Menu
Forums
New posts
Search forums
What's new
New posts
New media
New media comments
New profile posts
Latest activity
Media
New media
New comments
Search media
Members
Current visitors
New profile posts
Search profile posts
Log in
Register
What's new
Search
Search
Search titles and first posts only
Search titles only
By:
New posts
Search forums
Menu
Log in
Register
Forums
Cattle Boards
NCBA, R-CALF, COOL, USDA (No Politics!)
CJD USA UPDATE NOV. 2006
JavaScript is disabled. For a better experience, please enable JavaScript in your browser before proceeding.
You are using an out of date browser. It may not display this or other websites correctly.
You should upgrade or use an
alternative browser
.
Reply to thread
Help Support CattleToday:
Message
<blockquote data-quote="flounder" data-source="post: 307905" data-attributes="member: 3519"><p>New Mad-Cow Variant Is Suspected </p><p>February 17, 2004 The Wall Street Journal by ANTONIO REGALADO</p><p></p><p>Italian scientists have discovered that cattle may harbor a new form of mad-cow disease. </p><p>The research by scientists at the University of Verona, in Italy, builds on earlier work that raised the possibility of unusual cases of the fatal brain-wasting disease, formally known as bovine spongiform encephalopathy. The findings pose new questions about the risk of consuming tainted meat. </p><p></p><p>"If you eat cattle with this new strain, you could get a disease in humans," said Salvatore Monaco, a biologist who made the finding with colleague Gianluigi Zanusso. </p><p></p><p>Dr. Monaco said he found that the brains of certain infected animals looked similar to human brains destroyed by Creutzfeldt-Jakob disease, a neurological disorder that is believed to arise spontaneously and hadn't previously been linked to tainted meat. The human form of mad-cow disease is called variant Creutzfeldt-Jakob disease, which manifests itself differently. Now the question is whether the new form of BSE could be responsible for other Creutzfeldt-Jakob cases. </p><p></p><p>About 150 cases of variant Creutzfeldt-Jakob disease -- nearly all of them in Britain -- have been linked to eating infected cattle. But the majority of cases of Creutzfeldt-Jakob, which strikes about one in a million people each year, are termed "sporadic" because they don't have any known cause. </p><p></p><p>Consumer groups are likely to leap at the Italian finding, published in the Proceedings of the National Academy of Science. Some activists have long contended that humans are contracting mad-cow disease in the U.S., contrary to what public-health officials say. </p><p></p><p>"I have been waiting for this," said Terry S. Singeltary, a Bacliff, Texas, resident whose mother died in 1997 of Creutzfeldt-Jakob disease. Mr. Singeltary and others suspect that some cases of sporadic Creutzfeldt-Jakob are caused by something in the environment, perhaps contaminated meat. </p><p></p><p>BSE is believed to be caused by misshapen proteins called prions that can be spread by consumption of contaminated tissue. The U.S. found its first case of the cattle disease in December, after a Holstein in Washington state tested positive for the condition. </p><p></p><p>The Italian findings give some support to the theory that BSE could be responsible for some cases of Creutzfeldt-Jakob disease, Dr. Monaco said. The Italian group studied the brains of eight cattle that had tested positive for BSE using standard tests. Six of the animals' brains showed the usual signs, but the brains of two animals showed unusual deposits of prions. The distinctive patterns of deposits may indicate a new strain of mad-cow disease, which the Italian scientists have dubbed BASE, for bovine amyloidotic spongiform encephalopathy. </p><p></p><p>Linda Detweiler, a former senior veterinarian for the U.S. Department of Agriculture, said the finding isn't a complete surprise. Studies in the U.K., France and Japan have hinted that some cattle may have been suffering from atypical cases of mad-cow disease. </p><p></p><p>A related disease in sheep, called scrapie, is known to come in many different strains. </p><p></p><p>Dr. Detweiler said more research will be needed to confirm whether there is in fact a new strain of BSE. One possibility is that the disease simply looks different in the specific cattle breeds in the Italian study. "I think there are still a lot of questions," Dr. Detweiler said. </p><p></p><p>Stanley Prusiner, a leading researcher at the University of California, San Francisco, who is the