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From: TSS (216-119-136-145.ipset16.wt.net)
-------- Original Message -------- Editorial team (Eurosurveillance.weekly@hpa.org.uk Brain tissue samples from a sheep carcass in the United Kingdom (UK) Results so far show that some characteristics of this detected case are There is a theoretical risk that BSE could be present in sheep, masked References: 1. Department for Environment, Food and Rural Affairs. Defra 7 April 2004 The Veterinary Laboratories Agency (VLA) have informed Defra, the The VLA and other European laboratories with expertise in scrapie-like A meeting of the scientific experts who performed these analyses, held Defra's Chief Scientific Adviser, Professor Howard Dalton, said "The UK, The National Scrapie Plan remains unaffected by this new result and SEAC ------------------------------------------------------------------------ Notes for editors 1. Scrapie is a fatal neurological sheep disease belonging to a group of 2. There is a theoretical risk that BSE could be present in sheep, 3. There is as yet no definitive diagnostic method that can rapidly a. Western blot (WB) This involves taking a sample of the brain and treating it with an b. Immunohistochemistry (IHC) This involves taking thin slices of the brain, and by using special The Western blot method found that the sample did not appear to resemble 5. The tissue sample has now been analysed using a total of 5 different 6. The VLA is the European Reference Laboratory for TSEs and is 7. The genotype of the suspect sheep was ARQ/ARQ which is known to be END Public Enquiries: 08459 335577 back to top ------------------------------------------------------------------------ well, let's see. if you search the Gov. site, the urls have conveniently gone http://spider.aphis.usda.gov/compass?scope=scrapie+vermont&browse-category=ROOT&search-category=ROOT&ui=sr&chunk-size=&page=1&taxonomy=Compass 80% Relevant Vermont sheep-5/02 APHIS Factsheet 8AJAHE=HO 5AHLE?AI )FHE Imported Background APHIS' mission is to "Protect American Belgium/Netherlands Agriculture." As part of that mission APHIS regulates the importation of a http://spider.aphis.usda.gov/compass?scope=scrapie+vermont&search-category=ROOT&view-template=aphis&browse-category=ROOT&ui=sr&chunk-size=10&page=2&taxonomy=Compass Date: Thu, 11 Apr 2002 16:11:37 -0700 ######## Bovine Spongiform Encephalopathy 4/11/2002 USDA: Testing to Continue on Confiscated Imported Sheep by Julianne Johnston USDA today said that tests conducted on a flock of sheep confiscated last year from a farm in Vermont confirm that two of the 125 sheep tested positive for an atypical undifferentiated transmissible spongiform encephalopathy (TSE) of foreign origin. The flock of 125 sheep was confiscated in March 2001 after four animals from an associated flock tested positive for TSE in July 2000. USDA said it will continue to conduct additional tests to determine the type of TSE in these sheep. "These results confirm our previous conclusions were correct and that we took the appropriate preventative actions in confiscating these animals," said Bobby Acord, administrator of USDA's Animal and Plant Health Inspection Service. "USDA's actions to confiscate, sample and destroy these sheep were on target. As a result of our vigilance, none of these confiscated animals entered the animal or human food supply." The sheep, imported from Belgium and the Netherlands in 1996, were placed under certain federal restrictions when they entered the country as part of USDA's scrapie control efforts. In 1998, USDA learned that it was likely that sheep from Europe were exposed to feed contaminated with bovine spongiform encephalopathy. At that time, the state of Vermont, at the request of USDA, imposed a quarantine on these flocks, which prohibited slaughter or sale for breeding purposes. On July 10, 2000, several sheep from the flock tested positive for a TSE, a class of degenerative neurological diseases that is characterized by a very long incubation period and a 100 percent mortality rate in infected sheep. Two of the better known varieties of TSE are scrapie in sheep and BSE in cattle. There is no evidence that scrapie poses a risk to human health. On July 14, 2000, USDA issued a declaration of extraordinary emergency to acquire the sheep. This action was contested by the flock owners. A federal district court judge ruled in favor of USDA based on the merits of the case. The flock owners appealed to the Second Circuit Court requesting a stay, which was denied. The sheep were confiscated by USDA in March 2001 and transported to USDA's National Veterinary Services Laboratories in Ames, Iowa, where they were humanely euthanized. Tissue samples were collected from the sheep for diagnostic testing and USDA will continue with additional tests which could take up to 2 - 3 years to complete. In all, USDA has acquired 380 sheep from a total of three flocks. All of the animals were humanely euthanized, sampled and disposed and did not enter the animal or human food supply. http://www.agweb.com/news_show_news_article.asp?file=AgNewsArticle_20024111426_2812&articleID=87101&newscat=GN Greetings list members, > tested positive for an atypical undifferentiated transmissible > spongiform encephalopathy (TSE) of foreign origin. what the heck does this mean? so was it scrapie from Europe, or BSE in the sheep, or was it just like all the rest of the Scrapies in the USA? what made this an atypical undifferentiated TSE of foreign origin? kind regards, Terry S. Singeltary SR., Bacliff, Texas USA ########### http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############ ######## Bovine Spongiform Encephalopathy Greetings again list members, i notice here that they did; [[Meanwhile, the Faillaces and Freeman cannot put animals such as cattle, sheep or goats on the land