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From: TSS ()
11/28/2006 3:09:00 PM WASHINGTON (Dow Jones)--U.S. Department of Agriculture Secretary Mike Johanns said Tuesday that he "vented frustration" to South Korea over its rejection last week of a U.S. beef shipment. The nine-ton shipment from Creekstone Farms Premium Beef that was rejected was the first since South Korea lifted its nearly three-year ban on U.S. beef. Johanns complained that the rejection was the result of the discovery of a small piece of cartilage, something he argued should not have been important. "You can't trade under these circumstances," Johanns told a gathering of reporters. South Korea partially lifted its ban on U.S. beef on Sept. 8, but U.S. producers were hesitant to ship because of uncertainty over the country's import restrictions. There remained disagreements between the two countries on what constituted a "specified risk material" - material considered to be risky for the spread of mad-cow disease - and South Korea refused to agree to a tolerance level for bone fragments and cartilage. USDA officials said earlier this month that negotiators made progress in getting South Korea to agree that bovine material such as silver skin – a membrane separating muscle groups - is not a risk, but there was no success in getting the country to agree to tolerance levels for bone fragments and cartilage. And it was one "small piece of cartilage" that Johanns said prompted South Korea to reject the entire shipment from Creekstone. Johanns expressed sympathy for Creekstone. The company, he said was promised an open market, but "the market isn't even close to open." Creekstone had been hoping its first post-ban beef shipment would be successful and was already planning to send more. The demand from South Korean importers is strong, Creekstone Senior Vice President of Operations Kevin Pentz said earlier this month while the beef shipment was still being inspected. South Korea was the second-largest foreign market for U.S. beef until December 2003, when the country - along with most other major markets – banned U.S. beef. The bans came after Dec. 23, 2003, when the USDA announced finding the first case of mad-cow disease, or bovine spongiform encephalopathy, in the U.S. Source: Bill Tomson, Dow Jones Newswires; 202-646-0088; bill.tomson @dowjones.com > piece of cartilage, something he argued should not have been important. > "You can't trade under these circumstances," Johanns told a gathering of reporters. > South Korea partially lifted its ban on U.S. beef on Sept. 8, Johanns does not understand the ramifications of broken promises and lies. the USDA bse surveillance plan and bse ruminant to ruminant feed ban (should include all mammalians i.e. MTM feed ban), has been in shambles from day one, a total failure or sham, call it what you must. in reality the S. Koreans should be more concerned about all the tons and tons of tainted BSE feed that is still being fed to USA cattle. You have to hand it to the S. Koreans for wanting to protect there people, a far cry from what the USDA and the FDA has done. All of this has been well documented and believe me when i tell you, the S. Koreans know this. > Agriculture secretary faults S. Korea THERE is know one to fault but yourself sir. you and your boss. ... THE only reason Japan and the rest of Asia accepted USA beef was because they were force fed it through trade, and GWs BSE MRR policy, the legal trading of all strains of TSE. USDA is no different than Britain for poisoning the Globe. CDC DR. PAUL BROWN TSE EXPERT COMMENTS 2006 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 03-025IFA THE SEVEN SCIENTIST REPORT *** On the Question of Sporadic or Atypical Bovine SpongiformEncephalopathy and Creutzfeldt-Jakob Disease Paul Brown,* Lisa M. McShane,† Gianluigi Zanusso,‡ and Linda Detwiler§ Strategies to investigate the possible existence of sporadic bovine spongiform encephalopathy (BSE) require systematic testing programs to identify cases in countries considered to have little or no risk for orally acquired disease, or to detect a stable occurrence of atypical cases in countries in which orally acquired disease is disappearing. To achieve 95% statistical confidence that the prevalence of sporadic BSE is no greater than 1 per million (i.e., the annual incidence of sporadic Creutzfeldt-Jakob disease [CJD] in humans) would require negative tests in 3 million randomly selected older cattle. 