International meetings and the presentations given that concern BSE

• The meeting at the Royal Institute of British Architects in London in 1991 was the first to make it clear that little work was being done on BSE that was ready for presentation. Even though this was 4 years after the disease had begone, there was one speech on the epidemiology so far of BSE and another from Ray Bradley telling us that everything was all right and not to worry. The hall was full with people from all over the world.
• The meeting at Royal Society in 1993 was similarly packed but similarly there was little information about BSE. Again the hall was full.
• The meeting at the National Food Alliance in 1995 seems to have been the first at which the 'dont worry about it' group from the MAFF actually gave lectures to the 'do something about it' groups from around the country. A small lecture theatre was full and contained media people waiting to interview the experts.
• The meeting at Goettingen in 1995 contained various pieces of information that were clearly of use to research into BSE. This was the biggest yet and clearly more groups were becoming involved in the subject.
• The 1996 meeting of the Society for Risk Analysis contained lectures concerning the assessment of the risk associated with various foods and how the population view these risks (if they knew).
• The May 1996 meeting at Rochdale This is on a separate web page and is an important meeting with full documentation.
• Creutzfeldt-Jakob Disease, Decision-Making in Times of Uncertainty, June 5-6, 1996, Crowne Plaza, Toronto. This has a number of speakers indicating how little we know about the risk associated with blood transfusion.
• BSE and Public Health, (July 1996) the major meeting organised by the Public Health Association, was published. Copies are available from Dr. Karen Toque, North West Public Health Authority, Fazakerley Hospital, Lower Lane, Liverpool L9 7AL UK 0151 525 2323.
• Prions and Brain diseases in Animals and Humans. Nato Advanced Workshop. Erice, Sicily 19th to 22nd August 1996. This was actually organised through NATO and, although it was offered to put this on the Internet, it appears that copies of the documents will be released at a later date and will probably be available from Dr. John Collinge, St. Mary's Hospital, London W2.
• Les Encephalopathies Subaigues Spongiformes Transmissibles: etat actuel des connaissances. This was issued in November 1996 following the meeting in Bougival: 'Programme de Recherche sur les esst et les prions' "Methodes Diagnostiques et outils biologiques' I presume that copies can be got from Madame Jaqueline Dubot, InSERM, Service ICAR, 101 rue de Tolbiac-75654, Paris, Cedex 13. Paris - 44.23.61.40.
• The Royal Statistical Society Meeting on 26th November 1996

National Food Alliance, April 1995

No specifically new information was released but rather the various groups involved in the subject were actually in one room explaining their position. This seems to have been the first time that this took place during the epidemic and was, dispite the anger that it produced with some people, was a breath of fresh air