the sheep used for five years from the time the sheep left. And the property is being disinfected under the direction of the USDA.]] http://timesargus.nybor.com/Story/45252.html again, why does this not pertain to all scrapie infected lands in the USA??? how is this disinfection being carried out? are they taking two feet or more of topsoil away from entire quarantined land? how are they disinfecting environment? what about small critters that enter area? how are they keeping deer/elk and other animals from area? what is so special of the Fallice's sheep scrapie's??? [[But despite the positive finding, Detwiler said there was no risk to human or animal health in the United States.]] how in the world can she make such stupid statements, when she apparently does not know what type TSE she is even dealing with. this is what she insinuates by the atypical undifferentiated transmissible spongiform encephalopathy (TSE) of foreign origin. the next thing that will come from them is a _new_ name for same disease. please someone lurking from the USDA/APHIS explain this??? or can you$ my personal opinion, we need new blood (not related to industry), to be involved in TSE regulations$ look what has happened to date with the old regime. (nothing) yep, no BSE yet, but again, we have not looked to find it. apparently they don't have time with all the other human/animal TSEs they are dealing with. GBR II my XXX, USA should be re-evaluated to GBR III, and sooner than later... Terry S. Singeltary Sr., Bacliff, Texas USA Terry S. Singeltary Sr. wrote: > ######## Bovine Spongiform Encephalopathy ######## Bovine Spongiform Encephalopathy Greetings List Members, i must comment on Paul Browns ''afterthoughts''. i respectfully strongly disagree with some of his _assumptions_ and in my opinion, he should read up on the data on BSE to sheep and the _real_ threat this poses. i will not elaborate on his _assumption_ (one with no scientific data to back it up) that scrapie will not transmit to man. there has never been laboratory studies to prove this, BUT scrapie does transmit to primate. however, my concern is with his statements here; Products derived from nonbovine species, including sheep, pigs, and chickens (both meat and eggs) should also be entirely safe, as there is no evidence that any of these species is naturally susceptible to BSE. Scrapie-infected sheep tissues have been eaten by humans for centuries without causing disease (5 and his comments here are very disturbing to me $$$ ''Thus, the argument that undetected cases of BSE might be present in the United States, although impossible to disprove, is not supported by current evidence''... Paul, you have to first ''look to find'' 1 MILLION RAPID TSE TEST IN THE USA BOVINE ANNUALLY FOR 5 YEARS !!! Greetings again, in my humble opinion, there is indeed great concern for the potential for BSE in the sheep population, and current evidence DOES support the existence of a TSE in USA cattle, one that has been here for decades, but conveniently ignored or silently covered-up. i wish to kindly submit this data to you... TSS TSE in Sheep Contingency Planning Assessment of Risk due to BSE Infectivity from Disposal of Sheep A report for DEFRA November 2001 Management Summary It has been recognised for a considerable time that sheep in the United Kingdom may have been infected with BSE. To date no evidence has been found to demonstrate that the national flock is actually infected with the disease. DEFRA have prepared a draft contingency plan in the event that BSE were to be identified in UK sheep. The worst case scenario under this plan is the disposal of the entire UK flock, some 40 million sheep and lambs. This study has estimated the potential exposure of the UK population to BSE infectivity present in sheep in the event that this plan had to be put into effect. http://www.defra.gov.uk/animalh/bse/bse-publications/seac/DNVReport.pdf but who would have guessed that such an important experiment/study would have gotton so screwed up, by not being able to tell a sheep brain from a cow brain; © DEFRA 2002 Item 3- Scrapie Brain pool experiments- Update on current position and audits of samples 3.1 Members were updated on experiments conducted at the Institute of Animal Health (IAH) to examine a pool of scrapie brains collected in the early 1990s for evidence of BSE. SEAC had previously recommended that the material should be examined by DNA analysis to assess whether the pooled brain material may have been contaminated with bovine tissue. The Laboratory of the Government Chemist (LGC) had been asked to perform the work. Their results were completely unexpected as the analysis detected only bovine material in the sample. SEAC had intended to meet on the 19 October to Agreed version consider the experiment in detail. However, in view of the result, the meeting was cancelled. http://www.defra.gov.uk/animalh/bse/bse-publications/seac/mins21-11-01.pdf Executive Summary An audit of the sample handling procedures at IAH-E was carried out on 24 October 2001 at the request of the Department of the Environment, Food and Rural Affairs (DEFRA), by a team of two UKAS auditors. The scope of the audit was limited to the traceability of cow and sheep brain samples used in several experiments relating to transmissible spongiform encephalopathy (TSE) agents. In particular, the team focused on the audit trail of samples that had been sent to LGC, Teddington, the audit trail of brains collected in 1990/92 by Veterinary Investigation Centres and the audit trail for archived material held by IAH-E. In addition the audit team evaluated the IAH-E procedures against the specific requirements for sampling handling of international standard, ISO 17025 and identified opportunities for improvement. The audit established that there was no formal documented quality system covering this