discoverer of the prion and who reviewed the Italian report, has said the possibility of unusual BSE cases is an argument in favor of more comprehensive testing of cattle destined for human consumption. </p><p></p><p>Currently, the Agriculture Department tests only a tiny fraction of cattle for mad-cow disease. Its policy is to target animals that aren't able to walk, known as downer animals, based on the theory that those are most likely to have BSE. </p><p></p><p>But Dr. Monaco said his findings argue strongly for more testing in the U.S. The two animals found to have the new strain were 11 and 15 years old, "weren't acting abnormal, and were apparently free of neurological problems," Dr. Monaco said. </p><p></p><p>In Europe, all cattle slaughtered that are more than 30 months of age are tested for BSE. In Japan, all cattle turned into food are tested for the disease. </p><p></p><p>Scientists first discovered that BSE could affect humans in 1996, when doctors in Britain -- where mad-cow disease was ravaging herds -- found young people succumbing to Creutzfeldt-Jakob disease, which mainly strikes older people. Further research showed the disease, which remains extremely rare, was being caused by the same strain of prion as BSE -- the pattern of damage to the brain was similar in humans and cattle, as were the molecular signatures of the prions. </p><p></p><p>The existence of a second strain of BSE could mean some people are contracting it, but that the cases aren't being diagnosed properly. </p><p></p><p>Write to Antonio Regalado at <a href="mailto:antonio.regalado@wsj.com">antonio.regalado@wsj.com</a></p><p></p><p></p><p><a href="http://online.wsj.com/public/us" target="_blank">http://online.wsj.com/public/us</a></p><p></p><p></p><p></p><p>DECEMBER 2006</p><p></p><p></p><p>Volume 12, Number 12–December 2006</p><p> </p><p> </p><p>PERSPECTIVE</p><p></p><p>On the Question of Sporadic</p><p></p><p>or Atypical Bovine SpongiformEncephalopathy and</p><p></p><p>Creutzfeldt-Jakob Disease</p><p></p><p>Paul Brown,* Lisa M. McShane,† Gianluigi Zanusso,‡ and Linda Detwiler§</p><p></p><p>Strategies to investigate the possible existence of sporadic</p><p></p><p>bovine spongiform encephalopathy (BSE) require</p><p></p><p>systematic testing programs to identify cases in countries</p><p></p><p>considered to have little or no risk for orally acquired disease,</p><p></p><p>or to detect a stable occurrence of atypical cases in</p><p></p><p>countries in which orally acquired disease is disappearing.</p><p></p><p>To achieve 95% statistical confidence that the prevalence</p><p></p><p>of sporadic BSE is no greater than 1 per million (i.e., the</p><p></p><p>annual incidence of sporadic Creutzfeldt-Jakob disease</p><p></p><p>[CJD] in humans) would require negative tests in 3 million</p><p></p><p>randomly selected older cattle. A link between BSE and</p><p></p><p>sporadic CJD has been suggested on the basis of laboratory</p><p></p><p>studies but is unsupported by epidemiologic observation.</p><p></p><p>Such a link might yet be established by the discovery</p><p></p><p>of a specific molecular marker or of particular combinations</p><p></p><p>of trends over time of typical and atypical BSE and various</p><p></p><p>subtypes of sporadic CJD, as their numbers are influenced</p><p></p><p>by a continuation of current public health measures that</p><p></p><p>exclude high-risk bovine tissues from the animal and</p><p></p><p>human food chains. </p><p> </p><p> </p><p>SNIP...</p><p> </p><p> </p><p> </p><p> </p><p>Sporadic CJD</p><p>The possibility that at least some cases of apparently sporadic CJD might be due to infection by sporadic cases of BSE cannot be dismissed outright. Screening programs needed to identify sporadic BSE have yet to be implemented, and we know from already extant testing programs that at least a proportion of infected animals have no symptoms and thus would never be identified in the absence of systematic testing. Thus, sporadic BSE (or for that matter, sporadic disease in any mammalian species) might be occurring on a regular basis at perhaps the same annual frequency as sporadic CJD in humans, that is, in the range of 1 case per million animals.</p><p></p><p>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).</p><p></p><p>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).</p><p></p><p>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).</p><p></p><p>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.</p><p></p><p>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.