• Ray Bradley simply gave a very-practiced lecture about how BSE was simply going away and there was no risk anyway. There was no infectivity in the tissues we ate, and all the cattle with clinical disease were being slaughtered. How could there be a problem?
• John Wilesmith similarly told everyone how the disease had reached its peak and was dropping in incidence.
• Chris Bostock explained some of the genetics of disease.
• Harash Narang stated that his research had been tampered with, that attempts had been made to avoid testing cattle for disease, and that various tissues, not banned were still present in human food.
• Steve Dealler stated that, using MAFF data you could easily show that quite large numbers of BSE (clinically symptomatic) infected cattle were not being either reported or reaching MAFF statistics. He claimed that the numbers of infected cattle being eaten were unacceptably high, that the risk to humans could not be certainly stated, as Bradley had done, as being low, and, as such we should assume it to be a risk and get on with the research.
• Oskar Kaaden stated that many of the cattle showing signs of BSE had not received any infected food at all, and that the epidemiology was simply not acceptable as presented by Wilesmith. He was worried that infected cattle were reaching the German population and that Bradley's statements, being scientifically invalid, should not be presumed to be true by Government just because they would like them to be true.
• Professor Almond, who was chairman, gave an short review of the talks...and basically repeated what Dealler had claimed; That there was inadequate information at this time to be certain of BSE safety to humans
• Colin McLean (Once, junior minister for Agriculture in 1990, but now working for the Meat and Livestock Commission) Claimed that dispite all the scientists that seemed to know little about that actual goings on in the meat trade, British beef was doing well and getting better. He said little about BSE.
• Tim Lang (now from the Centre for Food Policy). Went through the information as it had appeared during the epidemic and it became clear that MAFF released the information that they wanted the people to hear. This seemes to have been true with other food 'scares' that have taken place in the UK.
• Carman Taboas (from the National Consumer Council) explained how they had been simply told all about BSE by MAFF and had believed what they were told. Various people in the audience were furious that this had happened. Afterall, the NCC was supposed to be on the side of the consumer not the side of the MAFF. Meldrum (Chief veterinary officer in the UK) was furious at this, stood up and stated that they had done their best.
• Derek Cooper (the well-known journalist) was the chairman and reviewed the afternoon as indicating that the information just did not seem to reach the populus and basically this may have been because there was no way for the journalists to work out who was telling them the truth. After all, if MAFF say everything is OK, and Lacey says that a plague is taking place, it is almost impossible for someone outside the subject to work out.
• The meeting was remarkably useful, with groups from the pet food industry, from environmental health, from the meat trade, from public health, from the Department of Health, and from other directions. All came away feeling that at least the groups had got together. Until then MAFF seems to have monopolised the media despite having given information that was known to be misleading.

Prion meeting at Goettingen, November 1995

This was a 2 day meeting with the experts from all over the world presenting the latest information. It was successful but too large to explain entirely here. Information about the conference can be obtained from Professor Hans Kretzschmar, Institut fur Neuropathologie University of Goettingen, Robert Koch Strasse 40, 37085 Goettingen, Germany. The only presentations shown here are those felt to be of special significance to BSE in the UK.