work at IAH-E and that record keeping was inadequate to give confidence in the chain of custody of samples used in the various rendering, genotyping and strain typing experiments audited. It was not possible to establish clear traceability between the samples that had been used in the individual experiments carried out by IAH-E or IAH-C with those analysed at LGC or with those that had been collected in 1990/92. The sample handling procedures covered by this audit at IAH-E did not meet the requirements of ISO 17025. http://www.defra.gov.uk/animalh/bse/bse-publications/audit/ukasrept.pdf explaining the brain mixup blunder; An Investigation of the Substitution of Scrapie Brain Pool Samples A report for DEFRA November 2001 Risk Solutions Page 19 Why did the experimenters not notice that they were working with cow brains not sheep brains? The simple answer is because for the most part they were working with brain pool macerate (minced brain material) not brains. It is not credible that staff collecting brains at VICs would have uniformly supplied cow brains or cow brain parts in mistake for sheep. We have interviewed staff at VICs and we understand from the VLA that records do not support the possibility that significant numbers of cow brains were sent to PDM in place of sheep brains. It is also very unlikely that the people preparing the scrapie brain pool would not have noticed if they were for the most part handling cow brains or cow brain parts in place of sheep brains. We cannot rule out the possibility that some cow brain material entered the brain pool at this stage but it is not feasible that the majority of the material was bovine. The substitution, if substitution occurred, must have involved brain pool macerate or rendered products. Why cant the results of the experiments tell us what material was used? The experiments had a number of features that make the results of the mouse bioassay difficult to interpret unambiguously and lead to the possibility that substitution of the samples would be difficult to detect by examining the results of the experiments: 1. The original experiments were not designed to determine whether BSE was present in sheep. Reasonable efforts were taken to ensure that the brain pool remained free from D5055 02 Issue 1 Risk Solutions Page 20 contamination during preparation but the level of control applied during the earlier experiments (272R and 372R) was not to the standard applied later. 2. Mouse bioassay as a method of diagnosing TSEs is not based on a full understanding of biochemical and physical processes. It is an empirical technique that has been widely applied, for example to show v-CJD is similar to BSE and different from scrapie. It is a complex process and the results need to be interpreted by experts. It can take several years to generate a firm result. The principal data collected in the experiments are lesion profiles (patterns of lesions in the mice brains) and incubation period (time from injection of mice to onset of clinical symptoms. The type of TSE is identified by comparing the results with those of known provenance. There is no good agreed test of sameness of lesion profile , so in marginal cases we are reduced to using subjective observations of the form somewhat similar and interpretation is difficult. The incubation times in principle give a more objective signal, but the effect of concentration has to be controlled. The mouse bioassay data that we understand has been collected and analysed at each stage of the experiments is summarised in Table 4.1. Several features of these experiments are not commonly encountered in mouse bioassay of TSEs and this makes determining the origin of the original material from the experimental results extremely difficult. They include: a. Mouse bioassay is generally carried out on individual brains; experience of working with brain pools is very limited. b. The BBP exhibited a low titre of infectivity, which can confound interpretation of results. c. The BBP comprised bovine brains with the hindbrains removed. By contrast most of the BSE strain typing has been carried out on the hindbrains, which may give a different pattern of results. d. The 272R titrations used a different strain of mice than the 372R titrations, so direct comparison of the resulting lesion profiles cannot be made. e. The 246 experiments used brain pool which was in an unsatisfactorily autolysed state. f. The strain typing data collected (incubation time and lesion profiles) are very sparse. Judging the sameness or difference of samples is a less challenging task for strain typing than identifying a strain and it may be possible to compare data from the 246 experiments with both the 272R and 372R experiments to determine whether the samples are similar or clearly different. However, the data are sparse and the result is unlikely to be clear cut. Much of this work is currently unpublished. http://www.defra.gov.uk/animalh/bse/bse-publications/audit/risksol.pdf RESPONSE TO THE UKAS REPORT FROM THE INSTITUTE FOR ANIMAL HEALTH The Institute is concerned, therefore, that the authors of this UKAS report may have based their findings on an unrepresentative and limited examination of procedures in place at IAH-E. http://www.defra.gov.uk/animalh/bse/bse-publications/audit/response.pdf http://www.defra.gov.uk/animalh/bse/index.html http://www.mad-cow.org/00/jul00_dont_eat_sheep.html Transmission of prion diseases by blood transfusion Nora Hunter,1 James Foster,1 Angela Chong,1 Sandra McCutcheon,2 David Parnham,1 Samantha Eaton,1 Calum MacKenzie1 and Fiona Houston2 http://www.socgenmicrobiol.org.uk/JGVDirect/18580/18580ft.pdf TSEs TRANSMISSION STUDIES what a coincedence , CONVENIENTLY, MORE FLUBBED UP BRAINS; HOUND STUDY b) Fibrillar material closely similar to SAF, found in BSE/Scrapie, was observed in 19 (4.3%) cases, all of which were hounds > 7 years of age. 14/19 of these suspected SAF results correlated with cases in the unresolveable histopathological catergory... http://www.bseinquiry.gov.uk/files/sc/seac19/tab07.pdf HOUND SURVEY (about 72 pages) http://www.bseinquiry.gov.uk/files/mb/m11a/tab08.pdf Also, at paragraph 17, it is noted that BSE had transmitted to the NPU negative line sheep (please not that as at January 1996, only one of six challenged sheep was clinically affected after oral challenge, four others have since died, and one remains alive. Following intracerebral challenge, three out of six were clinically affected, two confirmed only on pathology, while one was negative.) 