</p><p></p><p>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).</p><p></p><p>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. </p><p></p><p> </p><p></p><p>SNIP...</p><p></p><p></p><p></p><p></p><p>PLEASE READ FULL TEXT ;</p><p></p><p></p><p><a href="http://www.cdc.gov/ncidod/EID/vol12no12/06-0965.htm?s_cid=eid06_0965_e" target="_blank">http://www.cdc.gov/ncidod/EID/vol12no12 ... d06_0965_e</a></p><p></p><p> </p><p></p><p></p><p>3:00 Afternoon Refreshment Break, Poster and Exhibit Viewing in the Exhibit</p><p>Hall</p><p></p><p></p><p>3:30 Transmission of the Italian Atypical BSE (BASE) in Humanized Mouse</p><p></p><p>Models Qingzhong Kong, Ph.D., Assistant Professor, Pathology, Case Western Reserve</p><p>University</p><p></p><p>Bovine Amyloid Spongiform Encephalopathy (BASE) is an atypical BSE strain</p><p>discovered recently in Italy, and similar or different atypical BSE cases</p><p>were also reported in other countries. The infectivity and phenotypes of</p><p>these atypical BSE strains in humans are unknown. In collaboration with</p><p>Pierluigi Gambetti, as well as Maria Caramelli and her co-workers, we have</p><p>inoculated transgenic mice expressing human prion protein with brain</p><p>homogenates from BASE or BSE infected cattle. Our data shows that about half</p><p>of the BASE-inoculated mice became infected with an average incubation time</p><p>of about 19 months; in contrast, none of the BSE-inoculated mice appear to</p><p>be infected after more than 2 years. ***These results indicate that BASE is</p><p>transmissible to humans and suggest that BASE is more virulent than</p><p>classical BSE in humans.</p><p></p><p>6:30 Close of Day One</p><p></p><p></p><p><a href="http://www.healthtech.com/2007/tse/day1.asp" target="_blank">http://www.healthtech.com/2007/tse/day1.asp</a></p><p></p><p></p><p></p><p></p><p>SEE STEADY INCREASE IN SPORADIC CJD IN THE USA FROM</p><p>1997 TO 2006. SPORADIC CJD CASES TRIPLED, with phenotype</p><p>of 'UNKNOWN' strain growing. ...</p><p></p><p></p><p><a href="http://www.cjdsurveillance.com/resources-casereport.html" target="_blank">http://www.cjdsurveillance.com/resource ... eport.html</a></p><p></p><p></p><p></p><p>There is a growing number of human CJD cases, and they were presented last</p><p>week in San Francisco by Luigi Gambatti(?) from his CJD surveillance</p><p>collection.</p><p></p><p>He estimates that it may be up to 14 or 15 persons which display selectively</p><p>SPRPSC and practically no detected RPRPSC proteins.</p><p></p><p></p><p><a href="http://www.fda.gov/ohrms/dockets/ac/06/transcripts/1006-4240t1.htm" target="_blank">http://www.fda.gov/ohrms/dockets/ac/06/ ... 4240t1.htm</a></p><p></p><p></p><p><a href="http://www.fda.gov/ohrms/dockets/ac/06/transcripts/2006-4240t1.pdf" target="_blank">http://www.fda.gov/ohrms/dockets/ac/06/ ... 4240t1.pdf</a></p><p> </p><p> </p><p> </p><p> </p><p>JOURNAL OF NEUROLOGY</p><p> </p><p>MARCH 26, 2003</p><p> </p><p></p><p></p><p>RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob</p><p></p><p>disease in the United States</p><p></p><p></p><p>Email Terry S. Singeltary:</p><p></p><p></p><p><a href="mailto:flounder@wt.net">flounder@wt.net</a></p><p></p><p></p><p></p><p>I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to</p><p></p><p>comment on the CDC's attempts to monitor the occurrence of emerging</p><p></p><p>forms of CJD. Asante, Collinge et al [1] have reported that BSE</p><p></p><p>transmission to the 129-methionine genotype can lead to an alternate</p><p></p><p>phenotype that is indistinguishable from type 2 PrPSc, the commonest</p><p></p><p>sporadic CJD. However, CJD and all human TSEs are not reportable</p><p></p><p>nationally. CJD and all human TSEs must be made reportable in every</p><p></p><p>state and internationally. I hope that the CDC does not continue to</p><p></p><p>expect us to still believe that the 85%+ of all CJD cases which are</p><p></p><p>sporadic are all spontaneous, without route/source. We have many TSEs in</p><p></p><p>the USA in both animal and man. CWD in deer/elk is spreading rapidly and</p><p></p><p>CWD does transmit to mink, ferret, cattle, and squirrel monkey by</p><p></p><p>intracerebral inoculation. With the known incubation periods in other</p><p></p><p>TSEs, oral transmission studies of CWD may take much longer. Every</p><p></p><p>victim/family of CJD/TSEs should be asked about route and source of this</p><p></p><p>agent. To prolong this will only spread the agent and needlessly expose</p><p></p><p>others. In light of the findings of Asante and Collinge et al, there</p><p></p><p>should be drastic measures to safeguard the medical and surgical arena</p><p></p><p>from sporadic CJDs and all human TSEs. I only ponder how many sporadic</p><p></p><p>CJDs in the USA are type 2 PrPSc?