• Epidemiology of BSE. John Wilesmith. He gave a short explanation of the epidemiology that had taken place and showed graphs indicating that the feed ban in 1988 had been associated with a sudden drop in the number of cattle becoming infected. He explained that they simply were not sure just how the disease continued after that time and went through the explanations. Little was said about vertical transmission. It was felt that pig meal, which continued to be made partly from dead cattle, may have been fed to cattle and showed a (rather poor) relationship between the presence of pig feeding and the continuation of BSE cases after the ban. By rights, however, MAFF had been explaining that almost no infected cattle were being slaughtered in an abattoir (from where the pig meal tissue is taken). Wilesmith's research would suggest that infected cattle were being eaten by humans. He did not mention this. No mention was made of under-reporting of cases. It is clear, however, that large amounts of research had gone into his epidemiology and the audience was impressed.
• Epidemiology of CJD in UK. Rob Will. He explained that CJD has increased in the UK but the evidence that this is significant is poor. The prevalence in the UK seems to be about the same as in other countries of the EC and it may just be that we are reporting cases whereas previously the clinicians were not carrying out post-mortems. He claimed that no risk factors included an occupation. He said that the 3 farmers (of BSE infected herds) that had died of CJD recently could not yet be said to be significant, and specific foodstuffs eaten by CJD patients did not seem to be signficant, the data being fragile because the numbers are so small.He announced that a second teenager (only the fourth in the world) in the UK with CJD had died. This was international news. No mention was made of the 4th farmer or of the other 2 teenagers that were currently comatose. It was not clear how he managed to maintain the farmer statistics as not being significant. He said that other occupations (e.g. vicars) currently seemed to have too many cases but did not point out that this sort of result is expected with any study of this kind and, out of hundreds of occupations, to find that farmers with BSE herds were one of the small numers significantly more likely to die of CJD was going to be a problem with the press in the UK.
• The risk of blood-borne CJD: pros and cons. Paul Brown. He explained that, at the moment there was no evidence that CJD infected patients passed the disease to another person in a blood transfusion. He said that blood certainly contained infection but the statistics were so small with the 4 studies that had taken place until that time that no actual cases could be demonstrated in a recipient. At the end Dr. Dealler said that humans in the UK may be infected with BSE and asked if Dr. Brown felt that UK blood products should not be exported. He said that there was no risk to anyone from BSE and that UK blood was not a risk. He was also asked if he would take a blood transfusion from someone with CJD and he said he wouldn't.
• Comparison of physicochemical propeties of two strains of transmissible mink encephalopathy. Richard Marsh. The reason that this was so important was that you could actually tell the difference between two strains, known as the drowsy and hyper types, by exposing the agents to various chemicals or separation procedures. This was the first that this had been demonstrated. See Byron Caughey's article.
• Agent strian variation in scrapie and BSE. Moira Bruce. Hard work had been put into looking at the distribution of damage done to the brain of a mouse by various strains of TSE. One thing was found was that the damage distribution remained the same, even if the strain was derived from various species. For instance, if BSE was injected into a cat, and then the agent from the original cow and from the cat put into separate mice, what you find is that the distribtion of damage is the same from both sources. What was also found was that BSE distribution seemed to be totally separate from that produced by scrapie. They had known this for some time and had advised MAFF that they could not claim that BSE came from scrapie as a result as the evidence was against this. What is now to be done is to inoculate the disease from the humans (the farmers) into mice and see if it is the same as BSE.
• Transgenic investigations of prion diseases. Stan Prusiner. He put forward the resutls of some previous experiments showing that the prion gene, if carrying an alteration was associated with the animal developing a TSE apparently spontaneously. He showed that the insertion into a mouse chromosome of the gene from another animal would make the recipient then senstive to the TSE of that animal. Well, that was true with the hamster gene but when they tried with a human one things were much more difficult. Eventually, they found that by adding part of the gene the problem was solved. Prusiner claimed that he could look for a human TSE infection with a mouse and not suffer the problem of the 'species barrier' preventing the mouse becoming infected. This is very important in that it could be used to see if humans are already infected with BSE.
• Human molecular genetics and transgenic models of human prion disease. John Collinge. He went though the association between genetics and CJD, then the neurological changes seen in mice without the PrP gene, then explained that mice carrying the human gene (even many copies of it), when inoculated with BSE, did become infected, but produced the mouse prion not the human one. Nobody seemed to know how to interpret this. Clearly it would have been nice to be able to say that, as mice appear to be difficult to infect with BSE, this may show that humans are even more difficult to infect than mice. However, Prusiners speech suggested that this could not be taken as an interpretation, and we would have to wait until the mice carrying the human PrP and not the mouse one were inoculated with BSE in order to find a good indication if humans can be infected with BSE.
