rkaiser, don't get mad now and change the subject with all this valentines day stuff. but i still want you to be my valentine today, so lets keep this thread going, you probably will not get any tonight anyway :lol: :lol: :lol:
rkaiser wrote
>>>I don't feed ruminant by products dork - in fact guess what, that is illegal. And thank goodness it is. But if you think that the FEED BAN is going to stop BSE in it's tracks, you are more lost than I could ever imagine.<<<
there ya go again valentine, i never said it would stop all of it. but now if you can get that pea brain of yours to do any ciphering at all, you will see that the figures speak for themselves and there is not a op out there you can point to be a factor in that ciphering, did i loose you yet valentine :wink: :wink: :wink:
i was just discussing this with another rancher today matter of fact, course there are some out there that's brain is a bit bigger than a pea
========================
greetings 4th gen rancher,
there is much debate on this issue. but they cannot have there cake and eat there ice cream too.
as with the USDA et al on spontanoues BSE, nope, cannot happen they say in fairly strong terms in there lingo, but then they come back and say in humans it happens as sporadic cjd. bullshit! same with the vertical and lateral transmission, they implied it would not, but left a small opening as well, if so, only a small percentage, this with out any proof at all. but they are not looking very hard at this in my opinion.
my gosh, think what would happen if they did prove it. shame on them;-)
Vertical and lateral transmission of TSEs
This review was kindly provided on 10.8.96 by:
Phil Rogers MRCVS
Work Fax: 353-46-26154
Work Tel: 353-46-25214
Home Tel: 353-1-6281-222
The question of vertical and/or lateral transmission of TSEs is unresolved. Scrapie is almost certainly transmitted laterally and vertically (Constantin 1994).
MAFF workers (Bradley & Wilesmith 1993; Bradley 1994; Taylor 1994; Wells & Wilesmith 1995) state that the feeding of contaminated MBM was the only proven source of BSE in the UK and that lateral or vertical transmission of BSE in cattle is not proven. However, in June 1995, the UK Subgroup on BSE (chaired by Bradley) stated that "maternal and horizontal transmission cannot be excluded".
Lateral transmission may occur in some species: since 1970, a small herd of kudu at the London Zoo derived from 3 individuals. TSE was diagnosed in 5/8 kudu born in this herd since 1987. With the possible exception of the first confirmed case, none of these is thought to have been exposed to feeds containing ruminant-derived protein. Greater kudu are very susceptible to TSE and natural lateral transmission may have occurred among them (Kirkwood et al 1993).
Dealler & Lacey (1994) suggested vertical transmission of BSE. Ridley & Baker (1995) disagree: "The probability of maternal transmission of TSE in any species should be viewed with the greatest scepticism". No maternal or paternal transmission of was found in the progeny of mice inoculated with the agent of CJD (Taguchi et al 1993). However, research in MAFF (UK), released on Aug 10th 1996, has confirmed vertical (maternal, or cow-to-calf) transmission rates of about 10%, or about 1% per infected cow per year (Anon 1996).
Anon (1996) BSE research results suggest "enhanced risk" of
maternal transmission. Vet Rec AUG 10;139(...):126-127.
Baker,H.F. & Ridley,R.M. (1996) CJD and BSE: Study so far
provides no evidence for maternal and horizontal
transmission. Brit Med J MAR 30;312(7034):843. HF Baker,
Sch Clin Vet Med, MRC, Compart Cognit Team, Dept Exptl
Psychol, Cambridge CB3 0ES, England.
Bradley,R. (1994) Embryo-Transfer and Its Potential Role in
Control of Scrapie and BSE. Livest Prod Sci
MAR;38(1):51-59. R Bradley, MAFF Cent Vet Lab, New Haw,
Addlestone KT15 3NB, Surrey, England.
BSE is a new TSE of cattle resulting from consumption of a Scrapie-like agent in MBM of concentrate rations. There is evidence of a decline in the epidemic following the introduction of a feed ban in July 1988. Cow to cow transmission is not proven. Scrapie is an endemic disease of sheep known for over 250 years where maternal and horizontal transmission are responsible for the difficulty in controlling the disease.
Embryo transfer (ET) is a valued method of moving genetic material around the world with negligible risk of transmitting infectious diseases provided the International Embryo Transfer Society protocols are used. Data on ET and the control of SE in sheep and cattle is being investigated in the USA and the UK. In regard to sheep there are conflicting results. Washed embryos from experimentally infected sheep in the USA have not transmitted Scrapie to recipients though no account was taken of the genetic susceptibility of the embryo or recipient.
In contrast in the UK, using Sip and PrP genotyped experimentally-infected sheep and unwashed embryos, Scrapie resulted in the homozygous susceptible (sAsA) offspring within 979 d. The question as to whether ET can be used to control natural Scrapie in sheep is thus unresolved. Further studies to investigate the effect of washing embryos are in progress. In the UK, 1000 embryos have been collected from confirmed BSE cows and some have been transferred into 347 heifers imported from New Zealand as calves and subsequently held under quarantine conditions. Some embryos and uterine flushings have been inoculated into susceptible mice. No disease has resulted but the experiment will not be completed until 2001.
Constantin,A. (1994) A Short-Story of TSSEs. Bull Acad Natl
Med MAY 3;178(5):859-871. A Constantin, Intervet SA,
F-49125 Briollay, France.
Sheep Scrapie, the archetype of TSSE, has been described for more than 200 years but the first scientific papers appeared 60 years ago. The link between doctors and veterinary surgeons enabled our knowledge to develop. First, a Slow Virus was evoked, then Hadlow DVM (USA) suggested using brain filtrates from deceased patients of Kuru in order to inoculate primates or small rodents; this was carried out by Gajdusek's team.
The complete absence of an immune reaction has made the label "Slow Virus" give way to Unconventional Transmissible Agent (UTA). The few human cases of TSSE have all been transmitted to mice, rats, hamsters. Prusiner (San Francisco) has given us an enormous boost with the notion of prion, a protein molecule derived from an ordinary small membrane protein. Having recourse to transgenic mice has enabled American and European teams to demonstrate the essential role of genetics in the formation of the UTA. Those responsible for the Health of Cattle in U.K. will not contradict us. Future Research will be fascinating and will open a new chapter in the Medical Science concerning Mammals.
Dealler,S.F. & Lacey,R.W. (1994) Suspected Vertical
Transmission of BSE. Vet Rec FEB 5;134(6):151. SF
Dealler, York Dist Gen Hosp, Dept Microbiol, York YO3 7HE,
N Yorkshire, England.