</p><p></p><p></p><p><a href="http://www.neurology.org/cgi/eletters/60/2/176#535" target="_blank">http://www.neurology.org/cgi/eletters/60/2/176#535</a></p><p> </p><p> </p><p> </p><p> </p><p>Diagnosis and Reporting of Creutzfeldt-Jakob Disease</p><p></p><p>Singeltary, Sr et al. JAMA.2001; 285: 733-734.</p><p></p><p><a href="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" target="_blank">http://jama.ama-assn.org/cgi/content/fu ... lcode=jama</a></p><p></p><p></p><p></p><p></p><p>BRITISH MEDICAL JOURNAL</p><p></p><p></p><p>BMJ</p><p></p><p></p><p><a href="http://www.bmj.com/cgi/eletters/319/7220/1312/b#EL2" target="_blank">http://www.bmj.com/cgi/eletters/319/7220/1312/b#EL2</a></p><p></p><p></p><p>BMJ</p><p></p><p></p><p><a href="http://www.bmj.com/cgi/eletters/320/7226/8/b#EL1" target="_blank">http://www.bmj.com/cgi/eletters/320/7226/8/b#EL1</a></p><p></p><p></p><p></p><p></p><p>[Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk</p><p>Materials for Human Food and Requirement for the Disposition of</p><p>Non-Ambulatory Disabled Cattle</p><p></p><p><a href="http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf" target="_blank">http://www.fsis.usda.gov/OPPDE/Comments ... 5IFA-2.pdf</a></p><p></p><p></p><p>[Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine</p><p>Spongiform Encephalopathy (BSE)</p><p></p><p></p><p><a href="http://www.fsis.usda.gov/OPPDE/Comments/2006-0011/2006-0011-1.pdf" target="_blank">http://www.fsis.usda.gov/OPPDE/Comments ... 0011-1.pdf</a></p><p></p><p></p><p></p><p>THE SEVEN SCIENTIST REPORT ***</p><p></p><p></p><p><a href="http://www.fda.gov/ohrms/dockets/dockets/02n0273/02n-0273-EC244-Attach-1.pdf" target="_blank">http://www.fda.gov/ohrms/dockets/docket ... tach-1.pdf</a></p><p></p><p></p><p>PAUL BROWN M.D.</p><p></p><p><a href="http://www.fda.gov/ohrms/dockets/dockets/02n0273/02n-0273-c000490-vol40.pdf" target="_blank">http://www.fda.gov/ohrms/dockets/docket ... -vol40.pdf</a></p><p></p><p></p><p></p><p></p><p>9 December 2005</p><p>Division of Dockets Management (RFA-305)</p><p></p><p>SEROLOGICALS CORPORATION</p><p>James J. Kramer, Ph.D.</p><p>Vice President, Corporate Operations</p><p></p><p><a href="http://www.fda.gov/ohrms/dockets/dockets/02n0273/02n-0273-c000383-01-vol35.pdf" target="_blank">http://www.fda.gov/ohrms/dockets/docket ... -vol35.pdf</a></p><p></p><p></p><p></p><p>Embassy of Japan</p><p><a href="http://www.fda.gov/ohrms/dockets/dockets/02n0273/02N-0273-EC240.htm" target="_blank">http://www.fda.gov/ohrms/dockets/docket ... -EC240.htm</a></p><p></p><p></p><p></p><p>Dockets Entered on December 22, 2005</p><p>2005D-0330, Guidance for Industry and FDA Review Staff on Collection of</p><p>Platelets</p><p>by Automated ... EC 203, McDonald's Restaurants Corporation, Vol #:, 34 ...</p><p><a href="http://www.fda.gov/ohrms/dockets/dailys/05/Dec05/122205/122205.htm" target="_blank">http://www.fda.gov/ohrms/dockets/dailys ... 122205.htm</a></p><p></p><p></p><p>03-025IF 03-025IF-631 Linda A. Detwiler [PDF]</p><p>Page 1. 03-025IF 03-025IF-631 Linda A. Detwiler Page 2. Page 3. Page 4.</p><p>Page 5. Page 6. Page 7. Page 8. Page 9. Page 10. Page 11. Page 12.</p><p><a href="http://www.fsis.usda.gov/OPPDE/Comments/03-025IF/03-025IF-631.pdf" target="_blank">http://www.fsis.usda.gov/OPPDE/Comments ... IF-631.pdf</a></p><p></p><p></p><p>03-025IF 03-025IF-634 Linda A. Detwiler [PDF]</p><p>Page 1. 03-025IF 03-025IF-634 Linda A. Detwiler Page 2.</p><p>Page 3. Page 4. Page 5. Page 6. Page 7. Page 8.</p><p><a href="http://www.fsis.usda.gov/OPPDE/Comments/03-025IF/03-025IF-634.pdf" target="_blank">http://www.fsis.usda.gov/OPPDE/Comments ... IF-634.pdf</a></p><p></p><p></p><p>Page 1 of 17 9/13/2005 [PDF]</p><p>... 2005 6:17 PM To: <a href="mailto:fsis.regulationscomments@fsis.usda.gov">fsis.regulationscomments@fsis.usda.gov</a> Subject: [Docket</p><p>No. 03-025IFA]</p><p>FSIS Prohibition of the Use of Specified Risk Materials for Human Food ...</p><p><a href="http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf" target="_blank">http://www.fsis.usda.gov/OPPDE/Comments ... 5IFA-2.pdf</a></p><p></p><p>03-025IFA 03-025IFA-6 Jason Frost [PDF]</p><p>... Zealand Embassy COMMENTS ON FEDERAL REGISTER 9 CFR Parts 309 et al</p><p>[Docket No. 03-</p><p>025IF] Prohibition of the Use of Specified Risk Materials for Human Food and</p><p>...