• In vitro models of protease-resistant PrP formation, scrapie strains and species barriers. Byron Caughey. The most amazing thing here was that the two strains of TME (see above) could be produced by the presence of the relevant prion proteins in vitro. i.e. if the drowsy prion was put into a test tube with some chromosomal (normal) prion protein it was the drowsy form that was produced using the method published in Nature. The problem with prions up until now had always been that nobody could see how the prion could have a strain type. What seems to have been shown is that the prions can indeed have one, and can indeed produce further prions of the same strain.
• Fatal spongiform encephalopathy in a patient who ingested animal feed. Weis J, Schroder JM, Podoll K and Schwarz M. Inst of Neuropathology and Neurological clinic, Technical University (RWTH) Aachen, Germany. Apparently a patient who died of CJD was known to have tasted various feeds meant for animals over several years. No BSE was known to have been in the food.
• Risk factors for CJD: a reanalysis of case control studies. Many groups were authors including Wientjens, D from Erasmus University Medical School, Rotterdam, and Davanipour Z from University of Southern California, Los Angeles. Few associations were found between specific conditions and the development of CJD. Specifically, having other members of the family with CJD (or even perhaps other psychotic or dementing illness) was associated. Although not significantly increased (which would have been very difficult because of the small numbers of cases in the study) an elevated risk was found for subjects that were employed as health professionals and subjects ever exposed to cows and sheep.
• Vertical transmission of BSE: epidemiological evidence. Dealler S, 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).
• Scrapie in Iceland: epidemiology, main clinical and pathological features and eradication program. Georgsson G and Sigurdarson S. Institute for Experimental Pathology, Univ of Iceland, Keldur, Reykjavik, Iceland. He explained that the scrapie seemed to remain endemic in an area of the country even if the sheep were removed. They then decided to cull all the sheep in an endemic area farm, meticulously clean the and disinfect the premises and restock 2 years later. Since this has been introduced 200 farms that had been culled had not seen another case of scrapie (more than 4 years later) but some farms had seen some cases. The exact reason is unclear but a genetic as well as environmental factor seems to be needed for the development of disease. The final aim of total eradication of the disease i the country by culling and restocking may prove to be very difficult. Mr. Georggsson explained his worry about BSE and that MAFF may be being hopeful that BSE disappears and does not remain endemic.
• Detection of scrapie agent in theperipheral nervous system of diseased sheep. Groschup MH, Weiland F and Pfaff E. Federal Research Center for Virus Diseases of Animals, Paul Erlich Str 28, 72072 Tubingen, Germany. Although no sensitivity for the mouse assay was known, it was found that peripheral nerves may contain >10 thousand IU per gram. The most important factor here is that this represents one tenth of the amount found in the brain (by Hadlow) in sheep. The question must arise as to the absolute amount of infectivity that this represent to be present in peripheral nerves (i.e. taking the senstivity of the mouse assay into account) and from that the amount of BSE infectivity present in the peripheral nerves of cattle that are being eaten in the UK .
• Prion protein variation among primates, ungulates and rodents. Schatzi HM et al. Max von Pettenkofer Institute, University of Munich, Germany and University of California at San Francisco Medical School USA. Using PCR it is now possible to look at the primary structure of PrPc in many species at once. What was found was that many aspects of the PrP were retained throughout but some were variable. It was not, however clear that the PrP structure could be used to indicate which animals would be susceptible to the TSE derived from which other ones.
• The generation of poly- and monoclonal antibodies to prion proteins. Harmeyer S. Pfaff E and Groschup MH. Federal Research Centre for Virus Diseases of Animals, Paul Ehrlichman Str 28, 72072, Tubingen, Germany. They managed to make antibodies against various sections of both the PrPc and the PrPsc. The aim was to use the antibodies for diagnosis. Other groups have found it very difficult to produce adequate antibodies (except Proteus Co, UK) because the body generally sees the proteins as being normal and so their work may be of great use.
• Altered GABA distributio in hamster brainis an early molecular consequence of infection by scrapie prions. Li G, Lu P, Sturman JA, and Bolton DC. Dept of Molecular biology and Developmental biochmistry, NY state office of Mental Retardation and Developmental Disablities, INst for Basic Research in Developmental Disabilities, Staten Island, NY 10314, USA. This was an attempt to work out why the prion protein was needed in the first place and why it was so well retained in animals. They found that the GABA distribution changed very early in infection.