A female Friesian-Holstein cow aged 4 years with clinical signs suggestive of bovine spongiform encephalopathy (BSE) was slaughtered. Histological examination of the brain revealed findings typical of BSE with severe spongiform change. It is suggested that since the cow was born after the ruminant feed ban and since its dam had been a confirmed case of BSE the history is suggestive of vertical transmission of BSE.
Dealler S (1995) Vertical transmission of BSE: epidemiological
evidence. Prion meeting at Gottingen, November 1995.
Burnley General Hospital, UK.
He made it clear that various statistics in the epidemiology of BSE did not fit with the epidemiology that was expected for a disease that was passed purely through feed. What fitted much better was the model that it was the mothers that ate the infective material and they infected their offspring. The appearence of cattle in Portugal with BSE that were the offspring of exported UK cattle, the slow decay in the cases of BSE after the feed ban, the increased likelyhood of a herd that has had a case of BSE to have another compared with unaffected herd, the steady in-herd rate at approximately 25% (why not 100%?), and the apparent 2 peaks in the age distribution of cattle developing BSE.
A lot of ifs and buts were needed to fit the MAFF model to the epidemiology but it could be done. However, the vertical transmission model fitted it well. The added risk from BSE to a UK adult that continues to eat beef products is now less than 5% of the risk that has already been taken. Dealler S and Kent J. When the difference in risk for people stopping eating beef at specific dates is compared with the risk for those continuing it is seen that there is little difference by the time we reach 1996. By this time little difference is seen but only applies for people that have eaten beef throughout the epidemic until that point. It is also made clear that the apparent difference was quite wide in 1989. The statistics only used the human diet as liver, kidney, meat (and the nerves they contain).
Dealler S (1996, Internet): Aetiology of scrapie in cetain
circumstances is not evidence against another aetiology in
different circumstances. BMJ 20 Jan 1996 p 180. Ros Ridley
and Harry Baker, Dept of Exp Psychology University of
Cambridge. This is the continued argument that the findings
of various groups that suggest vertical transmission of
scrapie can be explained in a genetic manner.
Dealler S (1996, Internet): BSE is being maintained by vertical
and horizontal transmission. BMJ 20 Jan 1996 p 180.
Professor Lacey, University of Leeds He explains that the
epidemiological models used by MAFF had one by one been
shown not be be adequate to explain the huge number of
cattle that have developed BSE after being born after the
feed ban. He says that the recycling of remains would cause
the rapid rise of the disease but could not be the only
cause for the number of cases remaining so high.
IFST Bovine Spongiform Encephalopathy (BSE): Position Statement,
14 September 1996.
Placental transmission has been proposed as a likely route for vertical transmission for scrapie in sheep, although the existence of vertical transmission of scrapie has been disputed [Ridley and Baker (1995)]; but placental transmission has not been demonstrated with BSE in cattle. Until recently, there has been no evidence of maternal transmission in cattle.
A large-scale epidemiological study [Hoinville et al (1995)] should have brought to light the occurrence of vertical transmission if it occurred, but it did not, which was strongly suggestive of no significant occurrence. Preliminary results from the long-term experimental trials started in 1989, involving 315 calves born to BSE-infected dams (nearly all born within 13 months and many within 5 months before clinical onset of BSE in the dams) and 315 controls born of healthy dams, were the subject of a MAFF announcement and a SEAC report on 1 August 1996 [when the research paper is published, the reference will be given in an Editorial Footnote].
Some 550 animals, having reached their seventh birthdays had already been slaughtered and their brains histologically examined. BSE occurred in 15% of the test animals and 5% of the controls [presumed to be due to exposure to infected meat-and-bonemeal feed in their early years]. SEAC assumed that this represented 10% risk of maternal transmission in the trials, and, by assuming further that the risk is negligible in calves born through the earlier part of the dams' incubation period, estimated a risk of 1% in the field. However, the latter is unsubstantiated speculation, based on an unverified assumption, although some support for it may or may not be implicit in the results of a subsequently-published computer study [Anderson et l (1996)] [see later].
What the trial showed was a statistically significant association between BSE-infected dams and occurrence of BSE in the calves, but, on information currently available, did not establish the cause of that association. That cause may be maternal transmission or, for example, inherited genetic disposition coupled with exposure to infected feed. If it is in fact maternal transmission, that would raise the question of the mode of transmission, as yet unanswerable in the light of current knowledge and methodology.
Fortunately, whether the real risk was 10% or 1% or somewhere in between, will have no significant bearing on the continuing rapid decline in the number of new BSE cases and in the virtual eradication of the disease. Whatever the level of risk was, it has been operating throughout the period of rapid decline and is thus also, as the stock exchange analysts put it, already discounted in the epidemiological forecasts of further decline [e.g. Stekel et al (1996)]. Moreover, in the absence of horizontal transmission, of which there is no evidence, and in enforced absence of infected MBM feed, the effect found in this trial would be the only route for future infection.
Taking the figure actually found in the trial, 10%, and assuming the worst case situation that it applied throughout the calving lives of the dams, it means occurrence in one in ten of the offspring of BSE cows in 1989 (for the trial results are, of course, the belated findings on what actually happened in 1989).. Even assuming that, of that second generation (now 7 years old), all of the calves inheriting BSE survived and became dams for a full calving career (and it must be borne in mind that all are culled at 30 months, but even ignoring that), that means that there will have been occurrence in one in a hundred of the second generation's offspring. And in one in a thousand in the third generation's offspring, and so on. Of course, the geometric reductions in numbers of transmissions does not happen in large several-year-jumps like that, but in a smoother descending curve, because "generations" overlap and one must think in terms of annual cohorts, but over time the numbers must at least decline in that way.
Narang,H. (1996) Origin and implications of BSE. Proc Soc Exp
Biol Med APR;211(4):306-322. H Narang, Ken Bell Int, 22-40
Brentwood Ave, Newcastle Tyne NE2 3DH, Tyne & Wear,
England.
This is a review of TSEs. All animal and human SEs are slow-developing infectious diseases. The current working theory links the origin of BSE to the feeding of cattle with MBM prepared from the remains of scrapie-infected sheep. Recycling of cattle MBM essentially resulted in the selection of a single strain from the "wild type", a mixture of 20 strains. The BSE agent is easily transmitted through ingestion, with some evidence of vertical transmission.
Paradoxically, cattle have selected a major new strain which appears to be more virulent than an unselected strain found in scrapie sheep. The same strain of BSE agent is implicated in the occurrence of SE in domestic cats, tiger, and some exotic species of ruminants in zoos. The properties of BSE and its spread into cattle are still disputed. Since our understanding of the disease and its transmissibility in humans must await observations that will be made over some years to come, it is important to keep a reasonable perspective and ensure that any speculative comment is consistent with fact.
