There are always more articles than you can read about TSEs, and I can only make an apology that some may be missed. If you feel that your article is missing and should be here, please forward it
If you want an excellent quarterly bulletin "BSE, CJD, Scrapie: Prion related diseases" send a cheque for 22 pounds payable to the British Library to: Health Care Information Services, British LIbrary Document Supply Centre, Boston Spa, Weatherby, W. Yorkshire, UK LS23 7BQ (phone 0171 412 7470 for further info)If you want a monthly bulletin "BSE and CJD" send a cheque for 40 pounds payable to the 'PHLS Board' to the Library at the Public Health Laboratory, 61 Colindale Ave, Colindale, London NW9 UK.(phone 0181 200 4400 for further info)
If you want to go to the latest articles that I have added to the page, these are
Summary:
Symptomatic cases of BSE in British cattle now total more than
146,000. As BSE is one of a group of transmissible and fatal
spongiform encephalopathies (TSEs) affecting both animals and
humans this has raised concern regarding possible risks to human
health. The infective agent in TSEs, thought to be a prion has
not been clearly described. There are no early diagnostic
tests, incubation periods are prolonged (possibly up to 30 years
in humans) and the pathological process which leads to a rapidly
progressive and fatal encephalopathy has yet to be explained.
It is not yet known if the BSE agent can cross the human species barrier to infect humans. It has now been transmitted to 18 species and to 16 of these (possibly 17 if pigs are included) by mouth.
Given the importance of beef in the human diet, it is essential that control measures to protect health are rigorous, comprehensive and objective. In this respect there are four factors which are important in assessing risks. These are the likely magnitude of the species barrier between cattle and humans, the dose (single or cumulative) that are needed to transmit the disease, the method of exposure (oral or subcutaneous) and the likely period before symptomatic disease appears.
To assist knowledge and understanding in these areas we recommend the wider involvement of public health professionals in the existing nationally co-ordinated multi-agency research programme. We also recommend further studies into the oral transmissibility of the BSE agent to primates, an acceleration of the search for diagnostic tools and treatments for established prion infection and enhanced surveillance of neurological disease in humans.
It is now clear that probably a large percentage of the population will have been exposed to BSE in the UK.
Humans will have eaten 1,800,000 infected cattle by 2001 and
will have eaten tissues that have been shown to be infective in
other species, but inadequately tested in cattle.
Humans have already taken risks in eating bovine products that
have now been banned. The recurrent banning of foods or
procedures by MAFF will not help the people that have been
exposed before the ban. It is possible that further action such
as this by MAFF will seriously damage the public's respect for
its action.
The article's most important part is to show that the World Health Organisation's publicised opinions on how to decide whether or not the exposure of a human to a specific amount of an infective agent could not have been carried out as inadequate information was available with which to decide the action. As a result of this it was important that Government action should assume a tolerable level for human exposure to BSE to be very low indeed, possibly 10,000 times less then the amount felt acceptable by MAFF. Concerning the article in the British Food Journal 1995, volume 97, 3-18.
Review:
The most important aspect of the article seems to be the WHO directives as to how to decide what levels of an agent should be considered non-toxic to humans. Clearly a wide error margin is given by the WHO but still this would suggest the risk that is being taken with BSE as being unacceptable in public health terms.
British Food Journal 1995, volume 97, p3-18
The article explains that, as a fatal disease, with no method of treatment, inadequate methods of diagnosis and no method of prevention in any animal afer infection has taken place, this subject should be studied closely. Infectivity is presumed, if like in other TSEs, to be present in many tissues and to not be destroyed by cooking. One of the major problems is in trying to calculate the number of infected animals that are being eaten and at what point in their incubation period this takes place. It seems that there is adequate data now available from MAFF for this to found. The major findings of the article are:
Cases of BSE are becoming severely under-reported. For instance only 40% of clinical cases of BSE reached UK Government statistics in 1993.
BSE may continue in the UK for many years, with cases born each year, showing symptoms 3 to 8 years later.
BSE may not be derived from the disease of sheep, scrapie and if it is, we cannot rely on it to carry the same properties as that disease. The UK Government used the idea that BSE was scrapie originally to suggest that BSE would not infect humans although this was invalid at the time.
1,800,000 cattle incubating BSE will have been eaten before 2001 even if no cases are born after 1991. This figure assumes that all cattle with BSE were always reported by farmers to veterinary officers, that the VOs always accepted them, and that histological diagnosis was always correct (up to 1991). It is therefore likely to be an underestimate of the true BSE incidence. Many of the younger cattle incubating BSE would have been exported to Europe.
The epidemiology of BSE in the UK is that of an infection passed down from the mother to the offspring but where the mother would show symptoms later in life. It may be that BSE cases that we see are derived from infections in their mother and it was the mother that ate infected food. If this is true then the total number of infeced cattle eaten in the UK will be around 8,000,000 by 2001.
UK Government advisors have suggested that there is little risk from eating liver, kidneys, nerves and muscle from infected cattle. The article shows that this cannot be true if these tissues contain the same amount of infectivity as is found in other species with a similar disease.
The acceptable levels (UK Government) of infectivity to found in food may be 10,000 times the amount that could be seen as acceptable under WHO directives used for other potentially fatal diseases.
UK Governernment Advisory Committee on Dangerous Pathogens reported in October 1994 showing that cattle that may be infected should be treated as if they are infective. They say that some tissues should not be even touched (e.g. liver) that the UK Government continues to tell its population as being acceptable to eat.
The risk to humans in Europe from BSE is unacceptably high but cannot be stated precisely at this time. The article states again that the cumulative amounts of BSE in our diet in the UK is expected to be between 10,000 times and 100,000 times the amounts of scrapie that we would be eating.
No directions are given as to whether bovine tissue in the UK should be considered toxic.
Zentralbl-Veterinarmed-A. 1995;42:453-9
In about 5% of the cows showing clinical signs of BSE the histopathological examination is not conclusive (it is closer to 15% in the UK - Ed). In order to rule out BSE in these cases, additional methods are necessary. For that reason, non-radioactive in situ hybridization (ISH) was performed. In addition, for immunological testing a polyclonal antibody was raised against a synthetic peptide derived from bovine PrP. These two techniques were used on 4 cows with clinically suspect but histologically negative cattle. It is not completely clear what they found but it seems that the four cases were also shown to be negative by these new techniques, allowing BSE to be ruled out. The immunological technique can also be used with EM to look for SAF.
J. Gen. Virol. 1995;76:2567-76.
A complex study in which a 20-100mg sample of tissue could be used to extract TSE-specific amyloid, this would be concentrated and the material detected by Western blotting. It was discussed as a potential method of diagnosis.