</p><p><a href="http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-6.pdf" target="_blank">http://www.fsis.usda.gov/OPPDE/Comments ... 5IFA-6.pdf</a></p><p></p><p></p><p>In its opinion of 7-8 December 2000 (EC 2000), the SSC ... [PDF]</p><p>Page 1. Linda A. Detwiler, DVM 225 Hwy 35 Red Bank, New Jersey 07701 Phone:</p><p>732-741-2290</p><p>Cell: 732-580-9391 Fax: 732-741-7751 June 22, 2005 FSIS Docket Clerk US ...</p><p></p><p><a href="http://www.fsis.usda.gov/OPPDE/Comments/03-025IF/03-025IF-589.pdf" target="_blank">http://www.fsis.usda.gov/OPPDE/Comments ... IF-589.pdf</a></p><p></p><p></p><p></p><p> </p><p></p><p>Terry S. Singeltary SR.</p><p>P.O. Box 42</p><p>Bacliff, Texas USA 77518</p></blockquote><p></p>
[QUOTE="flounder, post: 307905, member: 3519"] New Mad-Cow Variant Is Suspected February 17, 2004 The Wall Street Journal by ANTONIO REGALADO Italian scientists have discovered that cattle may harbor a new form of mad-cow disease. The research by scientists at the University of Verona, in Italy, builds on earlier work that raised the possibility of unusual cases of the fatal brain-wasting disease, formally known as bovine spongiform encephalopathy. The findings pose new questions about the risk of consuming tainted meat. "If you eat cattle with this new strain, you could get a disease in humans," said Salvatore Monaco, a biologist who made the finding with colleague Gianluigi Zanusso. Dr. Monaco said he found that the brains of certain infected animals looked similar to human brains destroyed by Creutzfeldt-Jakob disease, a neurological disorder that is believed to arise spontaneously and hadn't previously been linked to tainted meat. The human form of mad-cow disease is called variant Creutzfeldt-Jakob disease, which manifests itself differently. Now the question is whether the new form of BSE could be responsible for other Creutzfeldt-Jakob cases. About 150 cases of variant Creutzfeldt-Jakob disease -- nearly all of them in Britain -- have been linked to eating infected cattle. But the majority of cases of Creutzfeldt-Jakob, which strikes about one in a million people each year, are termed "sporadic" because they don't have any known cause. Consumer groups are likely to leap at the Italian finding, published in the Proceedings of the National Academy of Science. Some activists have long contended that humans are contracting mad-cow disease in the U.S., contrary to what public-health officials say. "I have been waiting for this," said Terry S. Singeltary, a Bacliff, Texas, resident whose mother died in 1997 of Creutzfeldt-Jakob disease. Mr. Singeltary and others suspect that some cases of sporadic Creutzfeldt-Jakob are caused by something in the environment, perhaps contaminated meat. BSE is believed to be caused by misshapen proteins called prions that can be spread by consumption of contaminated tissue. The U.S. found its first case of the cattle disease in December, after a Holstein in Washington state tested positive for the condition. The Italian findings give some support to the theory that BSE could be responsible for some cases of Creutzfeldt-Jakob disease, Dr. Monaco said. The Italian group studied the brains of eight cattle that had tested positive for BSE using standard tests. Six of the animals' brains showed the usual signs, but the brains of two animals showed unusual deposits of prions. The distinctive patterns of deposits may indicate a new strain of mad-cow disease, which the Italian scientists have dubbed BASE, for bovine amyloidotic spongiform encephalopathy. Linda Detweiler, a former senior veterinarian for the U.S. Department of Agriculture, said the finding isn't a complete surprise. Studies in the U.K., France and Japan have hinted that some cattle may have been suffering from atypical cases of mad-cow disease. A related disease in sheep, called scrapie, is known to come in many different strains. Dr. Detweiler said more research will be needed to confirm whether there is in fact a new strain of BSE. One possibility is that the disease simply looks different in the specific cattle breeds in the Italian study. "I think there are still a lot of questions," Dr. Detweiler said. Stanley Prusiner, a leading researcher at the University of California, San Francisco, who is the discoverer of the prion and who reviewed the Italian report, has said the possibility of unusual BSE cases is an argument in favor of more comprehensive testing of cattle destined for human consumption. Currently, the