In risk assessment in such circumstances, it is tempting give too much credence to persuasive parallels when direct relevant information is not available. On the other hand, it would also be unwise to assume that the disease will die by itself and will have no effect on humans.
Ridley,R.M. & Baker,H.F. (1995) The Myth of Maternal
Transmission of SE. Brit Med J OCT 21;311(7012):1071-1075.
RM Ridley, Sch Clin Vet Med Cambridge, Innes Bldg,
Cambridge CB3 0ES, England.
It has long been accepted that the pattern of occurrence of Scrapie, the form of SE associated with sheep, is determined mainly by maternal transmission. This view has had a profound influence on policy decisions in the control of BSE and on public concern over the risk to human health from this disease.
The occurrence of maternal transmission is, however, not predicted by modern knowledge of the aetiology of SE, and even though claims of maternal transmission have been reiterated frequently in the literature, re-examination of the source data reveals that they are extremely scanty, unreplicated, and probably subject to ascertainment bias. The probability of maternal transmission of SE in any species should be viewed with the greatest scepticism.
Taylor,K.C. (1994) Suspected Vertical Transmission of BSE. Vet
Rec FEB 12;134(7):175. KC Taylor, MAFF, Govt Bldg, Toby
Jug Site, Surbiton KT6 7NF, Surrey, England.
Taguchi,F., Tamai,Y. & Miura,S. (1993) Experiments on Maternal
and Paternal Transmission of CJD in Mice. Arch Virol
130(1-2):219-224. F Taguchi, Kitasato Univ, Sch Hyg Sci,
Dept Microbiol, Sagamihara, Kanagawa 228, Japan.
No transmission of CJD in mice was observed in 75 offspring born to CJD agent-inoculated females or to normal females mated with inoculated males and in 19 normal offspring maintained by foster nursing with the inoculated mothers. The fertility of young adult female mice was lost by d 57 after the inoculation, whereas the reproductivity of male mice was maintained over 106 d after the inoculation.
Wilesmith,J.W., Wells,G.A.H., Hoinville,L.J. & Simmons,M.M.
(1994) Suspected Vertical Transmission of BSE. Vet Rec FEB
19;134(8):198-199. JW Wilesmith, MAFF Cent Vet Lab,
Addlestone KT15 3NB, Surrey, England.
The research which has been undertaken into potential sources of Infection and means of transmission is briefly described. Results of this research which are not yet complete, will estimate the risks of infection from feedstuffs, dams and as a result of horizontal transmission.
The results of monitoring histopathological changes in the brains of clinically suspect bovine spongiform encephalopathy have shown a remarkable consistency of lesion pattern which has confirmed that the diagnostic method currently used remains valid. Research on the pathology of the disease showed that mean lesion scores in all brain regions increase with clinical duration but there is no correlation between short clinical duration and mild or equivocal histological changes.
Will,R.G. (1995) The Myth of Maternal Transmission of SE:
Commentary: Scrapie Revisited. Brit Med J OCT
21;311(7012):1075-1076. RG Will, Western Gen Hosp, Dept
Clin Neurosci, Natl Ct CJ, Dis Surveillance Unit, Edinburgh
EH4 2XU, Midlothian, Scotland.
Will RG & Wilesmith JW. Response to the article: "Vertical
transfer of prion disease" by Lacey and Dealler. Human
Reproduction 1994; 9(10): 1792-1800.
http://www.mad-cow.org/lateral.html
Horizontal transmissionIf any transmission does take place at all, the evidence from sheep scrapie suggests that the calving cow probably represents the greatest risk to other cattle. A recent study has shown that lambs born to ewes introduced into a scrapie flock became infected and died at the same age as lambs born to native ewes, consistent with lateral transmission of scrapie to lambs (Research in Veterinary Science 76 (2004) 211–217). While there has been a study showing some evidence for horizontal transmissions up to three days after calving, there was no evidence of transmission to the cow's own calf, (Hoinville et al. 1995. Veterinary Record. 136, 312-318). However, the results were considered statistically insufficient to suggest that horizontal transmission was occurring.Another method of testing this theory involved the feeding of calves with placenta from confirmed cases of BSE. The calves that were challenged were clinically normal prior to slaughter and their tissues are being assayed for infectivity to find out if the cattle became infected without succumbing to clinical disease. Some preliminary tissue assays have been completed, without any infectivity being detected.Professor Anderson's group's work, has given rise to speculation about the possibility that horizontal transmission may arise on farms. The conclusion state quite clearly that:-"it should be emphasised that to date no evidence exists supporting the hypothesis of direct horizontal transmission." and,"produces no evidence to support the hypothesis that horizontal transmission is occurring at a rate sufficient to allow BSE to become endemic"Their, and previous studies have however indicated that bigger herds are at greater risk of acquiring BSE than smaller herds.This correlation of risk with herd size has in fact been known and published for several years. (Wilesmith et al, in Veterinary Record, 130. 90-94. Wilesmith, 1996, Bovine Spongiform Encephalopathy. The BSE Dilemma (p45-55). The finding is consistent with the original suggested explanation that the larger the herd the greater the probability of purchasing an infected batch of feed.Vertical transmission - from the sireEpidemiological studies have compared the incidence of BSE in the offspring of healthy bulls and those of bulls that later were confirmed to have BSE. There was no difference between the groups that could be attributed to the BSE status of the bull. Further data obtained from Artificial Insemination (AI) organisations have been analysed in order to expand and update previous studies, but no risk from semen used for commercial AI has been identified.Experimental transmissions have also been attempted using semen, seminal vesicles and prostate of bulls confirmed to have BSE, but no infectivity was detected in these samples. (Wilesmith, J. W. 1994. New Zealand Veterinary Journal. 42. 1-8).Maternal transmissionIn formulating BSE policy the UK has always assumed that maternal transmission could occur, but calculated that it would do so infrequently and so would not prevent the eradication of BSE. Apart from the general epidemiological analyses, and modelling of expected versus observed frequencies of disease in cattle that had BSE affected mothers, a specific study was established to study whether maternal transmission occurred, and if so at what rate. A summary of the findings were discussed at the Spongiform Encephalopathy Advisory Committee (SEAC) on 17 April 1997, and showed that calves which are the offspring of clinical cases have an enhanced risk of developing BSE. The overall risk difference was 9.6% as compared to non-BSE cases. In a separate study of the entire database, the risk was highest in calves born after clinical onset in the dam, and for calves born before clinical onset the risks decreased rapidly, with no maternal effect being detectable in calves born more than two years before the onset of clinical disease in the dam. It remains uncertain whether this effect represents true maternal transmission of infection from cow to calf or genetic susceptibility to a feed source of infection, or a mixture of both.Having considered the evidence, SEAC recommended that the Government should consider the options for a cull of offspring. The Committee confirmed however that it was satisfied that existing controls to protect the consumer were adequate. The scheme will have some benefits in terms of the eradication of BSE, although these are thought to be relatively small. It will prevent some cases of BSE occurring in offspring kept for breeding or milking and prevent any of those animals from infecting their calves.As