4. Meeting 16, on 26/1/94 - the update on research (16/5) confirmed that BSE had been transmitted to sheep, and that there was clinical evidence of transmission to mice from the spleen of the affected sheep. snip... IN CONFIDENCE A STUDY AIMED AT DETERMINING WHETHER OR NOT THERE HAVE BEEN SIGNIFICANT CHANGES IN THE NEUROPATHOLOGY OF SCRAPIE IN SHEEP AND GOATS DURING THE LAST TWO DECADES IN MATERIAL SUBMITTED TO CVL PATHOLOGY DEPARTMENT http://www.bseinquiry.gov.uk/files/sc/seac24/tab03.pdf EXPERIMENTAL TRANSMISSION OF BSE TO SHEEP http://www.bseinquiry.gov.uk/files/sc/seac25/tab05.pdf THE RISK OF TRANSMISSION OF BSE TO SHEEP VIA FEED http://www.bseinquiry.gov.uk/files/sc/seac31/tab01.pdf hell, they knew they were screwing up the sheep brains with cow brains in 1992; "The sensitivity of the project may be partially compromised by pooling of brains, but it is considered that the success of transmission to mice with BSE will prove advantageous." 'NOT'...tss http://www.bseinquiry.gov.uk/files/sc/seac31/tab01.pdf Personal $ Confidential -- Addressee only TO ALL MEMBERS OF SEAC THE EXPERIMENTAL TRANSMISSION OF BSE TO SHEEP http://www.bseinquiry.gov.uk/files/sc/seac33/tab02.pdf a) Summary of transmission studies. b) Update http://www.bseinquiry.gov.uk/files/sc/seac33/tab03.pdf The only circumstance in which infection with the natural isolate produces an higher incidence of disease compared to BSE, is in intracerebrally (and possibly orally) challenged ''positive'' line sheep. Notwithstanding the possibility of indigenous natural scrapie in some of these sheep, there are still sufficient numbers of transmission cases with PrP genotypes which preclude the natural disease developing i.e. those typed as VA136/RR154/QR171. As an extension to this study, it has been possible to recover BSE by passage in mice from brain and spleen taken from ''negative'' line sheep infected with BSAE by ic and oral challenge (Foster and others 1996). The close similarity of incubation periods and pathology from the passage of these tissues in mice to those seen in direct BSE transmission studies from cattle to mice suggests that passaging BSE in sheep does not alter its bilogical properties (Bruce and others 1994). IN FACT, because it has been possible to isolate BSE infectivity from ovine spleens, when this proved impossible from the spleens of naturally infected BSE cows (Fraser and Foster 1993), experimentally-induced BSE in sheep appears to behave more like the natural disease of scrapie.Whether this putative similarity to natural scrapie extends to the possibility of maternal transmission of experimentally-induced BSE in sheep, has till to be elucidated... http://www.bseinquiry.gov.uk/files/mb/m09/tab01.pdf we have found a link between BSE and CH1641, a C-group of scrapie. Disease susceptibility of sheep to these isolates is associated with different PrP genotypes compared to SSBP/1 scrapie... Transmission of BSE in sheep, goats and mice. snip... BSE has been transmitted in two lines of genetically selected sheep (differeing in their susceptibilities to the SSBP/1 source of scrapie), and to goats by intracerebral injection AND BY ORAL DOSING. snip... Also, intermediate passage of BSE in sheep or goats did not alter these primary transmission properties. Hamsters were susceptible to BSE only after intervening passage through mice... http://www.bseinquiry.gov.uk/files/mb/m09/tab11.pdf IN CONFIDENCE Perceptions of unconventional slow virus in the USA 3. Prof. A Robertson gave a brief account of BSE. The US approach was to accord it a very low profile indeed. Dr. A Thiermann showed the picture in the ''Independent'' with cattle being incinerated and thought this was a fantical incident to be avoided in the USA AT ALL COSTS. BSE was not reported in the USA...........(some good data on CWD) > avoided in the USA AT ALL COSTS and indeed they have and it continues today...TSS http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf BSE TRANSMISSION STUDIES http://www.bseinquiry.gov.uk/files/sc/seac18/tab02b.pdf Furthermore, we showed that the strain responsible for iCJD is closely related to that of one patient with sCJD, and, more unexpectedly, that these agents were similar to the French scrapie strain studied (but different from the U.S. scrapie strain). This finding requires a cautious interpretation for several reasons, not least because of the inevitably limited number of TSE strains that can be studied by such a cumbersome method as strain typing. Nonetheless, it also prompts reconsideration of the possibility that, in some instances, sheep and human TSEs can share a common origin. snip... http://www.pnas.org/cgi/content/full/041490898v1 STATEMENT OF DR HELEN GRANT MD FRCP ISSUED 13/05/1999 BSE INQUIRY http://www.bseinquiry.gov.uk/files/ws/s410.pdf http://www.bseinquiry.gov.uk/files/ws/s410x.pdf http://www.bseinquiry.gov.uk/evidence/ws/ws8.htm From: Terry S. Singeltary Sr. [mailto:flounder@wt.net] Sent: Tuesday, February 18, 2003 12:45 PM To: Freas, William Cc: Langford, Sheila Subject: Re: re-vCJD/blood and meeting of Feb. 20, 2003 http://www.fda.gov/ohrms/dockets/ac/03/slides/3923s1_OPH.htm and what about those USA MADCOWS; HOW