Agriculture Department tests only a tiny fraction of cattle for mad-cow disease. Its policy is to target animals that aren't able to walk, known as downer animals, based on the theory that those are most likely to have BSE. But Dr. Monaco said his findings argue strongly for more testing in the U.S. The two animals found to have the new strain were 11 and 15 years old, "weren't acting abnormal, and were apparently free of neurological problems," Dr. Monaco said. In Europe, all cattle slaughtered that are more than 30 months of age are tested for BSE. In Japan, all cattle turned into food are tested for the disease. Scientists first discovered that BSE could affect humans in 1996, when doctors in Britain -- where mad-cow disease was ravaging herds -- found young people succumbing to Creutzfeldt-Jakob disease, which mainly strikes older people. Further research showed the disease, which remains extremely rare, was being caused by the same strain of prion as BSE -- the pattern of damage to the brain was similar in humans and cattle, as were the molecular signatures of the prions. The existence of a second strain of BSE could mean some people are contracting it, but that the cases aren't being diagnosed properly. Write to Antonio Regalado at [email=antonio.regalado@wsj.com]antonio.regalado@wsj.com[/email] [url=http://online.wsj.com/public/us]http://online.wsj.com/public/us[/url] DECEMBER 2006 Volume 12, Number 12–December 2006 PERSPECTIVE On the Question of Sporadic or Atypical Bovine SpongiformEncephalopathy and Creutzfeldt-Jakob Disease Paul Brown,* Lisa M. McShane,† Gianluigi Zanusso,‡ and Linda Detwiler§ 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. SNIP... Sporadic CJD The possibility that at least some cases of apparently sporadic CJD might be due to infection by sporadic cases of BSE cannot be dismissed outright. Screening programs needed to identify sporadic BSE have yet to be implemented, and we know from already extant testing programs that at least a proportion of infected animals have no symptoms and thus would never be identified in the absence of systematic testing. Thus, sporadic BSE (or for that matter, sporadic disease in any mammalian species) might be occurring on a regular basis at perhaps the same annual frequency as sporadic CJD in humans, that is, in the range of 1 case per million animals. Whether humans might be more susceptible to atypical forms of BSE cannot be answered at this time. Experimentally transmitted BASE shows shorter incubation periods than BSE in at least 1 breed of cattle, bovinized transgenic mice, and Cynomolgus monkeys (12,13). In humanized transgenic mice, BASE transmitted, whereas typical BSE did not transmit (13). Paradoxically, the other major phenotype (H) showed an unusually long incubation period in bovinized transgenic mice (12). The limited experimental evidence bearing on a possible relationship between BSE and sporadic CJD is difficult to interpret. The original atypical BASE strain of BSE had a molecular protein signature very similar to that of 1 subtype (type 2 M/V) of sporadic CJD in humans (5). In another study, a strain of typical BSE injected into humanized mice encoding valine at codon 129 showed a glycopattern indistinguishable from the same subtype of sporadic CJD (15). In a third study, the glycopatterns of both the H and L strains of atypical BSE evidently did not resemble any of the known sporadic CJD subtypes (12). To these molecular biology observations can be added the epidemiologic data accumulated during the past 30 years. The hypothesis that at least some cases of apparently sporadic CJD are due to unrecognized BSE infections cannot be formally refuted, but if correct, we might expect by now to have some epidemiologic evidence linking BSE to at least 1 cluster of apparently sporadic cases of CJD. Although only a few clusters have been found (and still fewer published), every proposed cluster that has been investigated has failed to show any common exposure to bovines. For that matter, no common exposure has been shown to any environmental vehicles of infection, including the consumption of foodstuffs from bovine, ovine, and porcine sources, the 3 livestock species known to be susceptible to transmissible spongiform encephalopathies. Additional negative evidence comes from several large case-control studies in which no statistically significant dietary differences were observed between patients with sporadic CJD and controls (16,17). On the other hand, the difficulty of establishing a link