Foods section of the Society for Risk Analysis

• Perceived Food Risk: personal and general. Lennart Sjoberg, centre for Risk Resarch, Stockholm School of Economics, Sweden. A mailed survey about food risk. Complex in that many people saw the risks of food in different ways (e.g. being overweight).
• A study of food risk perception and its relation to purchasing behaviour. F. Bolger and AG Scliffe (City University, UK), P. Ayton, Dept of Psychology, City University, UK), P. Sparks, (Inst of Food Research, Reading, UK). This was more a description of what was going to be carried out as a study. A prediction is made that only a small number of factors will be given by people as influencing their purchasing behaviour and that a linear combination of weighted factors will be a good predictor of information search in the shopping task.
• Trust and risk communication on food issues. R. Shepherd, LJ Frewer and C. Howard. Institute of Food Research, Reading, UK. Because there can be many apparent risks associated with food (chemicals, bacteria, carcinogens, over-eating) it is almost necessary now for the people eating to have believed what the salesmen have told them i.e. that their the food is safe. An attempt was made to analyse this trust.
• Risk analysis, risk assessment, animal health and international trade. Marion wooldridge, Epidemiological Dept, Centra Veterinary Lab, New Haw, Addlestone, Surrey, KT15 3NB UK. Various groups decided that concerning trade of meat, the zero risk option was unworkable and hence a level of risk that should be looked on as acceptable should be used. A scenario tree of risk taking place throughout the production, transport, distribution, and shopping could be made and the risk to various groups assessed at each stage. The various international meat trade agreements were described and how these would prevent infected animals entering countries or not (e.g. the UK demanding to be able to export infected cattle with BSE when the EU prevented them).
• Microbiological risk assessment of meat: a veterinary perspective. Katheryn Christiansen Epidemiological Dept, Centra Veterinary Lab, New Haw, Addlestone, Surrey, KT15 3NB UK. The paper examines the usefulness of a risk assessment approach to evaluate the impact of control measures at the farm and slaughterhouse on therisk to public health from microbial hazards in meat. The one thing that could not be brought in to this was the fact that an 'acceptable' risk level could not be decided. For instance, with BSE any risk to humans at all could not be looked on as acceptable to the consumer, whereas to the government a minor risk would be acceptable and to macro-economists quite a large risk level could be accepable as long as the population that died were not wealth producers.

Bovine Spongiform Encephalopathy

The hall was absolutely packed with people, many of whom were from Public Health and the information given by the speakers was very useful indeed. All the reports have been fully published in the internet Journal of Transmissible Spongiform Encephalopathy except for that is below:

• Professor Anderson from Oxford University spoke on the subject of the epidemiology of the disease. This was after the withdrawal of John Wilesmith. He showed that the disease had almost certainly been in the UK since the begining of the 1980s and the number of cases had already started to rise shortly afterwards (but were not seen by vets). He explained that the cattle were not fed the infective material in large amounts when neonates (they get either colostrum, or tallow-milk initially) and only realtively small amounts of MBM in their diet until milking cattle. This did not fit in with the idea that they became infected when young unless they were more easily infected. He explained that infection could be taking place later than in early birth, he could not show that there had been any change in incubation period or the age distribution during the epidemic. He did not however touch on under-reporting, changes in compensation, or many other factors. One of the major things that didcome forward was that he felt the rate of vertical transmission might be in the range of 8% of the cattle seen and apparently had a method of working this out from the epidemiology data derived directly from CVL. He showed how the percentage might have risen to this level during the period after the feed ban.

Royal Statistical Soc. 26.11.96 Special Meeting on BSE and CJD

Synopses of speeches

John Wilesmith.

Christl Donnelly.

Robert Curnow

James Ironside

4 CJD cases in dairy farm workers since 1990 (all herds BSE positive)
2 CJD cases in beef suckler worker (one herd BSE positive)
Contact with meat and bone meal (p=0.003)
Contact with live BSE infected cattle (p=0.003)
This year there is an association between the eating of beef (p=0.01) and brain (p=0.005) and getting CJD. But the p values to up to 0.33 and 0.55 when compared with control groups.

PrP Genotype at position 129 of the population in the UK: MM 37%, MV 51%, VV 12%. In cases of sporadic CJD: MM 82%, MV 10%, VV 8%. So far in nvCJD all are MM.

Simon Cousens

Graham Medley

Sheila Gore

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Steve Dealler at deal@airtime.co.uk

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