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. 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... Models Qingzhong Kong, Ph.D., Assistant Professor, Pathology, Case Western Reserve Bovine Amyloid Spongiform Encephalopathy (BASE) is an atypical BSE strain 6:30 Close of Day One There is a growing number of human CJD cases, and they were presented last He estimates that it may be up to 14 or 15 persons which display selectively MARCH 26, 2003 RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment on the CDC's attempts to monitor the occurrence of emerging forms of CJD. Asante, Collinge et al [1] have reported that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD and all human TSEs are not reportable nationally. CJD and all human TSEs must be made reportable in every state and internationally. I hope that the CDC does not continue to expect us to still believe that the 85%+ of all CJD cases which are sporadic are all spontaneous, without route/source. We have many TSEs in the USA in both animal and man. CWD in deer/elk is spreading rapidly and CWD does transmit to mink, ferret, cattle, and squirrel monkey by intracerebral inoculation. With the known incubation periods in other TSEs, oral transmission studies of CWD may take much longer. Every victim/family of CJD/TSEs should be asked about route and source of this agent. To prolong this will only spread the agent and needlessly expose others. In light of the findings of Asante and Collinge et al, there should be drastic measures to safeguard the medical and surgical arena from sporadic CJDs and all human TSEs. I only ponder how many sporadic CJDs in the USA are type 2 PrPSc? Singeltary, Sr et al. JAMA.2001; 285: 733-734. http://jama.ama-assn.org/cgi/content/full/285/6/733?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=dignosing+and+reporting+creutzfeldt+jakob+disease&searchid=1048865596978_1528&stored_search=&FIRSTINDEX=0&journalcode=jama New Orleans District 404 BNA Drive, Building 200, Suite 500 Nashville, TN 37217 Telephone: 615-366-7801 Facsimile: 615-366-7802 October 26, 2006 WARNING LETTER NO. 2007-NOL-01 FEDERAL EXPRESS OVERNIGHT DELIVERY Mr. Christopher V. B. Smith Corporate President, CEO H. J. Baker & Bro., Inc. 228 Saugatuck Avenue Westport, Connecticut 06880 Dear Mr. Smith: On June 6, 8, 12-15, and 23, 2006, a U.S . Food and Drug Administration (FDA) investigator inspected your animal feed protein supplement manufacturing facility, located at 603 Railroad Avenue, Albertville, Alabama. The inspection revealed significant deviations from the requirements set forth in Title 21, Code ofFederal Regulations, Part 589.2000 (21 CFR 589.2000), Animal Proteins Prohibited in Ruminant Feed. This regulation is intended to prevent the establishment and amplification of Bovine Spongiform Encephalopathy (BSE). You failed to follow the requirements of this regulation, resulting in products being manufactured and distributed by your facility because they are adulterated within the meaning of Section 402(a)(4) [21 USC 342(a)(4)] of the Federal Food, Drug, and Cosmetic Act (the Act) and misbranded within the meaning of Section 403(a)(1) [21 USC 343(a)(1)] of the Act. Our investigation determined adulteration resulted from the failure of your firm to establish and implement measures sufficient to prevent commingling or cross-contamination . The adulterated feed was subsequently misbranded because it was not properly labeled. Specifically, we found : " Your firm failed to establish and use cleanout procedures or other means to prevent carry-over of products which contain or may contain protein derived from mammalian tissues into animal protein or feeds which may be used for ruminants, as required by 21 CFR 589.2000(e)(1)(iii)(B) . Specifically, you failed to establish and use such measures for a screw auger installed in February 2005 . This auger is used to convey both prohibited and non-prohibited material to bulk storage bins. In addition, you failed to follow the cleanout procedure your firm had developed for the receiving systems. Your feed is, therefore, adulterated under Section 402(a)(4) [21 USC 342(a)(4)] of the Act. " You failed to label all products which contained or may have contained prohibited materials with the BSE cautionary statement, "Do not feed to cattle or other ruminants," as required by 21 CFR 589.2000(e)(1)(i) . Such products are misbranded under Section 403(3) [21 USC 343(a)(1)] of the Act. These misbranded products include