between BSE and CJD may be compounded by our ignorance of the infectious parameters of a sporadic form of BSE (e.g., host range, tissue distribution of infectivity, route of transmission, minimum infectious dose for humans, whether single or multiple). Presumably, these parameters would resemble those of variant CJD; that is, high infectivity central nervous system and lymphoreticular tissues of an infected cow find their way into products consumed by humans. Transmissions that might have occurred in the past would be difficult to detect because meat products are generally not distributed in a way that results in detectable geographic clusters. Barring the discovery of a specific molecular signature (as in variant CJD), the most convincing clue to an association will come from the observation of trends over time of the incidence of typical and atypical BSE and of sporadic and variant CJD. With 4 diseases, each of which could have increasing, unchanging, or decreasing trends, there could be 81 (34) possible different combinations. However, it is highly likely that the trends for typical BSE and variant CJD will both decrease in parallel as feed bans continue to interrupt recycled contamination. The remaining combinations are thus reduced to 9 (32), and some of them could be highly informative. For example, if the incidence of atypical BSE declines in parallel with that of typical BSE, its candidacy as a sporadic form of disease would be eliminated (because sporadic disease would not be influenced by current measures to prevent oral infection). If, on the other hand, atypical BSE continues to occur as typical BSE disappears, this would be a strong indication that it is indeed sporadic, and if in addition at least 1 form of what is presently considered as sporadic CJD (such as the type 2 M/V subtype shown to have a Western blot signature like BASE) were to increase, this would suggest (although not prove) a causal relationship (Figure 5). Recognition of the different forms of BSE and CJD depends upon continuing systematic testing for both bovines and humans, but bovine testing will be vulnerable to heavy pressure from industry to dismantle the program as the commercial impact of declining BSE cases ceases to be an issue. Industry should be aware, however, of the implications of sporadic BSE. Its occurrence would necessitate the indefinite retention of all of the public health measures that exclude high-risk bovine tissues from the animal and human food chains, whereas its nonoccurrence would permit tissues that are now destroyed to be used as before, once orally acquired BSE has disappeared. SNIP... PLEASE READ FULL TEXT ; [url=http://www.cdc.gov/ncidod/EID/vol12no12/06-0965.htm?s_cid=eid06_0965_e]http://www.cdc.gov/ncidod/EID/vol12no12 ... d06_0965_e[/url] 3:00 Afternoon Refreshment Break, Poster and Exhibit Viewing in the Exhibit Hall 3:30 Transmission of the Italian Atypical BSE (BASE) in Humanized Mouse Models Qingzhong Kong, Ph.D., Assistant Professor, Pathology, Case Western Reserve University Bovine Amyloid Spongiform Encephalopathy (BASE) is an atypical BSE strain discovered recently in Italy, and similar or different atypical BSE cases were also reported in other countries. The infectivity and phenotypes of these atypical BSE strains in humans are unknown. In collaboration with Pierluigi Gambetti, as well as Maria Caramelli and her co-workers, we have inoculated transgenic mice expressing human prion protein with brain homogenates from BASE or BSE infected cattle. Our data shows that about half of the BASE-inoculated mice became infected with an average incubation time of about 19 months; in contrast, none of the BSE-inoculated mice appear to be infected after more than 2 years. ***These results indicate that BASE is transmissible to humans and suggest that BASE is more virulent than classical BSE in humans. 6:30 Close of Day One [url=http://www.healthtech.com/2007/tse/day1.asp]http://www.healthtech.com/2007/tse/day1.asp[/url] SEE STEADY INCREASE IN SPORADIC CJD IN THE USA FROM 1997 TO 2006. SPORADIC CJD CASES TRIPLED, with phenotype of 'UNKNOWN' strain growing. ... [url=http://www.cjdsurveillance.com/resources-casereport.html]http://www.cjdsurveillance.com/resource ... eport.html[/url] There is a growing number of human CJD cases, and they were presented last week in San Francisco by Luigi Gambatti(?) from his CJD surveillance collection. He estimates that it may be up to 14 or 15 persons which display selectively SPRPSC and practically no detected RPRPSC proteins. [url=http://www.fda.gov/ohrms/dockets/ac/06/transcripts/1006-4240t1.htm]http://www.fda.gov/ohrms/dockets/ac/06/ ... 