Monday, May 19, 2008



‘The first farmer’ – August 1992

5.7 At the beginning of August 1992, Dr Will confidentially informed Dr Ailsa Wight (DH, senior medical officer with responsibility for TSEs), that a probable case of CJD had occurred in a 60-year-old farmer whose farm, in the Manchester area, had a history of BSE. Dr Wight passed on this information to Sir Kenneth Calman (CMO) on 13 August 1992, stating that the CJD patient was alive and had been visited by the CJDSU.188 Although unconfirmed, the diagnosis was considered likely to be CJD on clinical grounds. Dr Wight advised that: There is no direct evidence that the two events (BSE and CJD) are linked and Dr Will feels they are probably a coincidence. Despite the rarity of CJD, it was perhaps only a matter of time before this situation arose, given the large numbers of people employed in the agricultural and related industries, and the fact that BSE cases now total over 65,000.189

5.8 This ‘first case’ of CJD in a cattle farmer was discussed by SEAC190 at their 13th meeting on 15 October 1992.191 Dr Will informed the meeting that one of the farmer’s cows had confirmed BSE in 1989 and that the farmer had developed CJD two years later.192

5.9 Dr Will informed SEAC that he intended to publish a report of his study of this case in a scientific journal ‘which would probably draw the conclusion that there was no evidence that this was not a chance occurrence of normal disease’. Dr Will also reported that his studies at the CJDSU had failed to reveal a correlation between occupational backgrounds and CJD to date.193

5.10 On 22 October 1992, a minute from Mr Thomas Murray (SEAC DH Secretariat) informed the Secretary of State about the SEAC meeting and the fact that the farmer had now died.194 He noted that the diagnosis of CJD had been confirmed by pathology and that the CJDSU had also ruled out iatrogenic or familial CJD, as well as exposure to cattle brain. He commented that the SEAC meeting had come ‘to the view that all indications suggested that it was a typical sporadic case of CJD. However in view of the history it is hoped to carry out further laboratory studies to try to confirm this.’ 185

YB89/10.26/3.1 186 YB89/10.26/3.2 187 YB89/11.20/11.1 188 YB92/8.13/2.1–2.2 189 YB92/8.13/2.1–2.2 190

SEAC – Spongiform Encephalopathy Advisory Committee. This Committee was set up after advice from the Tyrrell Committee. Dr Will was a member of SEAC from its outset 191

YB92/10.15/2.1–2.8 192 YB92/10.15/2.4 193 YB92/10.15/2.4 194 YB/92/10.22/1.1–1.2


Dr Will published his report of the case, ‘Creutzfeldt-Jakob Disease in an Individual Occupationally Exposed to BSE’, as a letter in The Lancet on 6 March 1993.195 The letter concluded that ‘CJD in our case is most likely to have been a chance finding and a causal link with BSE is at most conjectural’. The letter noted that the only possible direct route of cross-contamination was that the farmer had drunk pooled milk from his herd which included that from the affected cow, but that epidemiological evidence had largely precluded milk as a route of transmission in spongiform encephalopathies.

5.12 This letter created much media interest over the following few days, and its contents were reported in The Times,196 Today,197 Daily Express,198 Daily Mail,199 and Daily Telegraph which also reported Mr Kevin Taylor (Assistant Chief Veterinary Officer, MAFF) stating ‘I don’t think that a link between this case and BSE is even conjectural’ and rejecting fears that the farmer might have contracted the illness from milk.200

5.13 On 10 March 1993, Mr Jimmy Young of BBC Radio 2, interviewed microbiologist Professor Richard Lacey, who commented that: The good news is that this farmer, I think, got it too soon. If BSE produces this disease in people it will take, perhaps, another 5 or 10 years. So I think this is a one-off coincidence and I don’t think this farmer got his disease, CJD, from BSE. But nevertheless the underlying worries remain and I think it’s reasonable that this issue should be discussed. 201

5.14 The Second Annual Report of the CJDSU, published in July 1993, concluded that: 202 This is most likely to have been a chance occurrence rather than indicating any causal link with BSE.

5.15 It further noted that: A farmer’s wife who was diagnosed in 1992 had worked on a small holding for over 20 years but there had not been a case of BSE in the herd (Wilesmith, Personal Communication).203


‘The second farmer’ – July 1993

5.16 In early July 1993, Dr Will informed DH of a ‘second’ case of CJD in a farmer with BSE in his herd. The diagnosis had been confirmed by brain biopsy.204

5.17 Dr Wight described the case in a minute sent on 12 July 1993 to the private secretaries to Baroness Cumberlege and Sir Kenneth Calman. The minute was copied to others in DH and to Mr Howard of MAFF. The 64-year-old dairy farmer from the West Country was thought to have had at least two BSE cases in his herd, which were diagnosed in 1992. He was also thought to have assisted in calving and to have drunk the milk from his herd. His clinical symptoms had begun in May 1993. She commented that the history did not suggest anything other than a sporadic case of CJD but that DH was taking expert advice on the case.205

5.18 On 19 July 1993, Mr Kevin Taylor (MAFF) minuted the private secretary to Mrs Gillian Shephard, the MAFF Minister, in a response to a request for more detailed briefing.206 He noted that neither Dr Will nor the CJDSU intended to publicise the case at that time unless it attracted media attention, as they intended to include the information in their Third Annual Report due in approximately one year, ie, July 1994.

5.19 The minute attached a briefing note for the Minister. This specifically mentioned the consideration of occupational exposure to BSE as discussed in the CJDSU’s Second Annual Report which concluded that: . . . current information does not suggest that occupation is linked to an increased risk of developing CJD and it includes occupations which might involve an increased exposure to the agent of BSE.207

5.20 On 20 July 1993, SEAC held a meeting to consider this ‘second case’.208 They decided that a connection between occupation and CJD was unlikely and no conclusions could be drawn from the available statistical information. A paper by Professor Smith was presented which concluded that ‘the observation of two cases in workers in dairy farms with BSE-infected herds is disquieting, but the evidence is insufficient at this stage to draw any definite conclusions’.209

5.21 On 12 August 1993, the Daily Mail and Today publicised the story of the ‘second case’ of CJD in a dairy farmer.210 Both named the farmer and reported a DH spokesman saying that the Government’s experts had considered the case and ‘agreed that there are no features that give cause for undue concern’. The spokesman had also commented that it was most unlikely that there was any direct link between BSE and CJD in the patient.

5.22 In September 1993, the case study of this ‘second farmer’ was published in The Lancet. This letter gave the farmer’s age as 54.211 204

YB93/7.12/1.1 205 YB93/7.12/1.1 206 YB93/7.19/1.1 207 IBD2 tab 6 p. 6 208 YB93/7.20/1.1 209 YB93/7.20/1.5 210 YB93/8.12/1.3–1.4 211 Davies, P.T., Jahfar, S., Ferguson, I.T. and Windl, O. (1993) Creutzfeldt-Jakob Disease in an Individual Occupationally Exposed to BSE, The Lancet, 342, 680


Her note had a separate heading for ‘Comparison with young onset cases in world literature’. Here she noted that Creutzfeldt’s first patient was 23 years old (reported in 1920), and that there were other cases of CJD in young people which predated the emergence of BSE. These were a 20-year-old female and a 16-year-old female in the US and a 19-year-old female in France.219


‘The third farmer’ – December 1994

5.33 A ‘third case’ associated with farming where cattle in the herd had contracted BSE concerned a farm worker from Cornwall who had died in early December 1994, aged 54. There had been two confirmed cases of BSE on the farm, in August 1991 and October 1992. Additionally, a cow sold off the farm in December 1987 had been diagnosed with BSE in September 1988.224

5.34 On 1 December 1994, the case was reported in the local newspaper, The Cornishman, while the patient was still in hospital.225

5.35 On 19 December 1994, Mr Charles Lister, DH, minuted the private secretary to Baroness Cumberlege with information about this possible ‘third case in farmers/ farm workers who have had BSE cases in their herds’.226 This minute enclosed the article from The Cornishman and was copied to DH officials and to Mr Eddy at 219

YB94/1.14/1.2 220 YB94/1.26/3.1 221 YB94/1.26/2.3; YB94/1.14/1.2 222 YB94/1.26/2.2 223

The report formed Annex 2 to the CJDSU’s Third Annual Report (IBD2 tab 8) 224

YB94/12.19/3.1 225 YB94/12.19/3.4 226 YB94/12.19/5.1

EMERGENCE OF VARIANT CJD 39 MAFF. He noted that diagnosis would not be confirmed until post mortem, but the Surveillance Unit thought it highly likely to be CJD.

5.36 On the same day, Mr Thomas Eddy, MAFF secretary to SEAC, passed the newspaper article and basic information about the case on to MAFF Ministers and officials.227

5.37 On 13 January 1995, SEAC held a special meeting to discuss the significance of this third case of CJD in a farmer in the first four years of surveillance.228 Dr Sheila Gore, an epidemiologist from the MRC Biostatistic Unit, was invited as an independent expert.

5.38 Detailed consideration was given to the case itself and the epidemiological implications. Dr Will commented that the post-mortem results were not yet available, but it was highly likely that the diagnosis of CJD would be confirmed. He stated that the man had no significant medical history and that he had worked as a farm labourer on the same dairy farm since 1955: The man was known to have assisted with calving but never with any operative procedure; he rarely drank unpasteurised milk and never from BSE-affected animals. It was not known if he had ever eaten cattle feed.229

5.39 As to the epidemiological significance of the case, the members recalled the advice given by Professor Smith after SEAC had considered the second case of CJD in a farmer: Professor Smith had advised that if four cases arose in the first 5 years of the surveillance scheme the possibility of an association which was not due to chance had to be given very serious consideration.230

5.40 Dr Gore commented that: If the adult incidence of sporadic CJD in the UK was taken as one case per million (the figure used by Professor Smith) and if the same incidence applied to workers on dairy farms with BSE-affected herds, then the probability of observing three or more definite CJD cases in such workers in England and Wales in 5 years was low: 4 in 1,000. The probability was higher if the calculation was made using the total number of dairy farm workers in England and Wales. However, this was considered to be less relevant as the only reported cases of CJD in dairy farm workers since 1990 had been in lifetime dairy workers all with BSE-affected herds.


5.63 On 29 September 1995, various newspapers reported the third case of CJD in a dairy farmer.255 Reference was made to a letter published in The Lancet (dated 30 September 1995) by Dr (now Professor) Smith (LSHTM).

5.64 The letter reported: The occurrence of CJD in another dairy farmer with a potential occupational exposure to BSE is clearly a matter of concern. Statistical analysis indicates that the probability of discovering three or more dairy farmers with CJD by chance since 1990 in England and Wales ranges from 0.09 to 0.0002, depending on the occupational denominator (individuals who work on farms to full-time workers on BSE-affected dairy farms).256

5.65 Statistics for CJD in European farmers were also reported in the 30 September 1995 edition of The Lancet.257 The paper concluded that ‘there is no differential increase in the risk of CJD to farmers in the UK through potential occupational contact with cases of BSE’. On the continent there was also a slightly higher proportion of cases of CJD arising in farmers.258 This indicated that in the UK, CJD in farmers had probably not arisen from transmission of BSE.259

The fourth farmer – September 1995

5.66 On 28 September 1995, Dr Wright minuted the private secretary to the CMO about a probable fourth case of CJD in a farmer. The 59-year-old beef farmer lived in North Wales and was alive when the case was reported to the CMO. The farm, which had a 70-strong suckler herd, had a confirmed case of BSE about four years previously in a 4½ to 5-year-old cow.260

5.67 The minute recorded the urgency of dealing with the issue as the case was in the public domain and BBC Wales were making a programme referring to the case.261 An urgent meeting of SEAC was called for the following week.

5.68 On 4 October 1995, SEAC held a special meeting to discuss this further suspected case of CJD in a cattle farmer.262 Professor Smith (LSHTM) and Dr Cousens (LSHTM) were in attendance to provide the Committee with expert epidemiological advice.263 5.69 Dr Will advised that although the Unit had initially clarified the case as probable CJD, he felt that it was more appropriate to look at it as a suspect case. Consideration was given by SEAC to European data that showed 12 cases of BSE in France, along with a progressive neurological disease in a farmer associated with 255

YB95/9.29/12.1; YB95/9.29/10.1; YB95/9.29/14.1 256

Smith, P.E., Zeidler, M., Ironside, J.W., Estibeiro, P. and Moss, T.H. (1995) Creutzfeldt-Jakob Disease in a Dairy Farmer, The Lancet, 346, 898 257 Delasnerie-Laupretre, N., Poser, S., Pocchiari, M., Wientjens, D.P. and Will, R. (1995) Creutzfeldt-Jakob Disease in Europe, The Lancet, 346, 898 258 T71 p. 115 259 T24 p. 95 260 YB95/9.28/3.1 261 YB95/9.28/3.1 262 YB95/10.4/1.1–1.8 263 YB95/10.04/1.1

EMERGENCE OF VARIANT CJD 45 one of those cases. (In the eventuality, this farmer was not diagnosed with CJD. At the beginning of January 2000, there had been no reported cases of CJD in farmers in France where BSE had been found in that farmer’s herd.)

5.70 Mr Wilesmith gave SEAC information about the farm associated with the possible UK fourth case of CJD under discussion. The farm had not been visited by MAFF. It had one case of BSE in a purchased animal which died in September 1991. From available information, the animals had not been fed on concentrates (although this had not been double-checked). It was thought, however, that the farm did have a big poultry battery unit, which may have meant that ruminant-derived feed was available on the farm.

5.71 Dr Cousens made a presentation of the epidemiology.264 He had calculated age specific mortality rates for sporadic CJD from 1990 to 1994 and applied these to data on farmers to calculate the expected number of sporadic CJD cases in farmers. The following conclusions were reached: i. there had been an alarming number of cases in farmers who had had contact with cattle with BSE. However, other occupational groups, expected to carry greater risk (eg, abattoir workers, veterinary surgeons), did not appear to be affected; ii. it was now difficult to explain the cases as a chance phenomenon. Yet the absolute risk still remained extremely low; iii. it was unclear whether the possible risk factor might be associated with cattle with BSE or the food given to them; and iv. as there was a problem with establishing a causal link, transmission studies would be extremely important.

5.72 At this meeting, Dr Wight invited members of SEAC to make a fairly clear statement on how they viewed the significance of a fourth case and to consider whether they were satisfied that nothing else needed to be done in terms of practical measures.265 In evidence to the Inquiry, Dr Wight said that trying to get a clear statement as to what would be a significant number of cases in farmers was bound to be difficult. She said, ‘I do not think that SEAC any more than anybody else had any idea how to make sense of this at this stage.’266 At the meeting, Dr Tyrrell’s response was that although numbers were higher than expected, they were still extremely small. It would be irrational to take specific measures at the moment. Members of SEAC agreed to draw up a statement which the Department of Health could issue in response to media inquiries.267 The text of the statement included the following:268 The Committee concluded that it was difficult to explain this simply as a chance phenomenon. There is a statistical excess in cattle farmers compared with the general population but the absolute risk, even for farmers, is extremely low at about 2 cases per million per year. There may be other explanations for such an association besides infection with BSE, and the Committee noted that there are no recorded cases in other occupational 264

YB95/10.4/1.2–1.4 265 YB95/10.4/4.5 266 T71 pp. 135–6 267 YB95/10.4/4.5 268 YB95/10.4/4.9


46 groups such as veterinarians who might be expected to be similarly exposed. They also noted that the surveillance of CJD elsewhere in Europe has shown a similar incidence of CJD in farmers, including dairy farmers, in countries with no or very few cases of BSE. They therefore felt that it was important to undertake further epidemiological studies to detect any particular risk factors which might be involved, and reiterated their advice that the UK cases of CJD in cattle farmers and the strain of agent recovered from them should be studied in detail. The Committee have asked for further work to be done, but have not altered their advice to Government on the precautions necessary to protect either the public health, including farmers, and animal health.

5.73 Mr Eddy minuted the MAFF Minister and Parliamentary Secretaries advising them of the outcome of the SEAC meeting.269 He commented that SEAC had concluded that it would be worrying if the fourth case of CJD in a farmer from a BSE farm was confirmed. The chances of four CJD cases occurring randomly in farmers with BSE in their herds was . . . [since 1990] around 3/10,000. The Committee therefore concluded that it was difficult to explain the incidence as a chance phenomenon. This is a change to the Committee’s position; it had said that the most likely explanation of the three previous cases of CJD in dairy farm workers was that they were chance phenomena.270

5.74 Mr Eddy also stated that the SEAC did not recommend changes to any of the measures currently in place to protect human and animal health, including those of farmers and others handling cattle and BSE suspects.

5.75 On the same day, Mr Eddy prepared a second minute which was sent to Dr Matthews and Mr Keith Meldrum (CVO) amongst others about discussions during the SEAC meeting.271 Mr Eddy included a list of four ways in which the farmers might have been exposed to BSE that might have then led to their infection with CJD: i. cattle were excreting the agent in some form – no evidence for this; ii. meat and bone meal (MBM) in cattle feed – if so this would affect pig and poultry farmers equally (these feeds also contained MBM); iii. normal food – unclear why this discriminated in favour of farmers, although farmers could have been exposed to foods that other people might not have been routinely exposed to, such as unpasteurised milk; and iv. contact with animals – possibly animals killed on the farm.


5.93 Dr Will updated SEAC on CJD surveillance results at their 23rd meeting on 5 January 1996.292 He ‘reaffirmed that the incidence of CJD in dairy farmers in Europe showed an excess over the incidence for the population as a whole’. He confirmed that a 52-year-old abattoir worker from York was suspected of having CJD. The patient had worked mainly as a stockman in a mixed abattoir for 18 months in the late 1980s, and had occasionally pithed animals but had much less exposure than other abattoir workers. Dr Will believed that the patient was no more than a suspect at that stage.

5.94 The minutes of the meeting record that Professor Smith commented on this case: He [Professor Smith] felt that it was not possible to come to any conclusions on the basis of this case alone even if CJD is confirmed. Nevertheless, taking into consideration the affected farmers as well, and even though the abattoir worker was in an apparently relatively low risk category, the ‘box’ of ‘at 289 S61D Will para. 4 290 T138 p. 34 291 S61D Will para. 18 292

YB96/1.5/1.6–1.8; S61D Will paras 19–22

EMERGENCE OF VARIANT CJD 51 risk’ occupations was getting full compared to expectation on pure chance and could not be dismissed.293


Update on cases of CJD in farmers

5.152 During the period 1986–96, much attention and publicity was focussed on four cases of CJD in farmers (see above). Although those four cases were regarded as likely to be more than might be expected for the known population frequency of the disease, analysis of CJD in Europe showed the incidence of disease in farmers was similar to that in the UK.373 In addition, the clinical and pathological features of these cases were no different to those found in classical sporadic CJD.

5.153 It is understood that since 20 March 1996, at least two further cases of sporadic CJD in a relevant occupational group have been reported to the CJDSU, one in a farmer and another in an abattoir worker.374 Recent transmission studies in mice indicate that the causal agent in these cases has transmission characteristics (incubation period and neuropathology) which are distinct from both vCJD and BSE, and that the protein deposited in the brain in all of these cases has a glycosylation pattern distinct from the type 4 pattern observed in vCJD and BSE.


Is occupation a risk factor in vCJD?

5.192 One of the original proposals in the CJD surveillance project was to monitor occupational groups exposed to BSE-affected cattle and their products. Such groups include farmers, veterinarians, slaughtermen and butchers. This part of the project was given a low priority by the Tyrrell Committee and was not implemented. It was felt that rather than set up longitudinal study of a fixed number of individuals in each group, together with matched controls, it would be adequate to take an occupational history of each CJD case at the time of referral.

5.193 From 1990 to 1996, the CJDSU had referred to it four farmers affected with CJD who were known to have had cases of BSE on their farms. Assuming a total of 155,000 dairy farmers in the UK,384 the number of observed CJD cases is significantly higher than expected from population estimates. Counting only those farmers with affected cattle, the probability of observing four or more confirmed cases of CJD is estimated at less than one in 10,000.385 In addition, two farmers’ wives were known to have CJD from farms in which clinical BSE had not been reported (although preclinical cases of BSE on these farms might have been expected). 384 Gore, S. (1995) More than Happenstance: Creutzfeldt-Jakob Disease in Farmers and Young Adults, British Medical Journal, 311, 1416–8 385 Ibid.


5.194 The affected farmers were aged between 54 and 64 and had signs and symptoms typical of sporadic CJD. Two had EEG changes typical of the sporadic disease and all four had type 2 glycosylation patterns. Three farmers were homozygous for methionine at codon 129 and the fourth was a valine homozygote. None conformed to the phenotype characteristic of vCJD. The findings remained unexplained, although a European collaborative study showed a similar increased incidence in deaths due to CJD in farmers in several member states. It was noted that unexpected numbers of affected individuals occurred in other occupational groups, such as the clergy, but numbers in each occupation remained small.

5.195 Among occupational groups exposed to BSE, farmers remain unusual in having such an excess over the incidence of CJD for the population as a whole. No cases of CJD have been reported amount veterinarians exposed to BSE. Four people in the meat industry (butchers, abattoirs, rendering plants, etc) have been reported to have vCJD.386 The present evidence has been accepted by some as reassuring in that such occupations may not pose as serious a risk as might have been expected.

This was not simply another farmer but the third farmer......

suspect case of CJD in a farmer who has had a case of BSE in his beef suckler herd.

cover-up of 4th farm worker ???


now story changes from;

SEAC concluded that, if the fourth case were confirmed, it would be worrying, especially as all four farmers with CJD would have had BSE cases on their farms.


This is not unexpected...

was another farmer expected?

4th farmer, and 1st teenager

2. snip...

Over a 5 year period, which is the time period on which the advice from Professor Smith and Dr. Gore was based, and assuming a population of 120,000 dairy farm workers, and an annual incidence of 1 per million cases of CJD in the general population, a DAIRY FARM WORKER IS 5 TIMES MORE LIKELY THAN an individual in the general population to develop CJD. Using the actual current annual incidence of CJD in the UK of 0.7 per million, this figure becomes 7.5 TIMES.

3. You will recall that the advice provided by Professor Smith in 1993 and by Dr. Gore this month used the sub-population of dairy farm workers who had had a case of BSE on their farms - 63,000, which is approximately half the number of dairy farm workers - as a denominator. If the above sums are repeated using this denominator population, taking an annual incidence in the general population of 1 per million the observed rate in this sub-population is 10 TIMES, and taking an annual incidence of 0.7 per million, IT IS 15 TIMES (THE ''WORST CASE'' SCENARIO) than that in the general population...


20 year old died from sCJD in USA in 1980 and a 16 year old in 1981. A 19 year old died from sCJD in France in 1985. There is no evidence of an iatrogenic cause for those cases....

USA 2008

Prion surveillance in cattle has been reduced by 90% (from about 470,000 to 40,000 in the U.S. in 2007 out of about 35 million cattle slaughtered). Termination of human prion surveillance would therefore remove the second line of surveillance, thereby eliminating prion surveillance in the U.S. entirely. This development would be extremely worrisome in view of recent reports that precautions to limit the spread of the prion infectious agent may not have been followed in some slaughter houses in the U.S. Cattle affected with bovine spongiform encephalopathy (BSE) continue to be discovered in Canada, which has more rigorous BSE surveillance than the U.S. At the same time, Canada imposes few limitations in the trade of potentially prion-infectious cattle with the U.S.


Atypical forms of BSE have emerged which, although rare, appear to be more virulent than the classical BSE that causes vCJD.

please see full text with additional comments and links @ ;


There is a growing number of human CJD cases, and they were presented last week in San Francisco by Luigi Gambatti(?) from his CJD surveillance collection.

He estimates that it may be up to 14 or 15 persons which display selectively SPRPSC and practically no detected RPRPSC proteins.

PLEASE NOTE IN USA CJD UPDATE AS AT JUNE 2007, please note steady increase in ''TYPE UNKNOWN''. ...TSS

1 Acquired in the United Kingdom; 2 Acquired in Saudi Arabia; 3 Includes 17 inconclusive and 9 pending (1 from 2006, 8 from 2007); 4 Includes 17 non-vCJD type unknown (2 from 1996, 2 from 1997, 1 from 2001, 1 from 2003, 4 from 2004, 3 from 2005, 4 from 2006) and 36 type pending (2 from 2005, 8 from 2006,

*** 26 from 2007)

Diagnosis and Reporting of Creutzfeldt-Jakob Disease

Singeltary, Sr et al. JAMA.2001; 285: 733-734.


MARCH 26, 2003

RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob

disease in the United States

Email Terry S. Singeltary:

I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to

comment on the CDC's attempts to monitor the occurrence of emerging

forms of CJD. Asante, Collinge et al [1] have reported that BSE

transmission to the 129-methionine genotype can lead to an alternate

phenotype that is indistinguishable from type 2 PrPSc, the commonest

sporadic CJD. However, CJD and all human TSEs are not reportable

nationally. CJD and all human TSEs must be made reportable in every

state and internationally. I hope that the CDC does not continue to

expect us to still believe that the 85%+ of all CJD cases which are

sporadic are all spontaneous, without route/source. We have many TSEs in

the USA in both animal and man. CWD in deer/elk is spreading rapidly and

CWD does transmit to mink, ferret, cattle, and squirrel monkey by

intracerebral inoculation. With the known incubation periods in other

TSEs, oral transmission studies of CWD may take much longer. Every

victim/family of CJD/TSEs should be asked about route and source of this

agent. To prolong this will only spread the agent and needlessly expose

others. In light of the findings of Asante and Collinge et al, there

should be drastic measures to safeguard the medical and surgical arena

from sporadic CJDs and all human TSEs. I only ponder how many sporadic

CJDs in the USA are type 2 PrPSc?


Hardcover, 304 pages plus photos and illustrations. ISBN 0-387-95508-9

June 2003

BY Philip Yam


Answering critics like Terry Singeltary, who feels that the U.S. under- counts CJD, Schonberger conceded that the current surveillance system has errors but stated that most of the errors will be confined to the older population.

USA 2007-2008 sporadic CJD statistics revised to 1 in 9,000 in ages 55 and older !

The statistical incidence of CJD cases in the United States has been revised to reflect that there is one case per 9000 in adults age 55 and older. Eighty-five percent of the cases are sporadic, meaning there is no known cause at present.

Sent: Monday May 28, 2007


Sunday, March 16, 2008

MAD COW DISEASE terminology UK c-BSE (typical), atypical BSE H or L, and or Italian L-BASE

Subject: HUMAN and ANIMAL TSE Classifications i.e. mad cow disease and the UKBSEnvCJD only theory Date: January 29, 2006 at 9:03 am PST

HUMAN and ANIMAL TSE Classifications i.e. mad cow disease and the UKBSEnvCJD only theory

TSEs have been rampant in the USA for decades in many species, and they all have been rendered and fed back to animals for human/animal consumption. propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2007. With all the science to date refuting it, to continue to validate this myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, surgical, blood, medical, cosmetics etc. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.

This would further have to be broken down to strain of species and then the route of transmission would further have to be broken down. Accumulation and Transmission are key to the threshold from sub-clinical to clinical disease, and key to all this, is to stop the amplification and transmission of this agent, the spreading of, no matter what strain. In my opinion, to continue with this myth that the U.K. strain of BSE (one strain TSE in cows), and the nv/v CJD (one strain TSE humans) and that all the rest of human TSE are just one single strain i.e. sporadic CJD (when to date there are 6 different phenotypes of sCJD, and growing per Gambetti et al), and that no other animal TSE transmits to humans, to continue with this masquerade will only continue to spread, expose, and kill, who knows how many more in the years and decades to come. ONE was enough for me, My Mom, hvCJD i.e. Heidenhain Variant CJD, DOD 12/14/97 confirmed, which is nothing more than another mans name added to CJD, like CJD itself, Jakob and Creutzfeldt, or Gerstmann-Straussler-Scheinker syndrome, just another CJD or human TSE, named after another human.

WE are only kidding ourselves with the current diagnostic criteria for human and animal TSE, especially differentiating between the nvCJD vs the sporadic CJD strains and then the GSS strains and also the FFI fatal familial insomnia strains or the ones that mimics one or the other of those TSE? Tissue infectivity and strain typing of the many variants of the human and animal TSEs are paramount in all variants of all TSE. There must be a proper classification that will differentiate between all these human TSE in order to do this. With the CDI and other more sensitive testing coming about, I only hope that my proposal will some day be taken seriously. ...

Terry S. Singeltary Sr. P.O. Box 42 Bacliff, Texas USA 77518

Sunday, May 18, 2008


Sunday, May 18, 2008




2. We have identified one problem over where we are unable to act and this is the use of gonadotrophins in embryo transfer work. Some veterinary surgeons are quite legally using this exemption from the Medicines Act contained in Section 9(2) to prepare gonadotrophins from pituitary glands from various species, including cattle. These hormones are used to stimulate superovulation in donor cows.


3.2 Minute 5.3 - 5.4 Bovine Spongiform Encephalopathy

It was reported that some replies had been received from Companies using pituitary glands in their products. Copies of the BSE document had also been sent to DHSS and NIBSC.

and then another 3 + pages of blank space. ...TSS



There are three areas of particular concern, vaccines (including emergency vaccines), pharmaceuticals which are covered by MA licences and unlicenses hormonal products produced under exemptions claimed under (Section 9(2) Medicines Act).

1) Vaccines


another 6 pages of blank space. ...TSS



Medicines Act - Veterinary Products Committee










I was quite prepared to believe in unofficial pituitary hormones, also in the 1970's, whether as described by Dr. Little, or in other circumstances, for animal use.


The fact that there were jars of pituitaries (or extract) around on shelves is attested by the still potent 1943 pituitaries, described in Stockell Hartree et al. (J/RF/17/291) which had come from the lab. at Mill Hill. Having taken the trouble to collect them, they were not lightly thrown out...

more on the 1968 medicine act, they forgot to follow i.e. no Scrapie-like disease. ...TSS

Draft cover letter to product licence holders (considered by Human and Vet Medicines including deer)


(It was noted with concern that hormone extracts could be manufactured by a veterinary surgeon for administration to animals under his care without any Medicines Act Control.)




8. The Secretary of State has a number of licences. We understand that the inactivated polio vaccine is no longer being used. There is a stock of smallpox vaccine. We have not been able to determine the source material. (Made in sheep very unlikely to contain bovine ingredients).


From: TSS Subject: How many NHS patients as having received blood from a donor who later developed vCJD were people with haemophilia Date: December 21, 2006 at 9:13 am PST

Health: vCJD Lord Morris of Manchester asked Her Majesty's Government:

How many NHS patients identified by the National Blood Service as having received blood from a donor who later developed vCJD were people with haemophilia. [HL750]

19 Dec 2006 : Column WA291

The Minister of State, Department of Health (Lord Warner): No patient with haemophilia or other bleeding disorders have been identified as having received blood from a blood donor who subsequently developed vCJD, nor have there been any reported cases of vCJD associated with receipt of plasma products.

However, all haemophilia patients who received plasma products between 1980 and 2001 sourced from UK donor plasma have been designated as "at risk of vCJD for public purposes". All plasma products are now sourced from non-UK plasma. The United Kingdom Haemophilia Centre Doctors' Organisation is collecting data that will provide an estimate of the number of haemophilia patients who have been exposed to plasma products which may be implicated with vCJD.

Lord Morris of Manchester asked Her Majesty's Government:

What is their response to the findings of Professor John Collinge in the December 2006 edition of the Lancet on the transmission by infected blood of variant CJD; and what action they are planning to take. [HL751]

Lord Warner: The Lancet article refers to the third known case of vCJD transmission via blood transfusion from a vCJD-infected donor. This case was originally notified to the department in January 2006 and announced by the Health Protection Agency in a press release on 9 February 2006, a copy of which has been placed in the Library.

There are 24 living patients in a group of people who had received blood components from donors subsequently known to have developed vCJD. They were all notified in 2005 or earlier, through their GPs, of their risk status and have been provided with information and support. The Health Protection Agency contacted the GPs earlier in the year to notify them of this third case and the agency has ensured that the GPs are fully informed and briefed about the subsequent Lancet publication.

The department has implemented a series of measures to reduce the risk of vCJD being transmitted through the blood supply. Shortly after vCJD was first identified in 1996, the possibility of human-to-human transmission through blood was considered, and the department implemented precautionary measures to reduce what was, at that time, a theoretical risk. These measures have been strengthened since evidence of transmission via blood began to emerge from animal studies, and following the first case of transfusion-associated transmission in humans, reported in December 2003. An important additional step, introduced in March 2004, was to exclude from blood donation those people who had themselves received a blood transfusion since January 1980. Other precautionary measures include:

from December 1997, blood components, plasma products or tissues obtained from any individual who later develops vCJD, were withdrawn/recalled;

19 Dec 2006 : Column WA292

in July 1998, it was announced that plasma for the manufacture of blood products, such as clotting factors, would be obtained from non-UK sources;from November 1999, white blood cells, which may carry a significant risk of transmitting vCJD, were removed from all blood used for transfusion;in August 2002, it was announced that fresh frozen plasma for treating babies and young children born on or after 1 January 1996 would be obtained from the USA; in July 2004, the exclusion criteria for blood donation were extended to include previously transfused platelet donors, and donors who were unsure if they had previously had a blood transfusion;in September 2004, the department announced further precautionary measures for patients who had received certain batches of plasma products;in July 2005, the use of USA-sourced fresh frozen plasma was extended to all children up to the age of 16;in July 2005, the department announced further precautionary measures for those patients who donated blood to three people who later developed vCJD. The department continues to keep all the evidence in relation to transmission of vCJD by blood under close review.

Subject: Re: VACCINES/CHILDREN/TSE'S -- 'CONFIDENTIAL' Date: Wed, 6 Sep 2000 18:20:09 -0800 From: tom Reply-To: Bovine Spongiform Encephalopathy To: References: 1

######### Bovine Spongiform Encephalopathy #########

Just when I was thinking the Internet had reached a terminal condition of shallow pages and broken links, some young people come along and invent a really effective Internet search engine: This works quite well to search the entire site (or find 393 web sites such as GenBank that link to it, or 936 sites that cite it in text) back to 1996 as well as the BSE Inquiry

Thus for louping ill (unnecessary cites suppressed):

Witness Statements 537 - Coulthard

29.Pituitary FSH from pigs has been used in the USA prior to its use in the UK and much more extensively there and Canada.... 30.Thousands of embryos were exported from this country to the USA prior to the ban being imposed... 42. No cow pituitaries were used in the preparation of FSH [follicular stimulating hormone] products compared with the case of louping ill vaccine for scrapie.

In the 1930's: 18,000 UK sheep were inoculated against louping ill, a brain inflammatory illness spread by ticks. Despite formalin-treatment of the inoculated agent, the procedure gave rise to 1,500 cases of scrapie. Louping is a Scottish word for fleeing or leaping, related to loping. In humans, louping ill is called Russian spring-summer encephalitis, a meningo-encephalitis with muscular tremors and spasms followed by varying degrees of paralysis.... [John Lanchester 2 Dec 96 New Yorker]

In what the story calls a grand historical irony, this landmark series of experiments was being confirmed at the same time in England as a result of an outbreak of scrapie in several hundred sheep that had been immunized against louping ill with a vaccine prepared from tissue from the brain, spinal cord, and spleen of sheep that were belatedly discovered to have been exposed to natural scrapie infection.[6.Gordon WS. Advances in veterinary research. Vet Rec 1946; 58: 516-520] The transmissible nature of the scrapie agent was thus established beyond any doubt. [P Brown, 1755 and All That: A Historical Primer of TSE.

We need to look at the full text of the article and its cites to see how they actually made the vaccine, whether they exported vaccine-infected sheep to Canada and the US, and what became of the vaccinated flocks. Perhaps there is still sample available, Moredun Institute is still around.

Gordon WS. Advances in veterinary research. Vet Rec 1946; 58: 516-520 (not covered by Medline) Gordon, Bronlee and Wilson 1939 [full cite is available only in a letter we don't have)

Terry was reading Draft Factual Account 17

236. Mrs Alderman replied on 3 June 1988, listing products containing bovine insulin and noting there were two rabies vaccines listed but the species used in manufacture was not shown.[282] 237. On 6 June 1988 Mr Lawrence wrote to Sir Richard Southwood and enclosed some brief answers to the questions that had been tabled at the meeting on 19 May.[283] In relation to Q6, which asked OWhat is meat and other material from scrapie infected sheep used for - does it include pet food and material for biological products?¹ Part of the answer stated: ...

There has been one instance of inadvertant [sic] transmission of the scrapie agent to sheep through louping ill vaccine (Gordon, Bronlee and Wilson 1939). One of the three batches of vaccine made in 1935 at the Moredun Institute contained the scrapie agent resulting in 7% of the recipients of the 18, 000 doses in the batch developing scrapie. This vaccine was made from formalin-inactivated sheep brain, and brought to the attention of research workers that formalin, at a concentration of 0.35% for at least 3 months, which inactivated conventional viruses, did not totally inactivate the scrapie agent.


4. Questions we might want to have answered are: the highest risk would be from parenterals prepared from brain (eg rabies vaccine). Any species in which transmissible spongiform encephalopathies have been described would be suspect ("natural" infections in sheep, goats, cattle, deer, mink, but can be transmitted to hamster, mouse, guinea-pig etc). Are sterilisation processes adequate for the most resistant strain of scrapie agent or for CJD agent? Should companies be asked to include investigation for inclusion of scrapie agent (eg mouse innoculation [sic]) in at least some batches? If BSE behaves like scrapie, then we might expect other nervous tissue, spleen, lymph nodes and placenta to be contaminated. Infection has been described in other tissues too, eg gut wall, and we can not [sic] be sure blood is free. Do we know what bovine materials are used in which products, both as the active ingredient and in production? Bovine active ingredients in human products include insulin, vasopressin, bone, immune globulins, fibrin, dermal collagen, albumin. Bovine serum albumin and fetal calf serum must be used in preparation of very many products. For each of these products would any "BSE agent" be destroyed or eliminated in processing? If not, and the product is administered parenterally or topically into an open wound, might there be a risk? [For oral products, there would only be a trivially increased load on top of that taken in food in omnivores/carnivores including man. But for some herbivores, this might allow the agent to be introduced into yet another species].


Medicines and medical devises;

Subject: 2 known incidents of iatrogenic scrapie Date: Thu, 7 Sep 2000 09:51:14 -0800 From: tom Reply-To: Bovine Spongiform Encephalopathy To: References: 1

######### Bovine Spongiform Encephalopathy #########

One really has to wonder what went on in veterinary products produced during the peak BSE years. At this point, there are only 2 known incidents, both involving sheep brain vaccines.

I found a better source for needed references for iatrogenic scrapie in a nice review by Ray Bradley at Disclosure has been meagre on the 1998 vaccine incident in Italy. Note 3 of the 5 references are totally off Medline and the other 2 fail to have abstracts or links, due to journal ineptness, burial in conference proceedings, and age of article.

If anyone has the first 3, I would appreciate a fax 542-484-0669 US.


GORDON , W.S., 1959. Scrapie panel. In: Proceedings of 63rd Annual Meeting of the US Livestock Sanitary Association, 63, 286-294. [no medline record]

GORDON, W.S., 1946. Advances in Veterinary Research: Louping ill, tick-borne fever and scrapie. Veterinary Record, 58, 516-525. [no medline record]

GORDON , W.S., BROWNLEE, A.& WILSON, D.R., 1939. Studies in louping-ill, tick-borne fever and scrapie. 3rd International Congress for microbiology, 362-363. [no medline record]


CAPUCCHIO, M.T., GUARDA,F., ISAIA,M.C., CARACAPPĂ€, S. & DiMARCO,V., 1998. Natural occurrence of scrapie in goats in Italy. Veterinary Record, 143, 452-453. [title only]

AGRIMI, U., GLUSOPPE, R.U., CARDONE, F., POCCHIARI, M. & CARAMELLI, M., 1999. Epidemic transmissible spongiform encephalopathy in sheep and goats in Italy. Lancet, 353, 560-561. [title only]


Ray Bradley Private BSE Consultant Veterinary Laboratories Agency, United Kingdom

There have been two reported incidents of iatrogenic disease in animals, both involving scrapie. One was in Great Britain (Gordon, Brownlee and Wilson, 1939, Gordon 1946, 1959) the other in Italy (Capucchio et al, 1998, Agrimi et al, 1999). Both resulted from infection being introduced into vaccines, louping ill vaccine in Great Britain, Mycoplasma agalactiae vaccine in Italy. Each of these vaccines was prepared from tissues that included sheep brain. In both episodes it seems most likely that natural scrapie infection was present unknowingly in some brains used for the purpose. Once prepared and having passed all the conventional vaccine tests large numbers of sheep in Great Britain, and goats and some sheep in Italy were inoculated. After the necessary incubation period large numbers (> 1,000 in each case) of inoculated animals came down with scrapie. In the meantime some inoculated clinically healthy goats and sheep may have entered food and feed chains or have been used for other purposes. In the British outbreak there appears to have been no consequence for humans who may have consumed infected sheep. It is too early to say what may be the consequences in Italy but measures have been taken to reduce any risk there may have been. .........end

Louping-ill vaccine documents from November 23rd, 1946 FULL TEXT

THE VETERINARY RECORD 516 No 47. Vol. 58 November 23rd, 1946



The annual Congress, 1946, was held at the Royal Veterinary College, Royal College Street, London, N.W.I. from September 22nd to September 27th.

Opening Meeting

[skip to scrapie vaccine issue...tss]

Papers Presented to Congress


although 176 products do _not_ conform to the CSM/VPC guidelines.



8. The Secretary of State has a number of licences. We understand that the inactivated polio vaccine is no longer being used. There is a stock of smallpox vaccine. We have not been able to determine the source material. (Made in sheep very unlikely to contain bovine ingredients).



more on the 1968 medicine act, they forgot to follow

Draft cover letter to product licence holders (considered by Human and Vet Medicines including deer)

2.3.Iatrogenic exposure

Iatrogenic exposure of scrapie has probably occurred twice. The first report determined that the vehicle was a louping ill vaccine prepared from sheep tissues and this infected a large number of sheep sheep (Gordon, 1946, Greig, 1950). The second was more recent and in this case a vaccine against Mycoplasma agalactiae prepared from sheep tissues was incriminated (Agrimi et al 1999, Capucchio, 1998) but not all outbreaks could be linked to the use of the vaccine. In this episode goats were predominantly affected10.

5.3.3 The greatest risk, in theory, would be from parenteral injection of material derived from bovine brain or lymphoid tissue. Medicinal products for injection or surgical implantation which are prepared from bovine tissues, or which utilise bovine serum albumin or similar agents in their manufacture, might also be capable of transmitting infectious agents. All medicinal products are licensed under the Medicines Act by the Licensing Authority following guidance, for example from the Committee on Safety of Medicines (CSM), the Committee on Dental and Surgical Materials (CDSM) and their subcommittees. The Licensing Authority have been alerted to potential concern about BSE in medicinal products and will ensure that scrutiny of source materials and manufacturing processes now takes account of BSE agent.

BEFORE the BSE Inquiry went online, i was requesting the daily hearings and submissions, and they were sending them to me via air mail. then, when the BSE Inquiry finally went online, i was then able to go back and match up some of what i had with the YB numbers (above), with the official documents. ...TSS

BSE offals used in cosmetics, toiletry and perfume industry Sun, 3 Sep 2000. Unpublished Inquiry documents obtained by CJD activist Terry S. Singeltary Sr. of Bacliff, Texas Miss Marion Kelly Cosmetic, Toiletry and Perfumery Association 35 Dover Street London W1X3RA

Department of Trade and Industry 10-18 Victoria Street London SW1H ONN Enquiries 01-215 5000 Telex 8811074 DTHQ G 01 215 3324 1 February 1990

40,000 human heart valves a year from BSE herds Sun, 3 Sep 2000. Unpublished Inquiry documents obtained by CJD activist Terry S. Singeltary Sr. of Bacliff, Texas

Opinion (webmaster): Below are some shocking documents. Here is a British company preparing 40,000 heart valves a year from bovine pericardium, primarily for export, and they are not required to source this material from BSE-free herds even in peak epidemic years. It is amazing to watch health "authorities" grovelling on their bellies to wring petty concessions from middle management at obscure little companies. The main worry is not the practise of using 800 potentially infected cows a week for human heart transplant material but that the press or recipients will get wind of it, hurting business.

BSE wasn't the problem, it was awkward queries from importing countries like the US. The cows are stunned using brain penetration -- can't do anything about the chunks of bovine brain blasted into the circulatory system, it's the norm. Can't use younger lower-risk animals either, patch would not be big enough. It is fascinating to see the British government worrying about, but doing nothing, with pigs with BSE 10 years ago.

While scrapie was long used as an excuse for continuing with human use of BSE-tainted material, little sheep material was used medically. Bovine transplants, vaccines, insulin doeses, etc. are far more dangerous than dietary material as injections, and are done on a very wide scale. So scrapie was never a valid analogy to BSE, as MAFF knew full well.

The British government deferred to the manufacturer's rep for an opinion on how contaminated pericardium might be, just as this appeared showing that this tissue is extremely dangerous:

England worried briefly about infecting other countries 27 Aug 00 confidential correspondence obtained by Terry S. Singeltary Sr.

BSE11/2 020;


DEPARTMENT OF HEALTH AND SOCIAL SECURITY Richmond House, 79 Whitehall, London SWIA 2NS Telephone 01-210 3000 From the Chief Medical Officer Sir Donald Achson KBE DM DSc FRCP FFCM FFOM

Mr K C Meldrum Chief Veterinary Officer Ministry of Agriculture, Fisheries and Food Government Buildings Hook Rise South Tolworth Surbiton Surrey KT6 7NG 3 January 1990

Dear Mr Meldrum


You will recall that we have previously discussed the potential risks of BSE occurring in other countries as a result of the continuing export from the UK of meat and bone that may be contaminated by scrapie or possibly BSE.

I remain concerned that we are not being consistent in our attempts to contain the risks of BSE. Having banned the feeding of meat and bone meal to ruminamts in 1988, we should take steps to prevent these UK products being fed to ruminants in other countries. This could be achieved either through a ban on the export of meat and bone meal, or at least by the proper labelling of these products to make it absolutely clear they should not be fed to ruminants [or zoo animals, including rare and endangered primates -- webmaster]. Unless some such action is taken the difficult problems we have faced with BSE may well occur in other countries who import UK meat and bone meal. Surely it is short sighted for us to risk being seen in future as having been responsible for the introduction of BSE to the food chain in other countries.

The documents below were provided by Terry S. Singeltary Sr on 8 May 2000. They are optically character read (scanned into computer) and so may contain typos and unreadable parts.


Mr Cunningham CMP3 From: D O Hagger MBI Dr Salisbury MED/IMCD3 Mr Burton PD/STB/PG1B B/17/2 Date: 15.02.1989 Mr Dudley PD/AD4


Other US BSE risks: the imported products picture 24 Jul 00 Trade Statistics: UK to US Compiled by Terry S. Singeltary Sr of Bacliff, Texas

[Opinion (webmaster): The US has focused for years on tracing, containing, and eradicating live animal imports from the UK or other countries with acknowledged BSE like Belgium, including some 499 cattle and the Vermont sheep. This strategy does not acknowledge imports of rendered bovine products from England during the BSE period nor secondary products such as surgical catgut, which is to say surgical cowgut, or dairy cattle embryos, vaccines for veterinarian and human medicines. What has become of these?

Mr. Singeltary, who lost his mother to CJD of unexplained origin a few years back and went on to became a well-known TSE activist, has tracked down voluminous pertinent import data through correspondence with UK officials and searches of government web sites. Imports of such products are frequently cited by Europeans in rating BSE risks in the US and in shutting out US exports.

Many people's eyes glaze over when reviewing reams of sometimes older trade statistics. There is no proof that any of the imported products was contaminated with BSE nor if so, any evidence that any BSE product lead to infection in US livestock, surgical patients, or what not. Nonetheless, the data obtained by Mr. Singeltary establish that an appalling variety and tonnage of products that were imported by the US from the UK and othr BSE-affected countries during the peak of the BSE epidemic years.]




SURGICAL CATGUT SUTURES 2.1 At the first meeting of the Working Party on Bovine Spongiform Encephalopathy on 6 September 1989, detailed consideration was given to XXXXX Surgical Catgut. This arose from the Company's response to the Letter to Licence Holders, indicating that the bovine small intestine source material was derived from UK cattle, unlike 8 other licenced catgut sutures. In contrast XXXXX Surgical Catgut was stated to hold over 90% share of the market for catgut sutures, and to constitute approximately 83% of all sutures used in U.K. IMPORTS OF SUTURES FROM THE KNOWN BSE COUNTRY;

The documents below were provided by Terry S. Singeltary Sr on 8 May 2000. They are optically character read (scanned into computer) and so may contain typos and unreadable parts.


Mr Cunningham CMP3 From: D O Hagger MBI Dr Salisbury MED/IMCD3 Mr Burton PD/STB/PG1B B/17/2 Date: 15.02.1989 Mr Dudley PD/AD4


1. The purpose of this minute is to alert you to recent developments on BSE as they affect medicines and to invite representatives to a meeting in Market Towers on 22 February 1989.

2. The report of the Working Party on Bovine Spongiform Encephalopathy (BSE) was submitted by the CMO to the Secretary of State for Health and Minister for Agriculturer on 9 February.

3. The summary at the end of the report records, inter alia: 'we have drawn the attention of the Licensing Authority to the potential of transfer of BSE agent in human and veterinary medicinal products. In paragraph 7 of his submission (Annex A), the CMO notes:

"I am also putting work urgently in hand to satisfy myself that everything possible has been done to ensure .... that transfer of the BBE agent in human and veterinary medicinal products does not occur."

4. The Veterinary products Committee meets on 16 February and The committee on Safety of Medicines on 23 February when each will be considering a draft of some joint guidelines for manufacturers of medicinal products which use bovine material as an ingredient or an intermediate in the manufacturing process (Annex B).....

6. Although a wide range of medicines may be implicated - and the present proposal is to write to companies for more information - an "instant" telephone survey of manufacturer of vaccines used for children has already been undertaken in response to a request from Dr Harris. The results are in Dr Adams' minute of 14 February (Annex C) - the proviso in his second paragraph, last sentence should be noted. 89/02.15/11.1


1. I attach a list of questions on BSE and medicines compiled with the aim of providing question and answer briefing to DH and MAFF Ministers upon publication of the Southwood Report. I have suggested names of those who may be able to provide answers. All recipients are invited to consider which if any important areas have been missed. Also attached is copy QA briefing being proposed by MAFF. I understand MAFF have produced General QA briefing on the reports as a whole. ..

MF580439/1 0585 Question

1. Which medicines are affected? (person to provide reply) Dr. Jefferys

2. Are the risks greater with some medicines than others? Dr. Jefferys

3. Why are medicines affected? Dr. Jefferys

4. Are some affected products available over the counter from pharmacies or shops? Dr. Purves

5. Are only UK products at risk? Dr. Jefferys

6. Are existing stocks safe? Dr. Jefferys

7. Are pre 1980 stocks available? Mr. Burton

8. Are these alternatives to the use of bovine material? Dr. Purves

9. Why can't we throw away suspect stock and import or manufacture safe medicines? Dr. Jefferys

10. Which patients are at risk? Dr. Jefferys

11. Are some patients particularly vulnerable? Dr Jefferys

12. What risks exist to those who have already used these medicines? Dr. Jefferys

13. HOW might patients be affected? Dr. Jefferys

14. Can BSE be transmitted to patients by medicines? Dr. Jefferys

15. How long will it be before risks are quantified? Dr. Jefferys

100 89/02.17/10.2 MF580439/1 0586

16. What research is going on to find out if medicines can transmit this disease and if any patients have been affected? Dr Jefferys

17. Could recent cases of Creuuzfeld Jacob Disease have been caused by transmission of BSE through medicines? Dr. Jefferys

18. What action is the Licensing Authority taking to ensure proper scrutinising of source materials and manufacturing processes? Dr. Jefferys/Dr. Purves

19. Are the guidelines practical? Dr. Jefferys/Dr. Purves

20. Will the guidelines remove the risk? Dr. Jefferys

21. How will the guidelines be enforced? Dr. Jefferys/Dr. Purves

22. How soon will they come into force? Dr. Jefferys

23. Will the guidelines be published? Mr. Hagger

24. What is being done to reassure patients, parents etc? Mr. Hagger/Dr. Salisbury

25. What advice is being given to doctors, pharmacists etc? Mr. Hagger

26. What advice is the Government giving about its vaccination programme? Dr. Salisbury

27. Is the vaccination programme put at risk because of BSE? Dr. Salisbury


Q. Will government act on this?

A. Yes - thymus is not used in preparation of baby foods but it is contacting all manufacturers to seek their urgent views on use of kidneys and liver from ruminants. Will consider any necessary measures in the light of their response.


Q. Can medicines spread BSE to other cattle/animals?

A. The report describes any risks as remote.

Q. How can risks be avoided?

A. In liaison with the DOH the Veterinary Products Committee is examining guidelines for the veterinary pharmaceutical industry which will be issued shortly.

Q. What will Guidelines say?

A. In essence they call for non-bovine sources to be used if possible, including synthetic material of biotechnological origin. Where this is not possible the industry should look for sources which are free of BSE and which are collected in a manner which avoids risk of contamination by the BSE agent.

89/02.17/10.4 MF580439/1 0588

A. Bovine source material is used in [garbled, cannot read...TSS] and some other medicines.

Q. How many medicines are involved?

A. Computer records show that about 300 of the 3,050 veterinary medicines licensed in the U.K. are manufactured directly from bovine source material. However, other medicines may be produced from bovine sources and a letter is going to all license holders so that a comprehensive list can be drawn up.

89/06.19/8.1 BSE3/1 0191 Hr J Maslin (MAFF) Ref: Maslin3g

From: Dr H Pickles Med SEB/B Date: 3 July 1989


I was interested to see the list of by-products sent to the HSE. Those of particular concern included:

* small intestines: sutures (I thought the source was ovine but you are checking this)

* spinal cord: pharmaceuticals

* thymus: pharmaceuticals

Are you able to give me more information on which UK manufacturers use these materials? Our proposed ban on bovine offal for human consumption would not affect these uses, I assume.

Id No. 1934/RD/1 89/08.10/6.1 117A

BOVINE SPONGIFORM ENCEPHALAPATHY MEETING HELD ON 21 AUGUST 1989 AT 2;15 IN ROOM 720 Miss M Duncan (Chairman) Mr W Burton Dr E Hoxey Mrs J Dhell Ms K Turner Dr S Whittle Mr N Weatherhead ... 5. The MCA had sent 2700 questionnaires out, 1,124 had made valid returns; of these 122 use animal material of some kind and there are 582 products involved. ... 6. The MCA/BSE working group will meet on 6th September. Their aim is to review responses from professional officers in MCA who have suggested seven categories of importance (with 1 being the most important} for medical products:

ID 2267/NRE/1 89/08.21/10.1

1. Products with Bovine brain/lymph tissue administered by injection.

2. Products with bovine tissue other than brain/lymph administered by inection.

3. Tissue implants/open wound dressing/surgical materials/dental and ophthlamic products with bovine ingredients.

4. Products with bovine ingredients administered topically.

5. Products with bovine ingredients administered orally.

6. Products with other animal/fish/insect/bird ingredients administered by injection/topically/oral routes.

7. Products with ingredients derived from animal material by chemical processing (eg stearic acid, gelatine, lanolin ext.

The BSE working group will decide which of these are important, and should be examined more closely, and which categories can be eliminated.

The responses by the companies were presented by Ms Turner and were categorised by MCA standards, the products that were discussed were all low volume usage products eg sutures, heart valves.

8. As the responses included some materials of human origin it was decided that more information should be sought about CJD. There had been 2 recent deaths reported associated with human growth hormone. These were being investigated.

9. Re-editing of the Paper on "Incubation of Scrapie-like Agents"

It was suggested that the document could be sent out to companies with the non-standard sterilization Document. The document could have severe implications on the companies whose products have a high risk factor as decided by the MCA working group....

11. The Need for a list of High Priority Implantables The commitee decided that no list is necessary as all implantables, including ones from a human source are of high priority. Concern was shown over Killingbeck who use human material but had not yet responded. The company will be chased for a response. Concern was shown over the fact that there may be other scrapie-like organisms in other animals and further enquiries should be made.

2334q/RD/4 89/08.21/10.7


Glutaraldehyde, formaldehyde, and ethylene oxide are used in the sterilization of these devices.

However, glutaraldehyde 4,10,12,19 formaldehyde 5,10,11,13,19 and ethylene oxide 19,23 are all reported to be ineffective methods for sterilization of material infected with the agents of CJD or scrapie.

Previous advice and research using the agents of CJD and scrapie, has concentrated on the decontamination of equipment; protection of health care workers from contaminated human material; human growth hormone; and dura mater. The methods developed may not be directly applicable or transferable to material of bovine origin for use in human implantation.

2334q/RD/7 89/08.21/10.10 BSE11/2 020 SC1337

DEPARTMENT OF HEALTH AND SOCIAL SECURITY Richmood House 79 Whitehall, London SW1A 2NS Telephone 01-210-3000 From the Chief Medical Officer Sir Donald Acheson KBE DM DSc FRCP FFCM FFOM

Mr K C Meldrum Chief Veterinary Officer Ministry of Agriculture, Fisheries and Food Government Buildings Hook Rise South Tolworth Surbiton Surrey KT6 7NG

3 January 1990

Dear Mr. Meldrum,


You will recall that we have previously discussed the potential risks of BSE occurring in other Countries as a result of the continuing export from the UK of meat and bone that may be contaminated by scrapie or possibly BSE.

I remain concerned that we are not being consistent in our attempts to contain the risks of BSE. Having banned the feeding of meat and bone meal to ruminants in 1988, we should take steps to prevent these UK products being fed to ruminants in other countries. This could be achieved either through a ban on the export of meat and bone meal, or at least by the proper labelling of these products to make it absolutely clear they should not be fed to ruminants. Unless some such action is taken the difficult problems we have faced with BSE may well occur in other countries who import UK meat and bone meal. Surely it is short sighted for us to risk being seen in future as having been responsible for the introduction of BSE to the food chain in other countries.

I would be very interested to hear how you feel this gap in the present prcautionary measures to eliminate BSE should be closed. We should be aiming at the global elimination of this new bovine disease. The export of our meat and bone meal is a continuing risk to other countries.

Signed Sincerely Donald Acheson

Did the US import fetal calf serum and vaccines from BSE-affected countries? 3002.10.0040: FETAL BOVINE SERUM (FBS) U.S. Imports for Consumption: December 1998 and 1998 Year-to-Date (Customs Value, in Thousands of Dollars) (Units of Quantity: Kilograms)

<--- Dec 1998 ---> <--- 1998 YTD ---> Country Quantity Value Quantity Value

================================================================= WORLD
TOTAL . . . . . . . 2,727 233 131,486 8,502 Australia . . . . . . . . --- --- 19,637 2,623 Austria . . . . . . . . . --- --- 2,400 191 Belgium . . . . . . . . . --- --- 17 32 Canada . . . . . . . . . 900 110 30,983 3,220 Costa Rica . . . . . . . 500 20 4,677 169 Federal Rep. of Germany --- --- 105 21 Finland . . . . . . . . . 1 8 9 83 France . . . . . . . . . --- --- 73 7 Guatemala . . . . . . . . --- --- 719 42 Honduras . . . . . . . . --- --- 1,108 88 Israel . . . . . . . . . --- --- 24 165 Netherlands . . . . . . . --- --- 1 5 New Zealand . . . . . . . 26 5 65,953 913 Panama . . . . . . . . . --- --- 1,195 64 Switzerland . . . . . . . 971 8 1,078 23 United Kingdom . . . . . 329 82 743 756 Uruguay . . . . . . . . . --- --- 2,764 98 ------------------------------------------------------------------ 3002.20.0000: VACCINES FOR HUMAN MEDICINE U.S. Imports for Consumption: December 1998 and 1998 Year-to-Date (Customs Value, in Thousands of Dollars) (Units of Quantity: Kilograms)

<--- Dec 1998 ---> <--- 1998 YTD ---> Country Quantity Value Quantity Value ================================================================= WORLD TOTAL . . . . . . . 25,702 26,150 550,258 378,735 Austria . . . . . . . . . --- --- 45 225 Belgium . . . . . . . . . 14,311 12,029 248,041 199,036 Canada . . . . . . . . . 1,109 1,527 15,798 16,305 Denmark . . . . . . . . . 80 234 246 682 Federal Rep. of Germany 1,064 4,073 12,001 6,329 France . . . . . . . . . 3,902 4,859 87,879 92,845 Ireland . . . . . . . . . --- --- 120 478 Italy . . . . . . . . . . --- --- 2,359 81 Japan . . . . . . . . . . 445 1,903 11,350 11,298 Netherlands . . . . . . . --- --- 94 6 Republic Of South Africa --- --- 2 1 Spain . . . . . . . . . . --- --- 60 30 Switzerland . . . . . . . 716 353 9,303 4,271 United Kingdom . . . . . 4,075 1,172 162,960 47,148 ------------------------------------------------------------------ 3002.30.0000: VACCINES FOR VETRINARY MEDICINE U.S. Imports for Consumption: December 1998 and 1998 Year-to-Date (Customs Value, in Thousands of Dollars) (Units of Quantity: Kilograms)

<--- Dec 1998 ---> <--- 1998 YTD ---> Country Quantity Value Quantity Value ================================================================= WORLD TOTAL . . . . . . . 6,528 237 87,149 2,715 Canada . . . . . . . . . --- --- 2,637 305 Federal Rep. of Germany --- --- 104 5 Netherlands . . . . . . . 138 64 472 192 New Zealand . . . . . . . 6,390 173 83,882 1,895 United Kingdom . . . . . --- --- 54 318

Procedures Manual

Bovine Spongiform Encephalopathy (BSE)

Ongoing Surveillance Plan

Ongoing Surveillance Plan Implementation July 20, 2006


Personal Safety

If BSE is transmissible to humans in the occupational setting, the most likely routes would be through contact with infective tissues through wounds or open lesions on the skin, contact with mucous membranes (eyes and mouth), or exceptionally, by swallowing. .....snip...end

SO, looks like to me the most likely route of transmission of BSE to humans would be through inoculation i.e.

the most likely routes would be through contact with infective tissues through wounds or open lesions on the skin,

IF you look at all the successful transmission studies in the lab with TSE, inoculations was the most successful route.


Bovine Spongiform Encephalopathy

BSE-L is a discussion forum for scientists who are interested in Bovine Spongiform Encephalopathy (BSE). BSE-L has been created on 20th July, 1994 by Siegfried Schmitt. Impressum:

LISTS.AEGEE.ORG ( BSE-L: 484 matches (only the first 50 will be shown).. )

From: TSS ( Subject: Louping-ill vaccine documents from November 23rd, 1946 Date: September 10, 2000 at 8:57 am PST

Subject: Louping-ill vaccine documents from November 23rd, 1946 Date: Sat, 9 Sep 2000 17:44:57 -0700 From: "Terry S. Singeltary Sr." Reply-To: Bovine Spongiform Encephalopathy To:

######### Bovine Spongiform Encephalopathy #########

THE VETERINARY RECORD 516 No 47. Vol. 58 November 23rd, 1946



The annual Congress, 1946, was held at the Royal Veterinary College, Royal College Street, London, N.W.I. from September 22nd to September 27th.

Opening Meeting

[skip to scrapie vaccine issue...tss]

Papers Presented to Congress

The papers presented to this year's Congress had as their general theme the progressive work of the profession during the war years. Their appeal was clearly demonstrated by the large and remarkably uniform attendance in the Grand Hall of the Royal Veterinary College throughout the series; between 200 and 250 members were present and they showed a keen interest in every paper, which was reflected in the expression of some disappointment that the time available for discussion did not permit of the participation of more than a small proportion of would-be contributors.

In this issue we publish (below) the first to be read and discussed, that by Dr. W. S. Gordon, M.R.C.V.S., F.R.S.E., "Advances in Veterinary Research." Next week's issue will contain the paper on "Some Recent Advances in Veterinary Medicine and Surgery in Large-Animal Practice" by Mr. T. Norman Gold, M.R.C.V.S. In succeeding numbers of the Record will be reproduced, also with reports of discussions, that by Mr. W. L. Weipers, M.R.C.V.S., D.V.S.M., on the same subject as relating to small-animal practice, and the papers by Mr. J. N. Ritchie, B.SC., M.R.C.V.S., D.V.S.M., and Mr. H.W. Steele-Bodger, M.R.C.V.S., on "War-time Achievements of the British Home Veterinary Services."

The first scientific paper of Congress was read by Dr. W. S. Gordon, M.R.C.V.S., F.R.S.E. on Monday, September 23rd, 1946, when Professor J. Basil Buxton, M.A., F.R.C.V.S, D.V.H., Prinicipal of the Royal Veterinary College, presided.

Advances in Veterinary Research


W.S. GORDON, PH.D., M.R.C.V.S., F.R.S.E.

Agriculteral Research Council, Field Station, Compton, Berks.

Louping-ill, Tick-borne Fever and Scrapie

In 1930 Pool, Browniee & Wilson recorded that louping-ill was a transmissible disease. Greig et al, (1931) showed that the infective agent was a filter-passing virus with neurotropic characters and Browniee & Wilson (1932) that the essential pathology was that of an encephalomyelitis. Gordon, Browniee, Wilson & MacLeod (1932) and MacLeod & Gordon (1932) confirmed and extended this work. It was shown that on louping-ill farms the virus was present in the blood of many sheep which did not show clinical symptoms indicating involvement of the central nervous system and that for the perpetuation and spread of the disease these subclinical cases were probably of greater importance that the frank clinical cases because, in Nature, the disease was spread by the tick, lxodes ricinus L. More recently Wilson (1945, 1946) has described the cultivation of the virus in a chick embryo medium, the pathogenic properties of this culture virus and the preparation of louping-ill antiserum.

Between 1931 and 1934 I carried out experiments which resulted in the development of an effective vaccine for the prevention of louping-ill.* This vaccine has been in general use since 1935 and in his annual report to the Animal Diseases Research Association this year, Dr. Greig stated that about 227,000 doses of vaccine had been issued from Moredun alone.

Dr. Gordon illustrated this portion of his paper by means of graphs and diagrams projected by the epidiascope.

This investigation, however, did not begin and end with the study of louping-ill; it had, by good fortune, a more romantic turn and less fortunately a final dramatic twist which led almost to catastrophe. After it had been established that a solid immunity to louping-ill could be induced in sheep, a group of immunized and a group of susceptible animals were placed together on the tick-infected pasture of a louping-ill farm. Each day all the animals were gathered and their temperatures were recorded. It was anticipated that febrile reactions with some fatalities would develop in the controls while the louping-ill immunes would remain normal. Contrary to expectation, however, every sheep, both immune and control, developed a febrile reaction. This unexpected result made necessary further investigation which showed that the febrile reaction in the louping-ill immunes was due to a hitherto undescribed infective agent, a Rickettsia-like organism which could be observed in the cytoplasm of the granular leucocytes, especially the neutrophil polymorphs (MacLeod (1932), Gordon, Browniee, Wilson & MacLeod. MacLeod & Gordon (1933). MacLeod (1936). MacLeod collected ticks over many widely separated parts of Scotland and all were found to harbour the infective agent of tick-borne fever, and it is probable that all sheep on tick-infested farms develop this disease, at least on the first occasion that they become infested with ticks. When the infection is passed in series through susceptible adult sheep it causes a sever, febrile reaction, dullness and loss of bodily condition but it rarely, if ever, proves fatal. It is clear, however, that it aggravates the harmful effects of a louping-ill infection and it is a serious additional complication to such infections as pyaemia and the anacrobic infections which beset lambs on the hill farms of Northern Britain.

Studying the epidemiology of louping-ill on hill farms it became obvious that the pyaemic condition of lambs described by M'Fadyean (1894) was very prevalent on tick infested farms Pyaemia is a crippling condition of lambs associated with tick-bite and is often confused with louping-ill. It is caused by infection with Staphylococcus aureus and affected animals may show abscess formation on the skin, in the joints, viscera, meninges and elsewhere in the body. It was thought that tick-borne fever might have been a predisposing factor in this disease and unsuccessful attempts were made by Taylor, Holman & Gordon (1941) to reproduce the condition by infecting lambs subcutaneously with the staphylococcus and concurrently producing infections with tickborne fever and louping-ill in the same lambs. Work on pyaemia was then continued by McDiarmid (1946a, 1946b, 1946c), who succeeded in reproducing a pyaemic disease in mice, guinea-pigs and lambs similar to the naturally occurring condition by intravenous inoculation of Staphylococcus aureus. He also found a bacteraemic form of the disease in which no gross pyaemic lesions were observed. The prevention or treatment of this condition presents a formidable problem. It is unlikely that staphylococcal ???oid will provide an effective immunity and even if penicillin proved to be a successful treatment, the difficulty of applying it in adequate and sustained dosage to young lambs on hill farms would be almost insurmountable.

From 1931 to 1934 field trials to test the immunizing value and harmlessness of the loup-ill vaccine were carried out on a gradually increasing scale. Many thousands of sheep were vaccinated and similar numbers, living under identical conditions were left as controls. The end result showed that an average mortability of about 9 percent in the controls was reduced to less than 1 percent in the vaccinated animals. While the efficiency of the vaccine was obvious after the second year of work, previous bitter experience had shown the wisdom of withholding a biological product from widespread use until it had been successfully produced in bulk, as opposed to small-scale experimental production and until it had been thoroughly tested for immunizing efficiency and freedom from harmful effects. It was thought that after four years testing this stage had been reached in 1935, and in the spring of that year the vaccine was issued for general use. It comprised a 10 percent saline suspension of brain, spinal cord and spleen tissues taken from sheep five days after infection with louping-ill virus by intracerebral inoculation. To this suspension 0-35 percent of formalin was added to inactivate the virus and its safety for use as a vaccine was checked by intracerbral inoculation of mice and sheep and by the inoculation of culture medium. Its protective power was proved by vaccination sheep and later subjecting them, along with controls, to a test dose of living virus.

Vaccine for issue had to be free from detectable, living virus and capable of protecting sheep against a test dose of virus applied subcutaneously. The 1935 vaccine conformed to these standards and was issued for inoculation in March as three separate batches labelled 1, 2, and 3. The tissues of 140 sheep were employed to make batch 1 of which 22,270 doses were used; 114 to make batch 2 of which 18,000 doses were used and 44 to make batch 3 of which 4,360 doses were used. All the sheep tissues incorporated in the vaccine were obtained from yearling sheep. During 1935 and 1936 the vaccine proved highly efficient in the prevention of loup-ill and no user observed an ill-effect in the inoculated animals. In September, 1937, two and a half years after vaccinating the sheep, two owners complained that scrapie, a disease which had not before been observed in the Blackface breed, was appearing in their stock of Blackface sheep and further that it was confined to animals vaccinated with louping-ill vaccine in 1935. At that stage it was difficult to conceive that the occurrence could be associated with the injection of the vaccine but in view of the implications, I visited most of the farms on which sheep had been vaccinated in 1935. It was at this point that the investigation reached its dramatic phase; I shall not forget the profound effect on my emotions when I visited these farms and was warmly welcomed because of the great benefits resulting from the application of louping-ill vaccine, wheras the chief purpose of my visit was to determine if scrapie was appearing in the inoculated sheep. The enquiry made the position clear. Scrapie was developing in the sheep vaccinated in 1935 and it was only in a few instances that the owner was associating the occurrence with louping-ill vaccination. The disease was affecting all breeds and it was confined to the animals vaccinated with batch 2. This was clearly demonstrated on a number of farms on which batch 1 had been used to inoculate the hoggs in 1935 and batch 2 to inoculate the ewes. None of the hoggs, which at this time were three- year-old ewes. At this time it was difficult to forecast whether all of the 18,000 sheep which had received batch 2 vaccine would develop scrapie. It was fortunate, however, that the majority of the sheep vaccinated with batch 2 were ewes and therfore all that were four years old and upwards at the time of vaccination had already been disposed of and there only remained the ewes which had been two to three years old at the time of vaccination, consequently no accurate assessment of the incidence of scrapie could be made. On a few farms, however, where vaccination was confined to hoggs, the incidence ranged from 1 percent, to 35 percent, with an average of about 5 percent. Since batch 2 vaccine had been incriminated as a probable source of scrapie infection, an attempt was made to trace the origin of the 112 sheep whose tissues had been included in the vaccine. It was found that they had been supplied by three owners and that all were of the Blackface or Greyface breed with the exception of eight which were Cheviot lambs born in 1935 from ewes which had been in contact with scrapie infection. Some of these contact ewes developed scrapie in 1936-37 and three surviving fellow lambs to the eight included in the batch 2 vaccine of 1935 developed scrapie, one in September, 1936, one in February, 1937, and one in November, 1937. There was, therefore, strong presumptive evidence that the eight Cheviot lambs included in the vaccine although apparently healthy were, in fact, in the incubative stage of a scrapie infection and that in their tissues there was an infective agent which had contaminated the batch 2 vaccine, rendering it liable to set up scrapie. If that assumption was correct then the evidence indicated that:-

(1) the infective agent of scrapie was present in the brain, spinal cord and or spleen of infected sheep: (2) it could withstand a concentration of formalin of 0-35 percent, which inactivated the virus of louping-ill: (3) it could be transmitted by subcutaneous inoculation; (4) it had an incubative period of two years and longer.

Two Frenchmen, Cuille & Chelle (1939) as the result of experiments commenced in 1932, reported the successful infection of sheep by inoculation of emulsions of spinal cord or brain material by the intracerebral, epidural, intraocular and subcutaneous routes The incubation period varied according to the route employed, being one year intracerebrally, 15 months intraocularly and 20 months subcutaneously. They failed to infect rabbits but succeeded in infecting goats. Another important part of their work showed that the infective agent could pass through a chamberland 1.3 filter, thus demonstrating that the infective agent was a filtrable virus. It was a curious coincidence that while they were doing their transmission experiments their work was being confirmed by the unforeseeable infectivity of a formalinized tissue vaccine.

As a result of this experience a large-scale transmission experiment involving the ue of 788 sheep was commenced in 1938 on a farm specially taken for the purpose by the Animal Diseases Research Association with funds provided by the Agricultural Research Council. The experiment was designed to determine the nature of the infective agent and the pathogenesis of the disease. It is only possible here to give a summary of the result which showed that (1) saline suspensions of brain and spinal cord tissue of sheep affected with scrapie were infective to normal sheep when inoculated intracerebrally or subcutaneously; (2) the incubation period after intracerebral inoculation was seven months and upwards and only 60 percent of the inoculated sheep developed scrapie during a period of four and a half years; (3) the incubation period after subcutaneous inoculation was 15 months and upwards and only about 30 percent of the inoculated sheep developed the disease during the four and a half years: (4) the infective agent was of small size and probably a filtrable virus.

The prolonged incubative period of the disease and the remarkable resistance of the causal agent to formalin are features of distinct interest. It still remains to determine if a biological test can be devised to detect infected animals so that they can be killed for food before they develop clinical symptoms and to explore the possibilities of producing an immunity to the disease.


Greetings List Members,

pretty disturbing document. now, what would stop this from happening with the vaccineCJD in children???

kind regards,

Terry S. Singeltary Sr.

P.O. Box 42

Bacliff, Texas USA 77518