the three Pro-Pak products mentioned below, as well as Page 2 - H. J . Baker & Bro., Inc., Albertville, Alabama Warning Letter No. 2007-NOL-O 1 those bulk loads of individual feed ingredients processed through this common screw auger and distributed between the time it was installed in February 2005, and June 9, 2006 . This letter is not intended to serve as an all-inclusive list of violations at your facility. As a manufacturer of materials intended for animal feed use, you are responsible for ensuring your overall operation and the products you manufacture and distribute are in compliance with the law. You should take prompt action to correct these violations, and you should establish a system whereby violations do not recur. Failure to promptly correct these violations may result in regulatory action, such as seizure and/or injunction, without further notice. We acknowledge your June 16, 2006, voluntary recall of three products you manufactured from February 2005 to June 2006. The three products recalled were: Pro-Lak Protein Concentrate for Lactating Dairy Animals; Pro-Amino II for PreFresh and Lactating Cows; and, Pro-Pak Marine & Animal Protein Concentrate for Use in Animal Feed. Recall effectiveness checks and other measures will determine the merit of this recall . We recognize you now label all products with the required BSE cautionary statement and we also acknowledge your intent, given verbally to New Orleans District management of the FDA, to discontinue the production of supplements which do not contain prohibited materials. In your written response to this letter, please confirm in writing you have taken these steps. You should notify this office in writing within 15 working days of receiving this letter, outlining the specific steps you have taken to bring your firm into compliance with the law, including the steps we acknowledge above and any additional steps you have taken. Your response should include an explanation of each step taken to correct the violations and prevent their recurrence. If corrective action cannot be completed within 15 working days, state the reason for the delay and the date by which the corrections will be completed. Include copies of any available documentation demonstrating corrections have been made. Your reply should be directed to Kari L. Batey, Compliance Officer, at the address above. If you have questions regarding any issue in this letter, please contact Ms. Batey at (615) 366-7808. Sincerely, , Carol S . Sanchez Acting District Director New Orleans District Enclosure: Form FDA 483 cc: Craig R. Waterhouse Plant Manager H.J. Baker & Bros., Inc. 603 Railroad Avenue Albertville, Alabama 35951-3419 PRODUCT RECALLS AND FIELD CORRECTIONS: VETERINARY MEDICINE - CLASS II ______________________________ ______________________________ ______________________________ ______________________________ ______________________________ ______________________________ END OF ENFORCEMENT REPORT FOR AUGUST 9, 2006 ### ### ### ### END OF ENFORCEMENT REPORT FOR July 12, 2006 ### New Orleans District Telephone: 615-781-5380 WARNING LETTER NO. 2006-NOL-06 FEDERAL EXPRESS Mr. William Shirley, Jr., Owner Dear Mr. Shirley: On February 12, 17, 21, and 22, 2006, a U.S. Food & Drug Administration Our investigation found you failed to provide measures, including sufficient You failed to use clean-out procedures or other means adequate to prevent You failed to maintain written procedures specifying the clean-out As a result . the poultry meal you manufacture may contain protein derived This letter is not intended as an all-inclusive list of violations at your You should notify this office in writing within 15 working days of receiving Your reply should be directed to Mark W. Rivero, Compliance Officer, U.S. Sincerely, /S Carol S. Sanchez Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog, 100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg Primate (oral route)* 1/2 (50%) Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%) RIII mice (ic ip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%) PrPres biochemical detection The comparison is made on the basis of calibration of the bovine inoculum inoculated into mice and cattle.8 *Data are number of animals bioassays is generally judged to be about plus or minus 1 log. ic Table 1: Comparison of transmission rates in primates and cattle infected http://www.thelancet.com/journal/journal.isa
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