a result of the retrospective offspring cull that is taking place now and the on-going prospective cull that will follow it the number of animals on-farm with maternally derived infections will be reduced. These will be animals where the mother was known to have been infected and its calves were traced and culled before they were slaughtered for human consumption. http://www.defra.gov.uk/animalh/bse/science-research/epidem.html#horiz Review of the Evidence for the Occurrence of 'BARB' BSE Cases in CattleI was engaged as an independent consultant by the Animal Health and WelfareDirectorate General of Defra in November 2004 with the following remit: http://www.defra.gov.uk/animalh/bse/pdf/hillreport.pdf 5. In the section of my report entitled "BSE in North America" I draw attention to anecdotalevidence relating to Transmissible Mink Encephalopathy (TME) in the USA. (YB 88/07.00/6.12-6.14) This evidence suggested the possibility that a spongiform encephalopathy agent mayhistorically have been present in the bovine and, possibly because of a very low incidence ofencephalopathy in this species, the existence of the agent was not recognised. The anecdotalevidence suggests that the existence of such an agent was demonstrated through mink feeding onoffal from cattle; no sheep offal reportedly fed to such mink. In this report I also indicate that itwas reckoned from computer prediction that the CVL was picking up between 50 and 60% casesof BSE. I cannot recall the rationale of this but believe that this was information given to me atthe time. snip... Breeding from Offspring.23. Next I turn to the issue of breeding from offspring. Since the appearance of BSE, debatehas taken place as to whether or not maternal or vertical transmission takes place. In the minutedated 2 June 1988 (Annex 1) (YB 88/06.02/3.1-3.3) and entitled "Bovine SpongiformEncephalopathy (BSE)" I am quoted in paragraph 7 on this topic. At that stage there wasobviously no evidence of maternal or vertical transmission but one possibility was that the BSEagent might behave more like the scrapie agent than the CJD agent. In such circumstances thenthe potential for maternal transmission would exist. However, following much deliberation byscientists throughout the UK on this issue and in the absence of any evidence of maternaltransmission there was no prohibition on breeding from the progeny of BSE affected cows. >>>As aconsequence of the centralised computer system within Northern Ireland the majority ofoffspring of BSE affected cows have been clearly marked on the computer as offspring fromsuch affected animals. <<< Additionally, we were confident that if information became availableindicating maternal transmission and requiring action on the progeny of affected cows all suchanimals could be traced quickly on the computer and any necessary and appropriate actionimplemented immediately. http://www.bseinquiry.gov.uk/files/ws/s279a.pdf http://www.bseinquiry.gov.uk/files/yb/1988/06/02011001.pdf Statement- 16th April 1997 --------------------------------------------------------------------------------On 29 July 1996, the Spongiform Encephalopathy Advisory Committee (SEAC) issued a statement on maternal transmission of BSE following its consideration of an interim report on a study conducted by the Epidemiology Department, Central Veterinary Laboratory, Weybridge to investigate the occurrence and incidence of dam to calf transmission of BSE (the cohort study). SEAC established an Epidemiology Subcommittee to consider the final results from the cohort study. The Subcommittee was chaired by Professor Peter Smith (London School of Hygiene and Tropical Medicine), a member of SEAC. It included two further members of SEAC, Dr Richard H Kimberlin (SARDAS) and Professor Will Hueston (University of Maryland). The Subcommittee also included Professor Roy Anderson (Oxford University), Professor Robert Curnow (Reading University), Dr Peter Goodfellow (SmithKline Beecham Pharmaceuticals), Professor Dr. Ir. Aalt Dijkhuizen (Wageningen Agricultural University, the Netherlands) Professor Nicholas Day (Medical Research Council Biostatistics Unit), Dr John Williams (Roslin Institute), Dr Rosalind Ridley (Cambridge University) and Mr John Wilesmith (Central Veterinary Laboratory). The Subcommittee was assisted by Dr Sheila Gore (Medical Research Council Biostatistics Unit), Dr Neil Ferguson (Oxford University), Dr Christl Donnelly (Oxford University), Dr John Woolliams (Roslin Institute), and Ms Judith Ryan (Central Veterinary Laboratory). The Subcommittee met on four occasions, and submitted its final report on maternal transmission of BSE to SEAC on 11 April 1997. At its meeting on 15 April 1997, SEAC considered and accepted in full the report from the Epidemiology Subcommittee. SEAC noted that the results of the cohort study were not inconsistent with those of the case control study published in 1995 by Hoinville and others of the Epidemiology Department, CVL. That study, which involved cases of BSE born after the ruminant feed ban, did not identify significant evidence of maternal transmission, but the statistical confidence interval included a risk of up to 13 per cent (Veterinary Record (1995) 136, 312-318). The cohort study provides no information on the mechanism of direct maternal transmission of BSE. We recommend that further research should be undertaken to shed light on the mechanism. Some research has already been carried out into potential routes of transmission from dam to calf, by testing the infectivity of tissues from BSE-affected animals, including placenta, embryos, blood and milk: no evidence of infectivity has been found. However, given that the rate of transmission is probably low, some of these negative results may be due to the practical difficulties of detecting low levels, or a low prevalence, of infectivity. SEAC recognises that a low level of transmission would make research on mechanisms difficult, and that it would be complemented by a better understanding of the mechanisms of scrapie transmission in sheep. Any cull based upon the slaughter of calves born to cows in which BSE has been confirmed will have only a small effect on the incidence of BSE and the duration of the epidemic. Nevertheless, Government should consider the possibilities for such a cull, and its effects. SEAC noted that, in its statement of 29 July 1996, it had concluded that the evidence on maternal transmission did not call into question existing measures to protect public health. In the light of the Subcommittee's report, SEAC reconsidered the existing measures. With respect to consumption of bovine products the measures currently in place to protect the consumer are considered appropriate. In particular, the Committee considered the possibility of milk being a vehicle of transmission. SEAC concludes that no evidence has been found to suggest that milk from any species affected by transmissible spongiform encephalopathies is infectious. This concurs with the opinion of the Scientific Veterinary Committee, which advises the European Commission. With respect to occupational exposure, responsibility for assessing whether any amendments are needed to the existing Health and Safety Executive guidance rests with the Advisory Committee on Dangerous Pathogens. --------------------------------------------------------------------------------Epidemiology subcommittee statement to SEAC on maternal transmission of 11 April 1997 In July 1996 SEAC issued a statement on maternal transmission of BSE following an interim analysis of data from an ongoing study (called the "cohort study") being conducted by the Epidemiology Department, Central Veterinary Laboratory (CVL). The study was intended to determine whether maternal transmission occurred, and if so, to inform policy makers with respect to animal health implications. The study involved over 300 "matched-pairs" of calves. One calf in each pair was the offspring of a confirmed case of BSE and the other an animal born in the same herd in the same calving