Lancet November 4 1995, 1208-1209
It is suggested that scrapie is the source of all TSEs in animals and man but that, by passing from one species to another the agent is either selected or changed in such a way as to alter the range or type of disease that it might produce in a further animal species.
For instance it is suggested that scrapie does indeed cause the endemic types of CJD that seem to be present in some parts of the world (e.g. Slovakia) and partly associated with PrP gene aberrations. However, when scrapie is transmitted to cattle, it then becomes more infective to humans and is involved in the production of sporadic CJD in many parts of the world.
The cases of GSS that are not fully penetrant may be because the genes are correct but the agent (scrapie) is still required. In cases of fully penetrant GSS perhaps the agent also remains with the infected person.
Review:
The argument is fairly reasonable in that it will be very difficult to find groups that have not been exposed to meat at all, even though they think they have not. It will also take a long time to be able to carry out statistical research to say if beef is involved in sporadic CJD or not (because the controls will also eat a lot of beef and the difference between the groups will be small). Diringer recommends research as the way to find out what is going on but the current PrP research avalanche may only be of some use if animal inoculation studies are carried out similarly.
BMJ 25th November 1995 p1415-6
Jeffrey Almond. School of animal and Microbial Sciences, University of Reading.
He says that although TSEs do transmit, we still do not have proof that BSE will transmit to humans. He reviews the molecular biology of the PrP gene that may help us decide.
. BMJ 25th November 1995 p1416
Paul Brown. Lab of Central Nervous Studies NIH, Bethesda, MD
"In fact no one can say yet with any confidence whether the recent cases of CJD in adolescents and farmers are the results of infection with BSE.". he states that really young cases have been seen before and we should not assume that the new cases are anything to do with BSE. F "Finally there does not seeem to be any need for new governmental hearings, committee meetings or parliamentary debates about what more might be done because the precaustions taken some yars ago to eleiminate potentiallly inecvtious products from commercial distribution were both logical and thorough" (I hope he was right, but I doubt it-Ed)
BMJ 25th November 1995 1416-8
Sheila Gore. MRC Biostatistics Unit, Inst of Public Health, Cambridge
She demonstrates that the chance of getting two teenagers 'back to back' and four farmers with CJD in 4 years is so low that they could not have happened by chance. He work sparked off a lot of debate and it was felt from this that something was happening that theydid not know about.
BMJ 25th November 1995 1419
Ros Ridley, Harry Baker. MRC Comparative Cognition Team, Department of Experimental Psychology, Cambridge Univ
. They put forward the argument that the figures are simply not big enough for there to be any great risk. Four cases of apparently idiopathic CJD have been reported in teenagers in Europe and the USA. Obviously these were nothing to do with BSE. They felt that the CJD Surveillance Unit led to a higher level of reporting of cases and that these cases were of little significance.
BMJ 25th November 1995 1419
GW Roberts. Molecular Neuropathology, Smith Kline Beecham, prk North, Harlow.
He explains that we simply cannot know. The data islong and hard and at the end of going through it we still dit not end up being sure if BSE infected humans. He quoted the work of Dealler and Kent showing that the number of people that would have eaten various doses of BSE could be actually so variable as to be unhelpful but a worst case scenario would suggest a dreadful result. He discusses the problems that changes in environmental factors, changes in reporting levels, changes in many other factors may mislead us.
. BMJ 25th November 1995 1420
Kenneth Tyler. University of colorado, Health Sciences Center, Denver VA medical Center, Denver.
He looks at the inoculum size, the routes of inoculation the host factors (e.g. can humans be infected at all), the genetics and the implications for disease prevention. In the end he does not say if humans have caught CJD but says that really to avoid any risks we should avoid contact with nervous and lymphoreticular tissue. He does not even make the same pretece that MAFF does continually i.e. that there is no infectivity in any bovine tissue except brain and spinal cord. He says that meat is not expected to harbour major amounts of infectivity.
Federation of Infection Societies, Manchester Symposium, November 29th 1995
S. Dealler, Burnley General Hospital
By looking at other species and the incubation period that is produced by the transfer of infectivity it is possible to estimate when a rise in BSE cases in humans as CJD2 cases would be expectd to take place. This shows that we might be lucky to see any cases at all before the year 2000 and that the peak may be 15 years later. The reason for this is that humans have a very long life expectancy, BSE has been transmitted by mouth, and it has had to cross a species barrier. If cases of CJD2 were to appear earlier than 2000 that might be an indication of the size of the peak to come.
Research paper 95/132 Produced by the Science and Environment Section of the House of Commons Library. Christopher Barclay and Jane Cushion.Dec 1995
A rather poor review but attempts to go through all the possibilities of CJD and risks from BSE
Neurodegeneration vol 4 1995;357-368.
CJ Bruton, RK Bruton, SM Gentleman, GW Roberts. Corsellis Collection Brain Bank, Dept of neuropathy, Runwell Hosp, Wickford, Essex. etc.
Reliable identification of CJD in the UX has become essential following the suggestion that prion disease in cattle might transmit accidentally to humans who eat contaminated beef. recent data suggest that some cases f CJD may be conically unrecognized; in order to examine this proposal we reviewed all cases of dementia (n-1000+) collected between 1964 and 1990. We identified 19 cases of CJD of which only 11 were diagnosed before death. These 11 had a characteristic clinical history of CJD. Their brains showed little or no external abnormality. In contrast only 2 of the 8 clinically unrecognized cases had characteristic symptoms. The remaining six presented atypically; their illness lasted 3 years or more, motor signs were much less evidnt and simple dementia was the most promminent feature. the brains showed moderate or severe cereral atrophy. Our data indicate that only about 60% of prion disease cases with pathologically typical SE were identified clinically during life. This suggests that human prion disease may bemore common than previously supposed and that a further review of the epidemiology is required.
Annals of Neurology 1995;38:269-72
A 57 year old woman who died from CJD after 2 years after a liver transplantation. The liver donor had no history of neurological disease. In one albumiin donor, possible CJD disease develooped 3 years later. The patient intitially had cerebellar symptoms. Neuropathology includingn 'kuru--like plaques and prion protein deposits involving the cerebellum predominantly. The patient was homozygote valine at codon 129 of the PrP gene while the liver was methionine homozygote. This observation raises the possibility of transmission of CJD by the graft itself or the associated albumen transfusions and, on a wider extent by nonneural tissue. The article goes on to say that infectivity has been found both in the liver of humans with CJD and the blood. A minor review follows.