CAN PAUL BROWN IGNORE THIS; EVIDENCE OF TRANSMISSIBLE MINK ENCEHPALOPATHY RESULTS FROM FEEDING INFECTED CATTLE To be published in the Proceedings of the Fourth International Scientific Congress in Fur Animal Production. Toronto, Canada, August 21-28, 1988 Evidence That Transmissible Mink Encephalopathy Results from Feeding Infected Cattle _ - R.F. Marsh* and G.R. Hartsough "Department of Veterinary Science, University of Wisconsin-Madison, Madison, Wisconsin 53706; and ^Emba/Creat Lakes Ranch Service, Thiensville, Wisconsin 53092 ABSTRACT Epidemiologic investigation of a new incidence of transmissible mink encephalopathy (TME) in Stetsonville, Wisconsin suggests that the disease may have resulted from feeding infected cattle to mink. This observation is supported by the transmission of a TME-like disease to experimentally inoculated cattle, and by the recent report of a new bovine spongiform encephalopathy in England. INTRODUCTION Transmissible mink encephalopathy (TME) was first reported in 1965 by Hartsough and Burger who demonstrated that the disease was transmissible with a long incubation period, and that affected mink had a spongiform encephalopathy similar to that found in scrapie-affecied sheep (Hartsough and Burger, 1965; Burger and Hartsough, 1965). Because of the similarity between TME and scrapie, and the subsequent finding that the two transmissible agents were indistinguishable (Marsh and Hanson, 1969), it was concluded that TME most likely resulted from feeding mink scrapie-infecied sheep. The experimental transmission of sheep scrapie to mink (Hanson et al., 1971) confirmed the close association of TME and scrapie, but at the same time provided evidence that they may be different. Epidemiologic studies on previous incidences of TME indicated that the incubation periods in field cases were between six months and one year in length (Harxsough and Burger, 1965). Experimentally, scrapie could not be transmitted to mink in less than one year. To investigate the possibility that TME may be caused by a (particular strain of scrapie which might be highly pathogenic for mink, 21 different strains of the scrapie agent, including their sheep or goat sources, were inoculated into a total of 61 mink. Only one mink developed a progressive neurologic disease after an incubation period of 22 mon..s (Marsh and Hanson, 1979). These results indicated that TME was either caused by a strain of sheep scrapie not yet tested, or was due to exposure to a scrapie-like agent from an unidentified source. OBSERVATIONS AND RESULTS A New Incidence of TME. In April of 1985, a mink rancher in Stetsonville, Wisconsin reported that many of his mink were "acting funny", and some had died. At this time, we visited the farm and found that approximately 10% of all adult mink were showing typical signs of TME: insidious onset characterized by subtle behavioral changes, loss of normal habits of cleanliness, deposition of droppings throughout the pen rather than in a single area, hyperexcitability, difficulty in chewing and swallowing, and tails arched over their _backs like squirrels. These signs were followed by progressive deterioration of neurologic function beginning with locomoior incoordination, long periods of somnolence in which the affected mink would stand motionless with its head in the corner of the cage, complete debilitation, and death. Over the next 8-10 weeks, approximately 40% of alt the adult mink on the farm died from TME. Since previous incidences of TME were associated with common or shared feeding practices, we obtained a careful history of feed ingredients used over the past 12-18 months. The rancher was a "dead stock" feeder using mostly (>95%) downer or dead dairy cattle and a few horses. Sheep had never been fed. Experimental Transmission. The clinical diagnosis of TME was confirmed by histopaihologic examination and by experimental transmission to mink after incubation periods of four months. To investigate the possible involvement of cattle in this disease cycle, two six-week old castrated Holstein bull calves were inoculated intracerebrally with a brain suspension from affected mink. Each developed a fatal spongiform encephalopathy after incubation periods of 18 and 19 months. DISCUSSION These findings suggest that TME may result from feeding mink infected cattle and we have alerted bovine practitioners that there may exist an as yet unrecognized scrapie-like disease of cattle in the United States (Marsh and Hartsough, 1986). A new bovine spongiform encephalopathy has recently been reported in England (Wells et al., 1987), and investigators are presently studying its transmissibility and possible relationship to scrapie. Because this new bovine disease in England is characterized by behavioral changes, hyperexcitability, and agressiveness, it is very likely it would be confused with rabies in the United Stales and not be diagnosed. Presently, brains from cattle in the United States which are suspected of rabies infection are only tested with anti-rabies virus antibody and are not examined histopathologically for lesions of spongiform encephalopathy. We are presently pursuing additional studies to further examine the possible involvement of cattle in the epidemiology of TME. One of these is the backpassage of our experimental bovine encephalopathy to mink. Because (here are as yet no agent- specific proteins or nucleic acids identified for these transmissible neuropathogens, one means of distinguishing them is by animal passage and selection of the biotype which grows best in a particular host. This procedure has been used to separate hamster- adapted and mink-udapted TME agents (Marsh and Hanson, 1979). The intracerebral backpassage of the experimental bovine agent resulted in incubations of only four months indicating no de-adaptation of the Stetsonville agent for