season whose dam had reached the age of 6 years without developing clinical signs of BSE. The two groups of animals were born between August 1987 and November 1989, and were taken from their natal herds between July 1989 and February 1990, aged between 2 and 24 months. They were kept on one of three experimental farms until they reached the age of 7 years or were culled at an earlier age with BSE or another disease. All animals surviving to the age of 7 years were then slaughtered and their brains were examined pathologically for evidence of BSE. The preliminary results of the study, when most but not all of the animals had been followed to the age of 7 years, suggested that the offspring of BSE cases had an incidence of BSE that was about 10% greater than that of control animals, with statistical confidence limits (95%) ranging from 5-15%, the range reflecting the limited numbers of animals that developed BSE in the study. By November 1996 the last of the animals in the study had reached the age of 7 years, and by January 1997 the last of their brains had been examined. As had been anticipated, the final results were not markedly different from those on which the interim analysis had been based in 1996. Of the 301 offspring of BSE cases, 42 (14.0%) developed BSE. Among the 301 offspring of the "control" dams without BSE, 13 (4.3%) developed BSE. The difference between the two risks was thus 9.6%, and was highly statistically significant with a confidence interval ranging from 5.1% to 14.2%. A paper giving the results of the study will be published shortly in the Veterinary Record by the Epidemiology Department of CVL. The cohort study was set up to investigate the occurrence of maternal transmission, but interpretation of the results was confounded by the likely exposure of some of the experimental animals to contaminated feed. The results could be explained by two hypotheses, acting alone or in combination, namely direct maternal transmission of infection or inherited genetic variation in susceptibility to BSE via contaminated feed. Although most of the animals involved in the study had been born after the ruminant feed ban in July 1988, feed-borne transmission is thought to have continued beyond that date. This is consistent with the observation that the BSE risk in both of the groups was greater among animals born before the introduction of the feed ban than among animals born later. However, the difference in risk between the two groups was also greater in those born earlier, and this would not be expected if direct maternal transmission was the sole route of infection of the calves in the study. Such an effect might be apparent if cattle vary in their susceptibility to contracting BSE from infected feed. It is possible that the offspring of BSE cases may inherit, from their dams, genes associated with increased susceptibility to disease and that at least some of the difference in BSE risk between the offspring of BSE affected and non-affected dams in the study may be due to inherited factors, rather than because of direct transmission of BSE from dam to calf. The subcommittee has reviewed the evidence for variation in genetic susceptibility to BSE in cattle. There is variation in the risk of TSEs according to genotype in some species. For example, polymorphisms of the PrP gene are associated with substantial variation in susceptibility to infection with the scrapie (and in incubation period ) in sheep and mice and with differences in risk of CJD in humans. The subcommittee notes, however, that the limited research so far completed has failed to identify genetic factors as a major component in the epidemiology of BSE. To assist the CVL Epidemiology Department in the interpretation of the results of the cohort study, independent analyses of the data were conducted by three additional groups with expertise in statistical analysis (based in the Wellcome Trust Centre for the Epidemiology of Infectious Disease, University of Oxford; the MRC Biostatistics Unit, Cambridge; and the Department of Applied Statistics, University of Reading). In so far as was possible, they tried to evaluate the contributions to the risk difference between the animals in the two groups from inherited differences in susceptibility to disease caused by infected feed and from direct transmission of BSE from dam to calf. In the absence of detailed information on the genetic make up of the animals in the study, the possible genetic contribution could only be assessed by statistical modelling. The analyses by the three groups have been submitted for publication later this year. These analyses reached broadly the same conclusions. That there was a highly significant difference in risk between the two groups of animals was clear. The findings did not definitively establish direct maternal transmission as the sole explanation for the difference in risk. The statistical model which fitted the data best involved contributions from both direct maternal transmission and inherited susceptibility. The main evidence for direct maternal transmission is that the risk of BSE in the calf of an affected dam was greatest for calves born close to the onset of BSE in the dam. However, the power of the study to detect differences related to the time between BSE onset and the date of birth of a calf was limited by the design of the study which resulted in 83.4% of the calves being born within the six months prior to onset of clinical disease in the dam. Further investigation was necessary of the possible variation in the risk of BSE associated with the time between the birth of an animal and the onset of BSE in the dam. This was undertaken mainly by the group from the Wellcome Centre for the Epidemiology of Infectious Diseases, University of Oxford through analyses of data on all cases of BSE born after the ruminant feed ban, which are recorded on the BSE database held by the Epidemiology Department at the CVL. The findings will be submitted for publication shortly. Evidence was found that the subsequent BSE-risk was greatest in calves born after the date of BSE onset in the dam. For calves born before onset, the risk was lower, and diminished as the interval between birth and onset increased, and no risk was apparent more than two years before onset (see next paragraph). Thus, although possibly subject to some biases, these analyses also suggested that enhanced BSE-risk in the offspring of BSE dams involves a low level of direct maternal transmission in the late stages of the incubation period. In view of the findings of the analyses that are summarised above, the subcommittee concludes that there is some evidence for direct maternal transmission of BSE at a low level, but some variation in genetic susceptibility to BSE following feed-borne exposure may occur. The risk of transmission of BSE from dam to calf is likely to be less than 10%, and appears to be confined to animals born after the onset of BSE in the dam or up to two years beforehand. This level of transmission is not sufficient, by itself, to perpetuate BSE in the cattle population and is likely to have only a minor effect on the rate at which the incidence of BSE declines. It is inevitable that cases infected via animal feed will continue to appear in diminishing numbers for several years. Therefore, although the number of cases infected maternally will be small, they may represent an increasing proportion of the remaining cases detected. Given the evidence that variation in genetic susceptibility may have contributed to the results of the cohort study, and of the importance of genetic factors in TSEs in other species, the subcommittee considers that further research is necessary to clarify whether or not variations in the PrP gene or other genes may be influencing the transmission of, or susceptibility to, BSE in cattle. Research should seek to identify polymorphisms of the PrP gene which may be associated with BSE susceptibility, including stored samples from the cohort study. There should also be a search [AVMC1] for other genetic markers, outside the PrP gene, which may be associated with an increased BSE risk in cattle. http://www.seac.gov.uk/statements/state16apr97.htm THE POSSIBLE VERTICAL TRANSMISSION OFBOVINE SPONGIFORM ENCEPHALOPATHY (BSE)REPORT OF THE WORKING GROUPSUBMITTED TO THE SCIENTIFIC STEERING COMMITTEEAT ITS MEETING OF 18-19 MARCH 1999 http://europa.eu.int/comm/food/fs/sc/ssc/out44_en.pdf Statement- 29th July 1996 --------------------------------------------------------------------------------Maternal transmission of BSEThe Spongiform Encephalopathy Advisory Committee (SEAC) considered at its meeting on the 19 July 1996 an interim report on a study conducted by the Epidemiology Department, Central Veterinary Laboratory, Weybridge to investigate the possibility of cow to calf transmission of BSE. The study involved assembling two groups of animals with over 300 cattle in each. One group consisted of offspring of confirmed cases of BSE whilst the other group comprised animals born in the same herd and in the same calving season whose dam had reached at least 6 years of age without developing clinical signs of BSE. The animals in the two groups were kept until the age of 7 or until BSE or another disease intervened. BSE occurred in both groups as the cattle were born around the time of the ruminant feed ban in 1988 and the cattle, or at least some of them, in both groups would have been exposed to infected feed. As at the 14 July 1996, 273 animals in each group had reached the age of 7 and had been slaughtered or had developed disease. 55 animals are still alive and histological results are pending for 8 animals. Of the 273 animals born to dams with BSE, 42 have developed histologically confirmed BSE. In the 273 animals born to mothers who had not developed BSE 13 were histologically confirmed as having BSE. This provides evidence that the risk of maternal transmission is approximately 10% for the BSE infected cows whose calves were studied. The statistical confidence limits for that figure are 5-15%, this range being a reflection of the numbers of animals in the study and of the numbers developing BSE. It is highly unlikely that the results from the histological examination of the brains of the 63 remaining animals will materially alter these findings. An analysis has been made of the interval between the birth of the animals in the study and the onset of clinical BSE in their mothers. All of the calves in the study were born within 13 months of the clinical onset of BSE in their dams, and the great majority were born within 5 months of clinical onset. Thus the study does not provide a good estimate of the risk to animals born more than 6 months before the onset of BSE in the dam. However, the findings provide some, albeit limited, evidence that there is an enhanced risk of maternal transmission in the last 6 months of the BSE incubation period. It is plausible that the risk of maternal transmission reduces markedly as the interval between the birth of the calf and the onset of BSE in the dam increases. Therefore, the risk of maternal transmission observed under the study conditions is likely to be greater than would be expected for the entire population of cows. Under field conditions, only a fraction of the BSE-infected cows giving birth would be within 6 months of demonstrating clinical signs of BSE because of the long incubation period of the disease. The average incubation period is 60 months and, if the rate of cow to calf transmission over the last 6 months of the incubation is 10% and it is insignificant before that time, then the average transmission from cow to calf over the 60 months duration of infection in an animal prior to developing clinical disease will be 1%. This would be the rate of maternal transmission that would be observed under field conditions. Maternal transmission at the rates observed in husbandry conditions of the UK dairy herd will not lead to the permanent establishment of BSE even at a low incidence in the UK herd. It will die out, as it already clearly is doing, as a consequence of the restrictions on the primary mode of transmission through infected feed. The study itself provides no new evidence in relation to horizontal transmission. Since the meeting of SEAC on 19 July the Epidemiology Department at CVL has examined the data from this study and that pertaining to the herds from which study animals were taken and has found no evidence of horizontal transmission. The study tells us nothing about the route of maternal transmission, which could be in utero, at birth or soon after birth. In sheep scrapie where there is also evidence of maternal transmission, infectivity can be detected in the placenta. Furthermore in sheep scrapie there is evidence of in utero transmission from an experiment where the embryo from a scrapie infected sheep was transplanted into a healthy ewe and when that ewe gave birth the lamb eventually went on to develop scrapie. Similar embryo transfer experiments are underway in cattle but results are not yet available. Infectivity has however not been detected in the bovine placenta or in milk, or in blood (see Note 1). The Committee considered whether evidence of maternal transmission calls into question the existing recommendations to protect public health. These were drawn up on the assumption that BSE could be a risk to man, which is still not proven, and on the assumption that maternal transmission could occur. The Committee have concluded that there is no case for changing its recommendations (see Note 2) in relation to milk, meat, blood or any other product which is currently permitted. There is no evidence from any of the transmissible spongiform encephalopathies that infectivity can be transmitted through milk. In commercial dairy herds where the bulk of BSE cases arise calves do not receive their mothers milk except for the first few days of life when they receive the special milk produced at that time called colostrum. Colostrum is different in nature from ordinary milk and is not sold for human consumption. In the beef suckler herds it is common practice for calves to be suckled by their mothers for up to six months. Existing data do not provide evidence to suggest that the rate of maternal transmission in beef suckler calves who have prolonged exposure to their mother's milk is any different to that in dairy herds where the only exposure would be to colostrum in the first few days of life. The Committee was pleased to note that the Epidemiology Department at CVL is undertaking further detailed studies on this point, and that the results of these studies will be available very soon. The Committee recognise the role of the ACDP and the HSE in relation to the occupational risks. The Committee draws the attention of those bodies to these new findings but does not make any recommendations for further action other than that the two bodies should consider the evidence and any implications for occupational health. The Committee considered the position in relation to the measures to eradicate BSE, particularly in relation to any selective cull implemented by Government. It is clear from the new information that maternal transmission will not perpetuate the disease and that BSE will therefore die out even in the absence of any form of selective cull. The Committee were made aware that preliminary analyses of the effect of these new results on a culling policy had been undertaken but that these were as yet incomplete. Nevertheless the Committee recommends that the results of the completed analyses be taken into account before final decisions are made about the policy for a selective cull. Finally, the Committee considered what further research might be of high priority in the light of the results of this study and the matter will be the subject of a separate report. Note 1. Data from standard transmission experiments following parenteral inoculation into mice. Details are given in Table 7 of the latest MAFF Progress Report on BSE, published in June 