Veterinary Record. Dec 9. 1995. p605-8
DM Taylor, SL Woodgate, MJ Atkinson, Neuropathogenesis Unit, Edinburgh University
Bovine brain infected with the BSE was used to spike material processed in pilot scale facsimilies of 12 rendering processes which are used within the EU and 3 which are not. the raw material for experimental rendering represented those used inpractice, and consisted of appropriateproportions of BSE infected brain tissue, bovine or porcine intestine and bovine bone. Meat and bone meal and tallow were produced from the rendered tissue. Suspension sof all the meat and bone meal samples were assayed in mice for BSE. Four of the 15 processes produced MBM with detectable BSE infectivity. Neither of the tallow samples did. The problem with the results was that they did not show any great effect for themethods of talow extraction using solvents. This was the method that was blamed for rendering the MBM safe until the process was stopped at the beginning of the 1980s in the UK. Presumably the change in manufacturing cannot be now assumed to have had a specific effect.
Lancet 6 Jan 1996 p65
Stating that we should not assume that any new CJD would be similar to previous ones and that the epidemiology may be obscure initially. Hence we should ook harder at the significance of the new cases of CJD in young people.
Lancet 6 Jan 1996 p65
He felt that the new cases of CJD in younger people were not concerned with BSE and puts forward some of the various hypotheses as to where sporadic CJD comes from.
Lancet 6 Jan 1996 p65
Argues with Operalsky and Mosely's letter (Nov 4) about the risks from blood transfusion and point out that by the time recommendations to remove specific blood products from shelves has reached the pharmacies, the products have often been used.
Lancet 20 Jan, 1996 p.195-6
Shows that, assuming the disease to be cumulative it is possible to get an idea as to when the risk took place and as to what would be the added risk for beef eaters to continue doing so at this point. It shows that most of the risk is already taken and the advantage for stopping is minimal.
BMJ 20 Jan 1996 p 180
Terence Featherstone of the Department of Radiology, Darlington Memorial Hosp suggests that magnetic resonance imaging may be of value in diagnosis of CJD.
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.
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.
BMJ 20 Jan 1996 p 181
Janet Fraser, James Foster, Hugh Fraser, Institute for animal Health, Neuropathogenesis Centre Edinburgh
this was shown in mice.
Secret Government: the Scott report
BMJ 24 February 1996 p455-6.
Martin McKee (Health Secvices Research Unit, London School of Hygience and Tropical Medicine. Tim Lang
Links with industry cast doubt on the government's role in public health. The report said that everyone that mislead the House of Commons, misled the media, mislead the people, lied to the judges, and were determined to send arms to a country that had been banned from receiving them for political reasons throughout the world, were in fact doing it with a clear heart. They thought they were doing it for the best even when it came to allowing a group of men to go to jail even though they carried out the exports with the OK of the Government. The report suggests that the associaton between industry and Government may be too close to allow. The meaning of this for BSE is important.
A statement indicating to medical practitioners in the UK that in the last two weeks the CJD Surveillance Unit has described a distinct variant of CJD in 10 cases, in people aged under 42 with dates of onset of illness in the last two years. He states that still the risk of CJD in the UK is the same as in europe and hat it remains a rare disease. Patients presentig with the non-specific symptoms are no more likely to be suffering from CJD than previously. There is no reason for a change in referral patterns to neurologists or other specialist services. Neurologtists are aware that they can obtain advice from the CJD Unit. 20 march 1995
Mr Dorrell followed by Mr. Hogg speaking on the subject of BSE risk to humans. this was following the weekend discussion by SEAC concerning risks to children and various others. Hansard. 25th March 1996 3.31 pm.
Mr. Dorrell states that research into the subject would have to increase and that he had asked Professor Swales (now at Richmond House, Whitehall, DofH) formerly Prof of Gen Med at Leicester University, to produce a list of the research that would be required to be carried out.
Mr. John evans (St. Helens North) asks how Mr. Dorrell could accept advice from the same group that had been telling him for years that nobody would die of CJD (p722)
Mr. Hogg (p724) gives out the data concerning the number of cattle that would be expected to be slaughtered and what would be the sort of regulations that would be reqired.
This is the report on the statement as to the risk to children concerning BSE in food products. It concluded that there was no increases sceptibility to infection for pregnant women, hospital patients, the immunosuppressed, or children. there is nothing to lead the committee to change its advice on the sonsumption of milk andmilk products. SEAC also concluded that gelatin was safe. Children are no morelikely to become infected than adults. He states that further research isneeded and the WHO will organise an international seminar on the latest results from the CJD unit as soon as possible.
Nature 28 March 1996. 380;271
The scare in Britain over infections across species by rions was badly handled. whether the research community can do more to prevent future public crises of confidence needs to be examined in the light of the past influenceof interested parties.
The article makes it plain that the population has difficulty believing what is told to it by MAFF, which has too many vested interests in selling foods, no matter what the potential risk to them. Prion research must now be strengthened, denial of information from the people must be stopped, and external review will be essential.
Nature 28 March 1996. 380;273
A short article on what had gone on during the previous week. It pointed out that the Government's position to avoid specific research or to take severe action had been that there was no proof of BSE causing CJD...but there still was no proof.
Nature 28 March 1996. 380;273
A short review of the research that has not been done but requires to be done
British Medical Journal. 30 March 1996. 312 p 791-3
Failures of opidemiology must be remedied. The article makes it plain that the action so far taken in epidemiology was inadequate in order to work out the risk that has been taken in the UK. She calculates the chance of 10 cases developing CJD betwen the ages of 17 and 41 yrs and whether that should have been thought of earlier as abnormal. she goes back on her own work showing that there was excess risk to farmers and teenagers. With the amount of data currently available she says that it is not possible to assess the risks being taken by people in the UK by carrying out certain procedures (working on farms, eating beef, dringking milk) purely because the data was not adequate at the time. Mistakes were made with other epidemiological attempts e.g. with HIV and false reassurances were given (e.g. HIV and breast milk). The main aim of the article is to put forward the data that would be required in order to find out much more about the epidemiology of CJD2. One of the factors that is suggested is that the disease be made 'notifiable'. This means that doctors seeing a case must report it to officials and the data would be built up centrally. "Practically we do not have in vitro or in vivo tests for infected cattle and so have continnued to play Russian roulette with no information on the odds. Age specific prevalence of infected cattle has not even been monitored by random pathology after slaughter for which there is now the stronges case".
This is in the editorial section and is very aggressive in its demands
.
The risk is unproved but no better explanation is presently forthcoming.
British Medical Journal. 30 March 1996. vol 312. p790-1.
He admits that the cases that have been seen have been different clinically from the sporadic type of CJD and that the finding of neuropathology that is also different (but similar to each other) would make BSE the most likely explanation. Ill defined early emotional behavioural dymptoms of the new variant will obviously openthefloodgates to hundreds if not thousands of suspected cases of CJD over the next few years and it will be a matter o enormous practical importance that a screening test is produced. He says that a new test is soon to be reported with a sensitivity of 97% and s specificityof 98%. "A good deal of work remains to be done i order to esztablish the link between BSE and CJD, much of which has already been initiated. None of it will be ofany help to htose who may have been exposed to the agent in the 1980s.... Nor will it remedy the possible failure of the scientific pudits (including me) to forsee a potential medical catastrophe" (Ed-it was good of him to admit that he was wrong, as he had been denying any risk to humans from BSE for many years)
BMJ Vol 312 30 March 1996. p 843
Ridley, RM and Baker H. MRC Comparative Cognition Team, Dept of Experimental Psychology, Univ of Cambridge. Study so far shows no evidence for maternal and horizontal transmission. This is an argument with the previous article from Lacey suggesting that there was evidence. They quote the work of Hoinville and Wilesmith in which they compared the likelihood of a cow developing BSE as to whether their mother did so. '94.4% of animals with SE and 95.7% of controls were born to dams that did not subsequently develop BSE'. The difference was not significant. (Ed-The problem with this is that it would be needed to work out what percent were actually the offspring of infected mothers and in one of the major epidemiological models including vertical transmission, there would not be expected to be any difference between the groups, because such a high percentage of the dams in any herd were in fact infected)
BMJ Vol 312, 30 March 1996. p 843
John Wilesmith, Cenral Veterinary Lab
He says that the study will show if vertical transmission is taking place by comparing the offsppring of cattle known to have BSE with those that are the offspring of other cattle from the same herd. The results should be ready by the end of 1997. At the moment he denies any evidence of vertical transmission.
(Ed-this has come under considerable discussion. It is not clear why it is a blind study, as this should make no difference as to the diagnosis of the vet at the time. After all it is a fatal disease and the cow cannot be making it up. Similarly the histopathologists looking at the slides in diagnosis need not be told if they are looking at the slide of the dead cow or a control. A lot of demands have been made to un-blind the study. Also many people have made it cleat that the study cannot actually show if there is any vertical transmission or not as the control dam would also be infected i.e. both the case and the control will have come from infected mothers)
BMJ Vol 312. p 843
M. Bennett. Environmental Technology Centre, Depf of Chemical engineering, UMIST. Box 88, Manchester M60 1QD
He shows that the epidemiology actually shows that the number of cases of BSE born after the feed ban actually increased and it is not surprising that Lacey makes claims that the disease is not going away.
BMJ Vol 312. p 844
Martin Zeidler, RG, Will, J, Ironside, CJD Surveillance Unit Western General Hosp, Edinburgh and R. Sellar, J. Wardlaw Dept of clinical neuroscience, Western Gen Hosp
Replying to a previous letter sugesting that MRI would be useful.
BMJ, 312, 30 March 1996, p854-5
This goes through the days in which BSE was admitted to be a likely risk and the effect it had on the media.
Nature 4 April 1996. 380;370
Various European research groups say that the hiding of information by the UK groups does not help when trying to work out what is going on.
Editorial Lancet April 6 1996, 347; p915
Editorial. It explains the risks that have been taken and how the unfolding story of scrapie, BSE and CJD underscores the weakness of separating agricultural and medical science and of allowig one Government department to protect the intersts of both thefood consumers and the farming industry. Morover the advice of independenet scientists and the creation of political policy should not come from the same stable. this latest drama points to the need for a separate, independent agency that reports to the public not to the policy makers. Such an agency would be a forum for open scientific debate. the iformation andopinions proffered would be pubicly subjected to critical evaluation. we would all then have the opportunity to understand how expert opinion and recommendations are formed and politicians could begin at last to build foresight into their policy responses rather than simply react in confusion and haste to the latest scientific alarm." Excellent-ed.
Lancet April 6 1996, 347; p916
Lancet April 6 1996, 347; p917
JG Collee. Department of Med Micro, Univ of Edinburgh
Considering Collee wrote a major article in the Lancet in around 1990 indicating that the risks from BSE to humans, although possible should not be considered to any great degree, this article is absolutely excellent. It describes the way in shcih infection could take place, how it may pass into a pathogenic phase, how it could spread around the body, how it could develop into a clinical disease. A list of essential factors and key questions is put forward and he explains that we simply know quite inadequate amounts at present to know what isgoing on with the new CJD2.
Lancet April 6 1996, 347; p921-25
RG Will, JW Ironside et al . CJD Surveillance Unit, Edinburgh.
Summary: Background. Epidemiological surveillance of CJD was
reinstituted in the UK in 1990 to identify any changes in the
occurrence of the disease after the epidemic of BSE in cattle.
Lancet April 6 1996, 347; p945
Tabrizi. SJ. St. Thomas' Hospital, London
A 28 year old woman who had had various neurological problems
since the age of 14.
New Scientist. 13 April 1996 p4.
A journalistic news item. investigating why MAFF in the UK
failed to carry out the experiments to find out if BSE was
derived from scrapie and yet continued to claim that 'as BSE
came from scrapie, therefore we wont catch BSE either'.
Robert Rohwer who studies spongiform encephalopathies at the
veterans affairs Medical Centre in Baltiore Md said that the
xperiment should have been simple. You just feed scrapie to
cows. Iain Pattison suggested that happen in the UK but
Wilesmith simply dismissed this and said it would only tell us
what we knew already. In 1994 18 calves were injected with
scrapie. The cows became sick after 14-18nmonths and died
within 5 months. But the cattle did not die of BSE, as could be
seen by post mortem study. Mark Robinson of the Animal Disease
Research Unit in Pulman, Washington said "The pathology in the
brain did not resemble BSE at all" No strain of scrapie to date
produces a disease incows that resembles BSE. MAFF continue to
say that it could jsut be from a strian that they have not
tried. Rohwer agrees that the MAFF scientists explanation for
the origin of BSE is plausible 2but it doesnt excuse the fac
thay they have not doen the experiment2 He suggests that BSE is
in fact a new disease that first arose in a few British cows.
because cattle carcasses were also rendered into animal feed,
the agent would get to further cattle. Other influential
scientists share Rohwer's criticism that the Brit Govt were too
eager to accept the vfiew based on limited scientific
understanding"
New Scientist. 13 April 1996 p5.
Young women with CJD2 might pass ont the deadly cnodition to
their children before showing symptoms themselves warnds Sheila
Gore of the MRC
This was sent to allthe GPs and most other doctors in the UK.
It refers to the following article in the BMJ. showing that the
Mdicines Control Agency who have revisited the subject this
month. Their expert advice remains that medicines licensed for
tuse in the Uk are safe. Non-bovine material or bovine material
outside the UK is used. Tallow derivatives have gone through
rigorous extraction procedures to eliminate the causative agent
of BSE
Ed-It is not clear just how tallow can be rendered safe from
scientific literature
BMJ 312, 20 April 1996 p988-9
E Anne Wickham. Hox 246, Canterbury CT4 5YY
Editorial saying that patients can be reassured that measures
are in place to reduce risk. Measures aimed at minimising
exposure to TSEs via medicinal products were intoduced soon
after the report of the Southwood committee in 1988 in
guidelines for manufacturers issued by Britain's Comjittee on
Safety of Medicines in 1989 and essentially adopted by the
European Committee for Propriatary Medcinal Products in 1992.
Materials were to be sourced from cattle under the age of 6
months, from countries fee of BSE or where low number of cases
had been reported. The guidelines included a classification of
various tissues and body fluids according to potential risk of
infectivity based on expoerimental data from scrapie in sheep
and goats. Notably they did not use information from other
species e.g. mice, hamster, mink.
She talks about specific products that had been derived from
cattle. Notably heparins derived from lung (lung was found to
be highly infective in mice), insulin from the pancreas, and
various sources for gelatins, and serum and lactose. The
guidelines recommended purification procedures known to remove
or inactivate agents causing TSEs: autoclaving or treatment with
sodium hydroxide, these being more effective than other methods.
The Assn of British Pharmacutical Industry declare their
products to be safe.
Annals of Neurology
Nineteen cases of sporadic CJD were studied. The PrP gene, the
biochemical characteristics and the intracerebral distribution
of the PrPsc. Four grops of subjects defined by the genotype at
codon 129 were found with two of them differing not by PrP
genotype but by the size and glycosylation. The typical CJD
phenotype or myuoclonic variant and the Heidenhain variant were
linked to the met homozygozity and the type 1 PrPres. The
atypical and rarer variants such as that with dementia of long
duration, the ataxic variant, andthe variant with kuru plaues
were linked to different genotypes at 129 and shared type 2 of
PrPres. Our data indicate that the sporadic form of CJD
comprises a limited number of variants. The met/val
polymorphism at 129 of the PrP gene and two tpes of PrPrs are
the major determinants of these variants. These findings
suggest the existence of prion strains in humans and provide the
molecular basis for a novel classsification of sproadic CJD.
What isnt spelled out properly is that there are two forms of
the PrP, whereas you would expect that there could not be.
Hence it would be the actual structure of the PrP that might
indicate the strain of the disease, whatever the genetics of the
patient.
The work was followed up by Collinge et al in Nature in
September 1996.
New Scientist 20th April 1996
France ignored a warning 4 years ago abou tht erisks of BSE
passing to humans the minister Francois d'Aubert said last week.
The previous government dragged its feet apparently. In 1992
the Govt commissioned Dominique Dormont of the Atomic Energy
Commissionto write a report on human and animal forms of TSE.
The report was never made public but according to the research
ministry it warned of the "existence of risks from BSE". Marc
Cesbron who studied TSE at Pasteur Inst in Lille says he wrote
to the Government in 1991 warning them of the possibility that
BSE could pass to humans. the letter was forwarded to the
European Commission but little happened. D'Aubert said that an
extra 5 million franks (650,000 pounds) would bee earmarked for
research in 1996 and that next year spending would increase to
69 million francs (more than in the UK). D'Auberts said he was
also launching an action plan to improve surveillance.
New Scientist 20th April 1996
Four sites: Coneticut, Minnesota, Oregon and California were
chosen by CDC to check that their CJD patients were not really
CJD2 that had been exported from the UK!
New Scientist 20th April 1996 p18
Shigeru Katamine a virologist at Nagasaki University and
geneticist Tetsuo Noda showed that when the entire PrP gene was
removed specific damage appeared to happen to the mice after a
year. Purkinje cells were damaged and destroyed in the
cerebellum. (Nature 380, p528.)
This was one up on the Zurich team that removed on ly part of
the gene and the animal remained normal.
Irene Tobler of the University of Zureich looked a little harder
at the PrP mutant mice (nulls) she showed that they did not
sleep normally and repeatedly stayed awake for periods of up to
16 seconds. Perhaps this explained the fatal familial insomnia
syndrome Nature 380 p639.
The Lancet 347, April 20th 1996 p1114.
Wisniewski H.
Sigurdarson S
Rubenstein R
Kascsak R
Carp R
All from the Inst for basic res in development and disabil,
Staten Island, NY 10314, USA except for Siguardson, who is from
Inst of Experimental Pathology, Univ of Iceland, Reykjavik,
Iceland
This is a very important in that it shows the agent for scrapie
(or at least a strain of TSE) is present inside the hay mites
that are present on the land. It showed that a relateively high
proportion of the mites were infested, that mice could be
infected from them, that hte amount of prion protein was high
enough that the western blotting looking for it in the mite
could find it after dilution of the agent by 200 fold. This may
actually suggest that the agent can not just remain in the mites
but perhaps multiplies in them as well. This was required to
somehow explain why scrapie remained associated with the land
but gradually died out over many years (i.e. that sheep put on
such land gradually became less and less likely to develop the
disease).
What was not made clear in the article is that the hay mite does
not live on blood as a source of food and is not specifically
found in parts of the country or with specific groups of sheep
etc. Also the hay mite is very small and it would have been
very difficult to carry out the experiments. This major finding
may need a complex investigation.- Ed
Nature 380 25th April 1996 p675.
Krakauer DC, Pagel, M, Southwood TRE Dept of Zoology
Oxford. Zanotto PM Inst Virology Mannfield Rd Oxford.
Phylogenic analysis for the prion protein. It appears that the
PrP structure may actually be an indication on the ability of
the disease to transmit between animals. This may actually
explain why BSE infects humans and scrapie does not. This
clearly cannot be the whole story, however, as although it shows
specific parts of the DNA for the PrP in cattle and humans being
the same, they are actually different at around 23 other sites.
The chances of the specific similarity that was found having
arisen by accident was 1.2 in 10,000 and so the researchers
believe that the evolutionary pressures that drove the human PrP
to change in a specific way was similar to the pressure on the
bovine PrP. The researchers note that the two amino acid
substitutions occur within a region of protein that is known to
be involved in prion disease.
Nature 2 May 1996;381:15
They calculated the affect that ploughing in the soil on which
the cattle had been grazing and decided that it was too
detrimental. They calculated the carbon content effect on the
UK soil pool and felt that, without a strong scientific reason
this would be unwise.
Safety management. vol 12 May 1996.
Doublas Latto
This discusses why the British Government was determined not to
take into account the advice from safety groups earlier in the
BSE epidemic in the UK.
Stekel DJ, Nowak, MA, Southwood, TREDep tof Zoology, Univ
of Oxford, Oxford, UK, OX1 3PS
This is a statistical attempt, using the same method as Dealler
in 1993 (Br. Food J.) to calculate the number of cases of BSE
that are currently being incubated and will appear as clinical
cases .The data is derived from MAFF, is assumed to be fully
correct and is assessed using standard techniques. No attept is
made to show or calculate underreporting but they also show that
the age distribution of BSE appears to become younger in cattle
born after the feed ban, although this does not make a lot of
sense. A further 15,000-24,000 cases were predicted of BSE
between 1996 and 1999 assuming no cattle born after 1992 would
develop BSE. About 75% of future cases will occur in cattl
eborn in 1989 or later (at least 5 monhts after the feed ban).
No attempt was made to correalate the pattern with that expected
for specific epidemiological models e.g. vertical transmision or
to calculate when the initial cases of BSE were infected.
Lancet. May 11, 1996, vol 347 p 1332/3
Jean-Francois Foncin Laboratoir de Neurohisologie, Ecole
Pratique des hautes Etudes et Unite 106, 75651, Paris Cedex 13,
France
He is worried that the article by Will et al, claiming that CJD2
could be a result of the epidemic of BSE. He is extemely
critical of the methods used in stating that there was no
specific genetic link found in the patients with the disease.
He claaims that in the late 1970s he showed around the French
neuropatholigal circles an apparently sporadic erly onset case
with initial ataxia, terminal dementia and abundant plaques as
"le Kuru de Gonesse". It was published as GSS only after
protracted inquires had showen that four relatives had died with
similar symptoms in psychiatric hospitals..
Lancet. May 11, 1996, vol 347 p 1332/3
Jean-Phillipe Deslys, corrinne Ida lasmezas, Thierry Billette
de Villemeur, Alexandre Jaegly, Dominique Dormont Various
sources.
They explain that the reasons given by Will et al for the cases
of CJD2 appearing in younger groups were possibly not the only
possible story. Will et al felt it was because younger people
were more exposed to infective material (this has been shown by
other groups as well - Ed). This groups, however feel that
there may be another factor, a genetic one also, that made these
people more open to infection. Also, as almost all the
population would have been exposed to some degree, it may even
be that a factor is protecting the other members of the
community but missing in these people. They suggest that people
already carying non-virulent strians of disease may actually be
non-susceptible to BSE. Only young, gnetically susceptible
people who had not been previously exposed to this agent would
beinected with BSE. As a result the exposure of the whole
population to BSE would be apparent in an unusual form of CJD
ina small group under the age of 40 years. (this is actually
very similar to what was said by Harash Narang to the House of
Comons Select Committee on 17th of April 1996- Ed).
Lancet. May 11, 1996, vol 347 p 1332/3
Diringer H robert Koch-Institut, Nordufer 20, D 13353,
Berlin, Germany.
He puts over the fact that the population going down with CJD2.
He suggests that the reason for sporadic CJD having such a high
proportion of met/met may be because they did not really appear
out of the blue but caught the condition from animals in the
same way as the CJD2 patients may have done.
Lancet. May 11, 1996, vol 347 p 1332/3
Taylor DM Neuropathogenesis Unit, Inst for Animal
health, West Mains Rd, Edinburgh, EH9 3JF.
This is following the article suggesting that sterilisation of
medical devices contaminated with CJD need not be a problem. He
says that there is simply not enough known to make that sort of
statemet. He explains that in different TSEs the time needed to
sterilise products was not relaible for instance BSE in cow
brain dropped 3.5 logs whereas scrapie infected hamster brain
dropped 7.5 logs under the same action of heat. One of the
ideas was that there was always a small percentage of the agent
that was completely resistant to heat and hence he did not agree
with the original author.
Adjou, KT, Demaimay, R, Deslys, JP, Lasmezlas C, Seman M,
Dormont D. All are from Service de Nerovirologie, CEA,
Fontenay aux Roses, France (except Seman)
This is an attempt at testing the use of an amphoteracin
derivative, supposedly less toxic on the incubation period of
scrapie in mice. They looked for the accumlation of glial
fibrillary acidic progein (GFAP) and the accumulation of PrPres.
What they found was that the treatment during the incuabtion
period delayed all factors. The continuous treatment with the
drug in this experiment may make it impossible in humans,
however.
British Medical Journal. 25 May 1996 312:1358
It showed that many of the doctors that would be likely to see
patients with CJD were not aware of the surveillance system for
the disease. This was not true for neurologists, however.
Nature 30 May 1996 p353
A discussion of the various committees and groups including the
WHO that were going over the problem of BSE and how they, for
shortage of information could not make fully scientific
statements. As a result they did not feel that a wider ban on
the UK beef exports could be lifted
Nature 30 May 1996 p353
States that it surely should be postulated that BSE was not
derived from sheep but from other cattle. A French vet in
southern france, M. Sarradet described as early as 1883 a "case
of scrapie n an ox". Re. Veterinaire 3, 310-312; 1883.
Puts over the problems of being sure that the food we handle and
eat are actually safe. It shows that there is still too much
uncertainty for people that do not wish to take risks to
continue eating potentially risky meals. It is also quite
aggressively scathing about the way in which the controls the
MAFF said it was taking to avoid BSE infected tissue getting
into the human diet were inadequately enforced and indeed the
MAFF admits this.
Nature 6 June 1996 p453
The worry that information concerning CJD cases is not being
released for investigation by other scientists by the UK
Government groups has been found unacceptable, particularly in
France, where a number of cases may well have appeared. French
workers were complaining that htey had been left completely in
the dark over what was happening and the results from the new
cases that seem to have appeared in 1996 of CJD2.
Society of General Microbiology Quarterly May 1996;23 part
2;48-9
Goes over the reasons why we should assume BSE to be a cause of
the CJD2 form of disease until further evidence appears. A good
short review.
Lancet July 6 1996. 348;55
Reports a rhesus monkey that was in the UK from 1982 to 1986 and
then transferred to France. It died of a spongiform
encephalopathy with excess PrP apparently present. The authors
consider that this could be derived from the eating of another
TSE material such as BSE.
Lancet July 6 1996 348;56
Over 100 marmoset monkeys lived for over 5 years being fed
material that contained ruminant derived protein. None lived
for more than 10 years. The authors remind us that as BSE could
be transmitted to these animals by inoculation, the oral route
could well be highly inefficient. Unfortunately the previous
paper, with the animal 13-14 years old may suggest that this
paper was inadequate and that the animals may well have been
infected but were simply incubating the disease. None of the
marmosets in this report were tested for disease by inoculation
into further animals.
Lancet July 6 1996 348;56
None of the new CJD2 cases had any of the PrP gene variations
that had been found in vertically transmitted forms of CJD.
Vet Rec. 1996;138:407-8
Case control study techniques to compare the incidenceof BSE in
progeny of 2 sires and 110 afected dams with the incidence of
BSe in te progeny of animals known to be unaffected at the last
record. All the progeny born before the feed ban. The
results provide little evidence of differences between the
incidence in the progeny of presumed unaffected animals. Data
from 5 herds were used. The disease status of the dam did not
signifcantly affect the disease status of its progeny after
allowance had been made for the effects of herd, year and age at
the last record of the progeny. The difficulty of establishing
maternal transmission if a high proportion of the dams are
incubating the disease and transmission can ooccur early in the
incubation period are discussed.
What this shows is that there is little difference in the BSE
likelihood of the offspring depending on whether there had been
BSE in the mother (i.e. it was insignificant). This was not
actually true for 7 year old dams where there was an excess of
BSE in the offspring (p<0.05). The problem with this sort of
research is that it depends on the cattle that have symptoms of
BSE represent a major part of the ones with the disease. If
however a large porportion of the cattle are infected and we
only see the ones with symptoms then the research becomes
difficult to interpret. "The present analyses suggest that if
the majority of the dams can be assumed not to have been
incubating the disease, then there is little or no evidence for
the maternal transmission of the disease".
Vet Rec. 1996;138:546-8
This took sheep infected with BSE either by oral infection with
0.5g bovine brain or intracerebral inoculation with brain
homogenate. The lesion profiles in the brains of mice
inoculation with the tissues of these sheep were similar to that
of BSE similarly inoculated into mice. Notably the significant
levels of infectivity found in the spleens of sheep show that
the pathogenesis of BSE in sheep resembles that expected for
natural and experimental scrapie in sheep spleen.
Vet. Rec. 1996;138:175-7
1,500 from 1992-3 were compared with 1000 from 1993-4 and the
lesion profiles were found to be the same. As in previous
studies, 61.6% of the cattle with no BSE lesions found were not
found to have any other histological changes. The remainder
consisted of bilateral focal spongiosis of unknown significance
(26%), 8.1% with inflammatory conditions, and a small number
with tumours, cerebrocortical necrosis or idiopathic brain stem
neuroal chromatolysis.
By rights the proportion of cattle with BSE should have risen
during the epidemic but appears not to have done so (i.e.
illnesses with nothing to do with BSE should have been a lower
and lower proportion as the number of cases of BSE rises).
However, this does not seem to have taken place as in previous
studies i.e. there seems to have been epidemics of all these
other diseases as well as BSE.
Vet Rec 1996;138:160-1.
Vet Rec. 1996;138:559-62
Unfortunately relatively small numbers of embryos were taken
from mothers with scrapie and inoculated into mothers without
scrapie. The results suggested that in some way the
experimental and/or husbandry practices involved n the
production, lambing and maintainance of these animals blocked th
transmission of scrapie to almost one quarter of the susceptible
progeny. Washing the embryo appeared to make little
difference.
It is difficult to make determined results from these numbers
but environmental factors and the small numbers involved. The
discussion of the findings is probably worth reading and the
reference list.
Vet Rec 30.3.96 Government announcement sparks a crissi for
British beef. This gives the major list of directives from the
UK government at the end of March 1996.
Vet Rec 30.3.96 Statement issued by the Spongiform
encephalopathy Advisory Committee on March 24 1996. This is
very direct in that it makes it clear what is safe and what is
not. The determination that the directives should be carried
out are not present.
Vet Rec 6.4.96 European ministers consider options for
resolving the beef crisis
Vet Rec 13.4.96 WHO gathers international experts to review
the situation on BSE
Vet Rec 13.4.96 Minister outlines slaugher plans forolder
cattle.
Vet Rec. 20.4.96 Small steps forward on BSE.
Vet Rec. 20.4.96 Mass slaughter policy 'wholly unreal' says
agriculture miniser
Vet Rec. 27.4.96 Editorial. Waiting for a formula. About the
production of a formula for the destruction of BSE in the UK in
such a way as to impress the EU
Vet Rec. 4.5.96 Britain's slaughter proposals fail to impress
European ministers
Vet Rec 11.5.96 Europe unmoved as scheme for older cattle gets
underway
Vet Rec 18.5.96 MPs highlight problems in dealing with cattle
over 30 months old
Vet Rec 25.5.96 Beef ban stays despite further slaughter
proposals from Britain.
Vet Rec 8.6.96 Movement on by-products ban as Britain sets out
its proposals on BSE
Vet Rec 15.6.96 Commission agrees to partial lifting of the
beef export ban
Vet Rec 22.6.96 Commission to make its own proposals for
easing the exports ban
Vet Rec 29.6.96 Editorial. Progress of sorts. This follows
the agreement for the ban to be lifeted slowly on the export of
certain beef products from the UK but only when the Veterinary
Commission agrees to it. The Government thinks that this will
take place by October 1996 but this is unrealistic.
Vet Rec 29.6.96 European ministers agree on a framework for
lifting the exports ban
Vet Rec. 20.7.96 Maternal transmission experiment 'nearing
completion'
Vet Rec. 27.4.96 Ban on beef exports: Commission awaits
specific proposals from Britain.
Nature 1996;382:180-2
PrPsc is shown to have an anti-parallel structure of
beta-pleated sheet as well as 3 small alpha helices. PrPc is
thought to have nothing but alpha helices. The sections that
are altered in mouse genetic are involved in these sections.
Lancet 1996;348:326 (August 3)
The article explains how it is still possible to be unhappy with
the prion being the total explanation for the infective agent.
It goes through the short pieces of science that have been most
important in putting forward the virus, virion, and prion
theories.
Nature 1996;382:779-88
A comprehensive study of the epidemiology of BSE.. This is the
major article confirming the data published in 1993 and 1995 by
Dealler and Kent. It assumes that all the data concerning the
epidemiology of BSE as given by MAFF is correct i.e. that there
is no under-reporting. It shows that the epidemic in cattle
will be altogether around 903,000 by the end of 1995 and of
these around 5,100 are derived from vertical transmission. The
proportion of cattle with BSE that are VT, as the epidemic
progresses is rising slowly and estimates are quite high. If
the disease is not passed from a calf to its offspring then the
epidemic would disappear by the year 2001, although no evidence
is given for this. It explains how culling policies can never
destroy all the infected cattle but that they can decrease the
proportion of cattle that are infected that remain.
One of the most important factors from this paper is that the UK
MAFF were aware of vertical transmission and the high numbers of
infected cattle being eaten (and exported) early this year when
it was presumed not to take place when information was given to
the European Commission. Also, the data given must be looked on
as an under-estimate of the true figures, which could be much
higher depending on the rates of under-reporting that took
place. The EC is likely to take this seriously despite the news
data put out to the press giving the impression that the disease
is disappearing fast.
Further major findings:
Lancet 1996;348, August 31st, letters
Consistent with sporadic CJD. Discusses the excess of CJD in
farmers in various countries with and without BSE.
BMJ 1996;313:562
Shows that Gore's statistics published in the BMJ in December
1995 were based on there being too few farmers at risk. When
larger at-risk numbers are included then the excess of CJD in
farmers became insignficant.
J. Clin. Micro. May 1996;34:1228-31
The tonsils of the sheep seemed to be as good as other sources
of PrPsc as a method of diagnosis for scrapie. They looked at 55
necropsies and found PrPsc in a reticular pattern in 54 of the
tonsils. (this article was followed by one from Arya SC
suggesting that the system could be used for BSE, and CJD
diagnosis)
Creutzfeldt-Jakob disase in a young woman
Scrapie theory fed BSE complacency
Potential transmission of BSE via medicinal products
...now fears grow for unborn babies
Messsage from the deputy Chief Medical Officer
Potential transmisisonof BSE via medicinal products
She admits that people may well have
been at risk from products from before the regulations, that
there may be a risk in the produts still at a low level but
stopping the product may be a greater risk, and the SEAC were
happy that the guidelines were satisfactory to protect ..human
health.
She does ot seem to be able to show that any
methods of assay of infectivity in the produts has been carried
out, she suggests that assays in mice would be adequate when
this is very unlikely (only a very small amount can be
inoculated into a mouse), and does not provide any calculations
as to the number of infected cattle that would have been used
for manufacture (or the point in their incubation period at
which this would have taken place), even though this data could
now be calculated from MAFF data. This editorial is calming but
does not put forwards risk analyses, which are what is
required.Molecular basis of phenotypic variability in sporadic
CJD
Parchi P, Castellani R, Capellari S, Ghetti B, Young K, Chen
SG, Farlow M, Dickson DW, Sima AAF, Trojanowski JW, Peterson RB,
Gambetti, P Division of Neuropathology Insititute of
Pathology, Case Western Reserve University, Cleveland, Ohio,
USA.
France wakes up to mad cow risk
USA takes a close look at deaths from brain disease.
A role at last for mad cow protein
Lancet 20.4.96 Evidence from America and Iceland that
infection of scrapie can remain in 'infected' hay mites.
Phylogenesis of prion protein
Moving the British cattle herd
Pete Smith, JU Smith, David Powlson Soil science, ICR
Rthamsted, Harpenden, Herts
Two years ago we warned of the danger from BSE and were
criticised, now officialdom has changed its tune...
Prediction of future BSE spread
CJD
CJD
CJD
Polymorphism at position 129 of the prion protein.
% of investigated cases No investigated
Met/met Met/val Val/val
Normal population 48 42 10 1397
Sporadic CJD 78 12 10 73
CJD2 100 0 0 8
CJD
Chemotherapeutic trials with a new plyene antibiotic
derivative, MS-8209, in experimental prion diease
European Congress of Chemotherapy, Glasgow, 14-17 May, 1996
Half of physicians are unaware of surveillance system for
CJD
Franks, A, Schweiger M
Britain caught out by 'unscientific' reactions to Europe's
beef crisis
News article
BSE a specific bovine disease?
Claude E Chastel Lab de Virologie, Faculte de Medcine,
Univ de Bretagne Occidentale, 29285, Brest, France
BSE. What have we learned?
Health Which, June 1996;89-91.
CJD researchers seek greater access to data on cases.
News article
BSE: Does it transmit to humans
Almond, J School of Animal and Microbial Sciences,
Reading, RG6 2AJ
Spontaneous spongiform encephalopathy in a young adult
rhesus monkey
Noelle Bons, Nadine Mestre Frances, Yves Charnay, Fabrizio
Tagliavini
Failure to transmit BSE to marmosets with ruminant derived
meal.
Ridley RM, Baker HF, Windle CP.
Prion protein gene analysis in the new variant of CJD
John Collinge, Jonathan Beck, Tracy Campbell, Kathy
Estipeiro, Robert Will.
The incidence of BSE in the progeny of affected sires and
dams
Curnow RN, Hau CM
Univ of Reading and Ninewells Hosp Med Sch, Dundee.
Table 3: Relative chance of an offspring of dams of specific
ages developing BSE
Age of dams
2 3 4 5 6 7 8+
Number of dams 238 1302 265 159 118 79 49
Relative odds 2.1 1.0 1.0 1.2 0.6 2.6 0.5
The only one that is significant is the figure for 7yrs
The most important factors with this study is that the results
from Wilesmith concerning vertical transmission would simply not
give these results even though the numbers invovled are fairly
small (see news, July 1996). The worry is that the figures on
table 3 are more valid than the numbers present can show and
this would suggest that Wilesmith's statistics may be invalid.
Detection of BSE infectivity in brain and spleen of
experimentally infected sheep
Foster JD, Bruce M, McConnell I, Chree A, Fraser H.
Ogston Blg, BBSRC, Ogston Blg, Edinburgh EH9 3JF
BSE in BG: consistency of the neurohistopatholgical findings
in two random annual samples of clinically suspected cases.
Simmons MM, Harris P, Jeffrey M, Meek SC, Blamire WH, Wells
GAH.
Absence of detectable infectivity in trachea of BSE-affected
cattle
Taylor DM, Ferguson CE, Chree A.
BBSRC Unit Inst for Animal Health, Edinburgh Univ, W. Mains Rd,
Edinburgh EH9 3JF
Observations on the transmission of scrapie in experiments
using embryo transfer
Foster JD, Hunter N, Williams A, Mylne MJA, McKelvey WAC,
Hope J, Fraser H, Bostock C.
Veterinary Record articles concerning the politics of BSE
after the announcement that it may infect humans
Vet Rec 30.3.96 Editorial: A crisis of confidence.
NMR Structure of the mouse prion protein domain PrP
(121-231)
Roland Riek et al Insitut fur Molekular biologie und
Biophysik, Eidgenossische Technische Hochschule-Honggerberg,
CH-8093, Zurich.
Keeping an open mind about prions
Elizabeth Finkel (sceintific journalist article)
Transmission dynamics and epidemiology of BSE in British
cattle
Anderson R.M. et al (including many of the MAFF epidemiology
group)
CJD in a beef farmer
Young GR, Fletcher NA, Zeidler M, Estibeiro KL, Ironside
JW
Walton Neurological Centre, Liverpool 9
Rate of CJD in farmers is not significant
Morrison D
CERN. European Laboratory for Particle Physics, CH-1211, Geneva,
Switzerland.
Immunohistochemical detection of prion protein in lymphoid
tissues with natural scrapie
Van Keulen, JLM, Schreuder BEC, Meloen RH, Mooij-Harkes G,
Vromans MEW and Langeveld JPM. Dept of Patholobiology and
Epidemiology and Lab for Molecular Recognition, Institute for
Animal Science and Health, Lelystad, The NetherlandsReturn to the index
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