yet the only thing folks were worried about was the abuse to the animals. what about the children ???
    who will watch the children for the next 5 decades ???
    Members of The HSUS are also concerned about the meat products provided to their children through the National School Lunch Program. More than 31 million school children receive lunches through the program each school day. To assist states in providing healthful, low-cost or free meals, USDA provides states with various commodities including ground beef. As evidenced by the HallmarkNVestland investigation and recall, the potential for downed animals to make their way into the National School Lunch Program is neither speculative nor hypothetical.
    Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.
    The rancher was a ”dead stock” feeder using mostly (>95%) downer or dead dairy cattle…
    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
    Saturday, August 29, 2009
    FOIA REQUEST FEED RECALL 2009 Product may have contained prohibited materials Bulk Whole Barley, Recall # V-256-2009
    C O N F I R M E D
    —– Original Message —– From: “Terry S. Singeltary Sr.” To: Sent: Thursday, November 05, 2009 9:25 PM Subject: [BSE-L] re-FOIA REQUEST ON FEED RECALL PRODUCT contaminated with prohibited material Recall # V-258-2009 and Recall # V-256-2009
    Thursday, November 12, 2009
    BSE FEED RECALL Misbranding of product by partial label removal to hide original source of materials 2009
    PLEASE be aware, for 4 years, the USDA fed our children all across the Nation dead stock downer cows, the most high risk cattle for BSE aka mad cow disease and other dangerous pathogens. who will watch our children for CJD for the next 5+ decades ???
    kind regards,
    Terry S. Singeltary Sr.
    P.O. Box 42
    Bacliff, Texas USA 77518