1996. Note 2. In its statement of 20 March about the new variant of CJD the SEAC said: "The Committee does not consider that these findings lead it to revise its advice on the safety of milk.""If the recommendations set out above [i.e., for the proper enforcement of SBO controls on the deboning of cattle over 30 months] are carried out the Committee concluded that the risk from eating beef is now likely to be extremely small." http://www.seac.gov.uk/statements/state29jul96.htm HERE IS THE LATEST and prospects for the future ? UK Strategy for Research and Development on Human and Animal Health Aspects of Transmissible Spongiform Encephalopathies 2005-2008 snip... 3.2.3.7 In addition to experiments involving grazing sheep on potentially "contaminated" pasture, another study is looking at the persistence of TSEs in the soil environment. However, such work is limited, at the moment, by the lack of an efficient method for the extraction of PrPSc from soil although methods have been developed for clay and sand. In 50v6.1 April 2002, Defra convened a workshop on TSEs in the Environment . As a result of this workshop a number of research recommendations were made in order to address gaps in our knowledge. snip...full text 91 pages; http://www.mrc.ac.uk/pdf-about-tse_uk_strategy_june2005.pdf Statement- 29th July 1996 --------------------------------------------------------------------------------Maternal transmission of BSEThe Spongiform Encephalopathy Advisory Committee (SEAC) considered at its meeting on the 19 July 1996 an interim report on a study conducted by the Epidemiology Department, Central Veterinary Laboratory, Weybridge to investigate the possibility of cow to calf transmission of BSE. The study involved assembling two groups of animals with over 300 cattle in each. One group consisted of offspring of confirmed cases of BSE whilst the other group comprised animals born in the same herd and in the same calving season whose dam had reached at least 6 years of age without developing clinical signs of BSE. The animals in the two groups were kept until the age of 7 or until BSE or another disease intervened. BSE occurred in both groups as the cattle were born around the time of the ruminant feed ban in 1988 and the cattle, or at least some of them, in both groups would have been exposed to infected feed. As at the 14 July 1996, 273 animals in each group had reached the age of 7 and had been slaughtered or had developed disease. 55 animals are still alive and histological results are pending for 8 animals. Of the 273 animals born to dams with BSE, 42 have developed histologically confirmed BSE. In the 273 animals born to mothers who had not developed BSE 13 were histologically confirmed as having BSE. This provides evidence that the risk of maternal transmission is approximately 10% for the BSE infected cows whose calves were studied. The statistical confidence limits for that figure are 5-15%, this range being a reflection of the numbers of animals in the study and of the numbers developing BSE. It is highly unlikely that the results from the histological examination of the brains of the 63 remaining animals will materially alter these findings. An analysis has been made of the interval between the birth of the animals in the study and the onset of clinical BSE in their mothers. All of the calves in the study were born within 13 months of the clinical onset of BSE in their dams, and the great majority were born within 5 months of clinical onset. Thus the study does not provide a good estimate of the risk to animals born more than 6 months before the onset of BSE in the dam. However, the findings provide some, albeit limited, evidence that there is an enhanced risk of maternal transmission in the last 6 months of the BSE incubation period. It is plausible that the risk of maternal transmission reduces markedly as the interval between the birth of the calf and the onset of BSE in the dam increases. Therefore, the risk of maternal transmission observed under the study conditions is likely to be greater than would be expected for the entire population of cows. Under field conditions, only a fraction of the BSE-infected cows giving birth would be within 6 months of demonstrating clinical signs of BSE because of the long incubation period of the disease. The average incubation period is 60 months and, if the rate of cow to calf transmission over the last 6 months of the incubation is 10% and it is insignificant before that time, then the average transmission from cow to calf over the 60 months duration of infection in an animal prior to developing clinical disease will be 1%. This would be the rate of maternal transmission that would be observed under field conditions. Maternal transmission at the rates observed in husbandry conditions of the UK dairy herd will not lead to the permanent establishment of BSE even at a low incidence in the UK herd. It will die out, as it already clearly is doing, as a consequence of the restrictions on the primary mode of transmission through infected feed. The study itself provides no new evidence in relation to horizontal transmission. Since the meeting of SEAC on 19 July the Epidemiology Department at CVL has examined the data from this study and that pertaining to the herds from which study animals were taken and has found no evidence of horizontal transmission. The study tells us nothing about the route of maternal transmission, which could be in utero, at birth or soon after birth. In sheep scrapie where there is also evidence of maternal transmission, infectivity can be detected in the placenta. Furthermore in sheep scrapie there is evidence of in utero transmission from an experiment where the embryo from a scrapie infected sheep was transplanted into a healthy ewe and when that ewe gave birth the lamb eventually went on to develop scrapie. Similar embryo transfer experiments are underway in cattle but results are not yet available. Infectivity has however not been detected in the bovine placenta or in milk, or in blood (see Note 1). The Committee considered whether evidence of maternal transmission calls into question the existing recommendations to protect public health. These were drawn up on the assumption that BSE could be a risk to man, which is still not proven, and on the assumption that maternal transmission could occur. The Committee have concluded that there is no case for changing its recommendations (see Note 2) in relation to milk, meat, blood or any other product which is currently permitted. There is no evidence from any of the transmissible spongiform encephalopathies that infectivity can be transmitted through milk. In commercial dairy herds where the bulk of BSE cases arise calves do not receive their mothers milk except for the first few days of life when they receive the special milk produced at that time called colostrum. Colostrum is different in nature from ordinary milk and is not sold for human consumption. In the beef suckler herds it is common practice for calves to be suckled by their mothers for up to six months. Existing data do not provide evidence to suggest that the rate of maternal transmission in beef suckler calves who have prolonged exposure to their mother's milk is any different to that in dairy herds where the only exposure would be to colostrum in the first few days of life. The Committee was pleased to note that the Epidemiology Department at CVL is undertaking further detailed studies on this point, and that the results of these studies will be available very soon. The Committee recognise the role of the ACDP and the HSE in relation to the occupational risks. The Committee draws the attention of those bodies to these new findings but does not make any recommendations for further action other than that the two bodies should consider the evidence and any implications for occupational health. The Committee considered the position in relation to the measures to eradicate BSE, particularly in relation to any selective cull implemented by Government. It is