mink after bovine passage. Mink fed infected bovine brain remain normal after six months. It wili be essential to demonstrate oral transmission fiom bovine to mink it this proposed epidemiologic association is to be confirmed. ACKNOWLEDGEMENTS These studies were supported by the College of Agricultural and Life Sciences, University of Wisconsin-Madison and by a grant (85-CRCR-1-1812) from the United States Department of Agriculture. The authors also wish to acknowledge the help and encouragement of Robert Hanson who died during the course of these investigations. REFERENCES Burger, D. and Hartsough, G.R. 1965. Encephalopathy of mink. II. Experimental and natural transmission. J. Infec. Dis. 115:393-399. Hanson, R.P., Eckroade, R.3., Marsh, R.F., ZuRhein, C.M., Kanitz, C.L. and Gustatson, D.P. 1971. Susceptibility of mink to sheep scrapie. Science 172:859-861. Hansough, G.R. and Burger, D. 1965. Encephalopathy of mink. I. Epizoociologic and clinical observations. 3. Infec. Dis. 115:387-392. Marsh, R.F. and Hanson, R.P. 1969. Physical and chemical properties of the transmissible mink encephalopathy agent. 3. ViroL 3:176-180. Marsh, R.F. and Hanson, R.P. 1979. On the origin of transmissible mink encephalopathy. In Hadlow, W.J. and Prusiner, S.P. (eds.) Slow transmissible diseases of the nervous system. Vol. 1, Academic Press, New York, pp 451-460. Marsh, R.F. and Hartsough, G.R. 1986. Is there a scrapie-like disease in cattle? Proceedings of the Seventh Annual Western Conference for Food Animal Veterinary Medicine. University of Arizona, pp 20. Wells, G.A.H., Scott, A.C., Johnson, C.T., Cunning, R.F., Hancock, R.D., Jeffrey, M., Dawson, M. and Bradley, R. 1987. A novel progressive spongiform encephalopathy in cattle. Vet. Rec. 121:419-420. http://www.bseinquiry.gov.uk/ Is there a Scrapie-like disease in cattle in USA http://www.bseinquiry.gov.uk/files/mb/m09a/tab01.pdf who's testing what; Cattlemen to finalize BSE research contracts (WHAT'S THE RUSH, LET'S WAIT ANOTHER 30 YEARS) - TSS 1/17/03 (0) http://www.vegsource.com/talk/madcow/messages/9912336.html In Reply to: Docket No. 01-068-1 Risk Reduction Strategies for Potential BSE Pathways Involving Downer Cattle and Dead Stock of Cattle and Other Species [TSS SUBMISSION] January 21, 2003 http://www.vegsource.com/talk/madcow/messages/9912358.html and where are my dang mad cow feed ban warning letters and what happened to the F.O.I.A.; re--FDA RUMINANT-TO-RUMINANT FEED BAN VIOLATION FEE WAIVER REQUEST http://www.vegsource.com/talk/madcow/messages/330.html and who's looking for CJD in the USA and asking any questions as to route and source; # Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States [FULL TEXT] - TSS 2/22/03 (0) http://www.vegsource.com/talk/madcow/messages/9912538.html still disgusted in Bacliff, TEXAS USA Terry S. Singeltary Sr. Date: Mon, 5 May 2003 16:50:28 -0500 Reply-To: Bovine Spongiform Encephalopathy Sender: Bovine Spongiform Encephalopathy From: "Terry S. Singeltary Sr." Bovine Spongiform Encephalopathy --------------010200020009060703070801 Content-Type: text/plain; charset=windows-1252; format=flowed Content-Transfer-Encoding: 8bit Commentary Afterthoughts about Bovine Spongiform Encephalopathy and Variant Creutzfeldt-Jakob Disease Paul Brown Senior Investigator, National Institutes of Health, Bethesda, Maryland, USA ------------------------------------------------------------------------ The recent review (1 Advice for Travelers to Europe The most frequently asked question concerned travel to Europe this summer: what is safe to eat, and what should be avoided. In principle, beef and beef products should no longer carry any risk because the European Community, as well as individual European countries, have taken measures to prevent the entry of potentially contaminated products into the human food chain. These measures include regulations to end the recycling of mammalian protein into ruminant feed (extended by some countries to feed used for all mammalian species); removal of the heads and vertebral columns of slaughtered cattle before further processing; and prohibition of certain nervous system and visceral tissues for human consumption. In the United Kingdom, mechanically removed meat, even after removal of the vertebral column, is prohibited for human use. Nevertheless, because the extent of BSE outbreaks in most European countries is still not known--more and more cases are being discovered through active surveillance using sensitive immunologic tests--and because there is always an imprecise lead time before the implementation of precautionary measures, it would probably be wise to remain wary of beef products in continental European countries (and certain other countries) in which BSE already exists or is likely to appear, and in which safeguards may not yet be fully implemented. The European Commission of Food Safety has published a global country-by-country BSE risk analysis, with continuing web site updates as new information becomes available http://europa.eu.int/comm/food/fs/sc/ssc/outcome_en.html). It is also important to reemphasize that beef as such is not dangerous; the villains were almost certainly beef products that (in the past) contained mechanically recovered meat contaminated by nervous system tissue. These beef products were often added to such precooked items as sausages, hot dogs, bologna and other luncheon meats, canned beef products, beef stews and broths, and meat pies-in short, any product containing beef in a precooked and often unrecognizable form. Cooking cannot be guaranteed to sterilize BSE infectivity: experiments using different strains of spongiform encephalopathy agents have shown only partial inactivation at temperatures as high as 350°C (662°F) (2,3 Dairy and Other Bovine-Derived Products Many readers asked about the safety of milk and dairy products. Persuasive evidence indicates that these important consumables are risk free: milk from infected cows has been fed to, and injected into the brain of, susceptible RIII mice without transmitting disease. Even more convincingly, calves suckling gallons of milk from their infected mothers have not contracted the disease (4 Questions have also arisen about the safety of other products derived from bovine sources, such as gelatin and tallow derivatives, which find their way into a dazzling array of items eaten or used by humans. These include products as varied as jellybeans, cosmetics, and vaccines. Scientific advisory committees in many countries, including the United States, have addressed these questions and have concluded that infectivity in the tissues used as sources of these products is either low or nonexistent, and that even if existent, infectivity would in most cases be destroyed by the processes used in product manufacturing. Nevertheless, depending on estimates of risk inherent in tissue sources and use of different products, industry has been either obliged or strongly urged to ensure BSE-free status of source cattle and to include processing steps known to destroy infectivity. Nonbovine Products Products derived from nonbovine species, including sheep, pigs, and chickens (both meat and eggs) should also be entirely safe, as there is no evidence that any of these species is naturally susceptible to BSE. Scrapie-infected sheep tissues have been eaten by humans for centuries without causing disease (5 The American Scene Concerns have been raised about BSE status in the United States and about the safety of foods and other products from domestic bovine sources. BSE could occur in the Unites States only as a result of 1) cases arising de novo in domestic cattle, 2) cases arising from exposure to spongiform encephalopathies in other domestic species, or 3) cases arising from the importation of infected cattle or livestock feed. With respect to de novo cases, it is possible that cattle (and perhaps all mammals) are subject to the same rate of spontaneously occurring disease as that of CJD in humans, approximately one case per million animals per year. If true, this incidence has so far escaped detection, despite extensive recent search for cases. One oft-repeated but misguided objection to this statement is that very few apparently healthy cattle have been examined. However, if we wish to know whether or not a given disease exists in a population, we do not concentrate on asymptomatic persons, but instead on population subsets at highest risk. For example, if we wished to know whether or not cases of Alzheimer's disease occurred in a given country, we would first examine older adults, not the general population. The same principle applies to BSE. Although asymptomatic cattle with BSE might be infected, it is far more probable that BSE will be diagnosed in animals with neurologic signs or at least some indication of illness (even if atypical), and it is precisely these animals that are being tested. Microscopy examination of brain specimens from >12,000 cattle categorized as downers (abnormal recumbency from any cause) or with suspected neurologic disease has failed to reveal a single case of BSE. Brain specimens from >3,000 of these cattle have also been tested immunologically for prion protein. By way of comparison, in Switzerland (a country in which BSE has been carefully researched), tests for the protein have been carried out in 40,000 animals, including 15,000 downer cattle, and yielded approximately one diseased cow for every 1,000 examined, half of these from the downer group. The comparison is statistically significant; that is, testing already completed in the United States would have detected BSE if it existed at the incidence level of Switzerland. Testing of cattle in the United States will continue, and many thousands more animals will be examined in the next few years, which will provide increasing assurance of BSE-free status. With respect to cattle or cattle feed imported from the United Kingdom (or other countries in which BSE has occurred), the United States led the way in taking measures to prevent or correct any such occurrences. During the years before the importation of live ruminants and ruminant products was banned (in 1989), 500 cattle and a single shipment of 12 tons of meat and bone meal feed were imported from the United Kingdom. Almost all of the cattle were traced, and if still living, were slaughtered and destroyed. We can say today that any animal or animal feed that might have been contaminated did not transmit the infection because with an incubation period of approximately 5 years, BSE would already have spread through recycled carcass cattle feed to cause a recognizable outbreak of disease. Import barriers have since been extended to include all countries in which BSE exists or which have not convincingly demonstrated its nonexistence. Thus, the argument that undetected cases of BSE might be present in the United States, although impossible to disprove, is not supported by current evidence. Because of the everpresent risk for human error, vigilance is still required to see that all established preventive measures are properly and continuously monitored. Allied Diseases Three varieties of spongiform encephalopathy present in the United States, scrapie in sheep, transmissible mink encephalopathy (TME), and chronic wasting disease (CWD) of deer and elk, under the right circumstances may be capable of infecting other animal species. Scrapie first appeared in the United States in 1947 in Michigan sheep of British origin that had been imported from Canada and has since spread to most regions of the country. Scrapie has not been convincingly shown to cause disease in any other species (apart from goats), despite its certain inclusion in rendering mixes for livestock until the 1997 mammalian to ruminant feed ban. Exactly why species barriers have not been crossed is unclear but may be due to a relatively low flock incidence of scrapie and a relatively small proportion of sheep to cattle in rendering plants, such that the very low amount of infectivity entering the total rendering mix does not survive processing into livestock feed. TME was also first reported in 1947 on a Wisconsin mink ranch and has occurred in several further outbreaks on mink ranches both in the United States and abroad. TME was originally thought to have resulted from feeding (scrapie-infected) sheep carcasses to the mink, but in one U.S. outbreak in 1985, epidemiologic study indicated that the dietary source might have been downer cattle carcasses (7 CWD was first recognized in 1967 in captive deer on a Colorado wildlife research facility. It occurs endemically in wild deer in contiguous sections of northcentral Colorado and southeastern Wyoming and episodically on elk farms along the eastern border states of the Rocky Mountains. No disease in humans or other animals has been attributed to CWD, but the potential for disease is very real: infected tissues could be eaten by predators or enjoyed by aficionados of wild game, and carcasses could be rendered for feed that (by error) could find its way to cattle. Regional hunters and elk farmers have been alerted to the risks, but more attention at the national level is urgently needed. What if&? What would result from the mistaken feeding of contaminated mammalian protein to a herd of cattle? During the 1980s, millions of cows in the United Kingdom were eating at least half pound of meat and bone meal dietary supplement each day, some of which was certainly contaminated, yet the incidence of BSE in affected herds never exceeded 2% to 3%. Today in the United States, the worst that could happen after a contaminated feed incident would be that a few cattle might be infected and come to slaughter unrecognized, but without a sequence of similar errors, no infectious tissue would be recycled in the livestock food chain, and a regulatory breakdown of this magnitude is virtually impossible. Nevertheless, if even a single case of BSE were to be discovered in the United States, the economic and perceived public health consequences could be immense. How would the current package of preventive measures stand up to future judgment? With generally high marks, although a few points of vulnerability still exist (the elimination of which would substantially dislocate segments of the rendering and livestock industries): * The 1997 ban on using mammalian protein in ruminant feed exempts plate waste from restaurants (which could contain bovine brain or paraspinal ganglia in the uneaten remains of some cuts of meat). They could be recycled to cattle in feed produced by rendering plants. * Feed for ruminants and nonruminants can be processed in the same feed mills, creating the potential for cross-contamination. Rendered carcasses of deer and elk with chronic wasting disease could conceivably in this way be fed to cattle. * If farmers or ranchers mistakenly or deliberately use nonruminant feed for ruminants, the mammalian to ruminant feed ban would be bypassed. Spontaneous TSE occurring in nonmammalian species, if it occurs, would also escape the mammalian to ruminant feed ban. * Unlike the European Union, the United States does not mandate that the rendering process be capable of sterilizing BSE infectivity. (Most feed mills render carcasses at 134°C without the concomitant use of steam and pressure, and thus cannot be guaranteed to sterilize). * Mechanically separated meat expressed from crushed carcasses can be added to cooked and uncooked meat products, up to a concentration of 30% by weight. Since 1997, spinal cord has been removed, but the vertebral column (including the paraspinal ganglia) can still be processed and used in many products: hot dogs, sausages, canned beef, luncheon meats, and soups and stews. A recently introduced and much safer process (advanced meat recovery) has not yet completely replaced the crushing method. * Organs known to be infectious in cattle with BSE (including brain) are not prohibited from human consumption. * Glandular dietary supplements containing various animal organ powders, including cattle brain, were often imported from the United Kingdom or countries in continental Europe until the U.S. Department of Agriculture import ban in 1989. The ban relies on proper labeling of the shipment and can be abused. As an alternative to the entire issue of precautions against the occurrence and spread of BSE, we must finally ask, what would be the economic consequences of eliminating animal protein from livestock feed or replacing it with plant protein? The rendering industry would disappear, and the incineration industry would expand in conjunction with the production of nutrition crops such as soybeans. Would plant protein be as effective as animal protein? Is the public prepared to pay more for meat or eat only as much as can be produced from range-fed animals? These are not trivial questions, and the answers will need to be weighed against the overarching issue of public health. Paul Brown Senior Investigator, National Institutes of Health, Bethesda, Maryland, USA References 1. Brown P, Will RG, Bradley R, Asher DM, Detwiler L. Bovine spongiform encephalopathy and variant Creutzfeldt-Jakob disease: background, evolution, and current concerns. J Gen Virol 1991;72:589-94. http://www.cdc.gov/ncidod/eid/vol7no3_supp/brown.htm TSS ########### http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############ http://www.vegsource.com/talk/madcow/messages/9911708.html UK SHEEP GOAT EXPORT http://www.vegsource.com/articles/sheep_exports.htm
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