4240t1.htm[/url] [url=http://www.fda.gov/ohrms/dockets/ac/06/transcripts/2006-4240t1.pdf]http://www.fda.gov/ohrms/dockets/ac/06/ ... 4240t1.pdf[/url] JOURNAL OF NEUROLOGY MARCH 26, 2003 RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States Email Terry S. Singeltary: [email=flounder@wt.net]flounder@wt.net[/email] 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? [url=http://www.neurology.org/cgi/eletters/60/2/176#535]http://www.neurology.org/cgi/eletters/60/2/176#535[/url] Diagnosis and Reporting of Creutzfeldt-Jakob Disease Singeltary, Sr et al. JAMA.2001; 285: 733-734. [url=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]http://jama.ama-assn.org/cgi/content/fu ... lcode=jama[/url] BRITISH MEDICAL JOURNAL BMJ [url=http://www.bmj.com/cgi/eletters/319/7220/1312/b#EL2]http://www.bmj.com/cgi/eletters/319/7220/1312/b#EL2[/url] BMJ [url=http://www.bmj.com/cgi/eletters/320/7226/8/b#EL1]http://www.bmj.com/cgi/eletters/320/7226/8/b#EL1[/url] [Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk Materials for Human Food and Requirement for the Disposition of Non-Ambulatory Disabled Cattle [url=http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf]http://www.fsis.usda.gov/OPPDE/Comments ... 5IFA-2.pdf[/url] [Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine Spongiform Encephalopathy (BSE) [url=http://www.fsis.usda.gov/OPPDE/Comments/2006-0011/2006-0011-1.pdf]http://www.fsis.usda.gov/OPPDE/Comments ... 0011-1.pdf[/url] THE SEVEN SCIENTIST REPORT *** [url=http://www.fda.gov/ohrms/dockets/dockets/02n0273/02n-0273-EC244-Attach-1.pdf]http://www.fda.gov/ohrms/dockets/docket ... tach-1.pdf[/url] PAUL BROWN M.D. [url=http://www.fda.gov/ohrms/dockets/dockets/02n0273/02n-0273-c000490-vol40.pdf]http://www.fda.gov/ohrms/dockets/docket ... -vol40.pdf[/url] 9 December 2005 Division of Dockets Management (RFA-305) SEROLOGICALS CORPORATION James J. Kramer, Ph.D. Vice President, Corporate Operations [url=http://www.fda.gov/ohrms/dockets/dockets/02n0273/02n-0273-c000383-01-vol35.pdf]http://www.fda.gov/ohrms/dockets/docket ... -vol35.pdf[/url] Embassy of Japan [url=http://www.fda.gov/ohrms/dockets/dockets/02n0273/02N-0273-EC240.htm]http://www.fda.gov/ohrms/dockets/docket ... -EC240.htm[/url] Dockets Entered on December 22, 2005 2005D-0330, Guidance for Industry and FDA Review Staff on Collection of Platelets by Automated ... EC 203, McDonald's Restaurants Corporation, Vol #:, 34 ... [url=http://www.fda.gov/ohrms/dockets/dailys/05/Dec05/122205/122205.htm]http://www.fda.gov/ohrms/dockets/dailys ... 122205.htm[/url] 03-025IF 03-025IF-631 Linda A. Detwiler [PDF] Page 1. 03-025IF 03-025IF-631 Linda A. Detwiler Page 2. Page 3. Page 4. Page 5. Page 6. Page 7. Page 8. Page 9. Page 10. Page 11. Page 12. [url=http://www.fsis.usda.gov/OPPDE/Comments/03-025IF/03-025IF-631.pdf]http://www.fsis.usda.gov/OPPDE/Comments ... IF-631.pdf[/url] 03-025IF 03-025IF-634 Linda A. Detwiler [PDF] Page 1. 03-025IF 03-025IF-634 Linda A. Detwiler Page 2. Page 3. Page 4. Page 5. Page 6. Page 7. Page 8. [url=http://www.fsis.usda.gov/OPPDE/Comments/03-025IF/03-025IF-634.pdf]http://www.fsis.usda.gov/OPPDE/Comments ... IF-634.pdf[/url] Page 1 of 17 9/13/2005 [PDF] ... 2005 6:17 PM To: [email=fsis.regulationscomments@fsis.usda.gov]fsis.regulationscomments@fsis.usda.gov[/email] Subject: [Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk Materials for Human Food ... [url=http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-2.pdf]http://www.fsis.usda.gov/OPPDE/Comments ... 5IFA-2.pdf[/url] 03-025IFA 03-025IFA-6 Jason Frost [PDF] ... Zealand Embassy COMMENTS ON FEDERAL REGISTER 9 CFR Parts 309 et al [Docket No. 03- 025IF] Prohibition of the Use of Specified Risk Materials for Human Food and ... [url=http://www.fsis.usda.gov/OPPDE/Comments/03-025IFA/03-025IFA-6.pdf]http://www.fsis.usda.gov/OPPDE/Comments ... 5IFA-6.pdf[/url] In its opinion of 7-8 December 2000 (EC 2000), the SSC ... [PDF] Page 1. Linda A. Detwiler, DVM 225 Hwy 35 Red Bank, New Jersey 07701 Phone: 732-741-2290 Cell: 732-580-9391 Fax: 732-741-7751 June 22, 2005 FSIS Docket Clerk US ... [url=http://www.fsis.usda.gov/OPPDE/Comments/03-025IF/03-025IF-589.pdf]http://www.fsis.usda.gov/OPPDE/Comments ... IF-589.pdf[/url] Terry S. Singeltary SR. P.O. Box 42 Bacliff, Texas USA 77518 [/QUOTE]
Insert quotes…
Verification
Post reply
Forums
Cattle Boards
NCBA, R-CALF, COOL, USDA (No Politics!)
CJD USA UPDATE NOV. 2006
Top