clear from the new information that maternal transmission will not perpetuate the disease and that BSE will therefore die out even in the absence of any form of selective cull. The Committee were made aware that preliminary analyses of the effect of these new results on a culling policy had been undertaken but that these were as yet incomplete. Nevertheless the Committee recommends that the results of the completed analyses be taken into account before final decisions are made about the policy for a selective cull. Finally, the Committee considered what further research might be of high priority in the light of the results of this study and the matter will be the subject of a separate report. Note 1. Data from standard transmission experiments following parenteral inoculation into mice. Details are given in Table 7 of the latest MAFF Progress Report on BSE, published in June 1996. Note 2. In its statement of 20 March about the new variant of CJD the SEAC said: "The Committee does not consider that these findings lead it to revise its advice on the safety of milk.""If the recommendations set out above [i.e., for the proper enforcement of SBO controls on the deboning of cattle over 30 months] are carried out the Committee concluded that the risk from eating beef is now likely to be extremely small." http://www.seac.gov.uk/statements/state29jul96.htm 1POSITION STATEMENTMATERNAL TRANSMISSION OF vCJDIssue1. The Chief Medical Officer for England asked SEAC to considercurrent evidence and comment on the potential transmission ofvCJD from mother to child via human breast milk. In uterotransmission was also considered. The committee alsocommented on the scientific basis of a risk reduction measure forpossible transmission of vCJD via banked breast milk.Background2. No diagnostic test is currently available for the detection ofabnormal PrP in milk. Research is under way to develop tests toscreen for the possible presence of abnormal prion protein (PrP) inmilk samples from cattle experimentally infected with BSE1. Thesemodified tests may also be applicable to human milk. However, it isnot yet clear when/if a reliable test will be available.3. A small number of breast milk banks in the UK supply highlyvulnerable premature babies for whom no milk may be availablefrom the mother. A model developed by the Department of Healthto assess the effect of pooling breast milk from multiple donors onthe possible risks of transmission of vCJD via breast milk bankswas considered.4. There is some, albeit limited, published epidemiological andexperimental research on maternal transmission of prion diseases.There are also unpublished surveillance data of children born tovCJD cases from the National CJD Surveillance Unit and UKsurveillance of neurological illness in children which might inform onpotential risks of maternal transmission.1 A joint FSA/SEAC milk working group is monitoring and providing advice on this researchcarried out at the Veterinary Laboratories Agency.2Breast milk banks5. There is no evidence that vCJD infectivity has ever beentransmitted through breast milk. However, a theoretical risk exists.Modelling studies clearly show that the practice of pooling breastmilk increases the number of donors to which a recipient isexposed and thereby increases the potential risk of an infantreceiving milk contaminated with vCJD infectivity. The theoreticalrisk of infection can be minimised by not pooling the milk, by theuse of individual hand operated breast milk pumps for singledonors, and by the use of single-use sterilised bottles for collection.In addition, available evidence suggests that infection/inflammationof the breast results in increased lymphocytes in milk and thereforeincreased risk of infectivity. This risk would be minimised if milkfrom donors showing signs of infection is not used.6. The committee suggested that, if practicable, milk could be storedfor an appropriate period of time to allow the health status of donorsto be monitored, before it is released. However, information wasnot available to the committee on whether long-term storage ofhuman milk is detrimental to its nutritional quality.Maternal transmission7. There is evidence from animal studies for low level maternaltransmission of prions in cattle and sheep. This transmission mayoccur in utero, via milk and/or perinatally. However, the possibilitythat this putative maternal transmission might have been due toanother mode of transmission, for example through a contaminatedenvironment or feed, cannot be ruled out.8. In contrast, in humans there is no evidence for maternaltransmission in cases of familial prion disease, other than thetransfer of a mutant form of the PrP gene, and there is no evidenceof maternal transmission of Kuru. However, compared with otherhuman prion diseases vCJD may pose a greater risk because ofthe greater involvement of the lymphoreticular system in vCJDpathogenesis. Although, breast tissue (and placenta) from a singlevCJD case tested negative for PrPvCJD, transfer of infectivity tobreast milk may depend on the physiological status of themammary gland. Similar tests or infectivity bioassays have notbeen conducted on breast tissue from lactating patients with vCJD.39. A published study suggesting transmission of sCJD in colostrum2was considered unreliable because tissues not normally associatedwith high levels of infectivity (blood and placenta) showedequivalent infectivity to that of the brain in this study.10. Analysis of prospective surveillance data of UK children born tomothers with, or that had subsequently developed clinical vCJD,provide no evidence for maternal transmission of vCJD. However,the number of cases is very small and the incubation period ofvCJD, if transmitted from mother to child, is unknown and so thechildren may yet be too young to have developed symptoms.11. The phenotype of BSE infection in humans expressing PrPgenotypes other than M/M at codon 129 is not known. Givenrecently published studies in mice expressing the human PrPgene3, which suggest that the human PrP genotype may affectdisease phenotype, the committee considered it very important thatundiagnosed neurological diseases be carefully monitored. In thisrespect, amongst others, it is recommended that the carefulmonitoring of neurological illnesses through the PIND surveillanceof children4 continue.Conclusions12. In summary, there is currently no epidemiological evidence formaternal transmission of vCJD, including transmission via breastmilk. However, there is a hypothetical risk. Although availableevidence is limited and mostly indirect rather than direct, this risk, ifany, appears to be low. As a risk cannot be excluded, a watchingbrief should be maintained.SEACJanuary 20052 Tamai Y et al. Demonstration of the transmissible agent in tissue from a pregnant womanwith CJD. New Eng J Med 1992 327, 649.3 Wadsworth et al. Human prion protein with valine 129 prevents expression of variant CJDphenotype. Science. 2004 306, 1793-1796.4 Devereux G et al. Variations in neurodegenerative disease across the UK: findings from thenational study of Progressive Intellectual and Neurological Deterioration (PIND). Arch DisChild. 2004 89, 8-12. http://www.seac.gov.uk/statements/cjdtransmissionfinal.pdf 4th generation rancher, in my opinion, the most disturbing factor is the real potential for CWD to cattle and the risk of cwdTSE tocattle. IF the transmission of CWD happens in the same way with cattle as to deer and elk, the chancesstopping the spread of this agent in the wild will become much more difficult. you have to consider, the USAhas a most unique and dangerous situation, and that is it's multiple TSE in species, all of which have beenrendered and fed back to animals for human/animal consumption. the long incubation is what is fooling everyone. hope i am wrong. ..... gotta gooooooooooooo.............later, terry
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hey there rkaiser, when you come of your heavy metals dream,
will you still be my valentine :heart: :heart: :heart:
