Volume 6: Human Health, 1989-96
7. Human health developments from January 1996 to 20 March 1996
The response to the reports of the January meeting
Discussion
Reactions outside government
SEAC meeting: 1 February 1996
Communication of concerns expressed at SEAC meeting on 1 February 1996
Discussion

Discussion

Reaction to Mr Eddy's minute of 8 January

7.117 Mr Meldrum had this to say in evidence about the concerns felt at Tolworth in relation to the cases of CJD in young people:

I also was concerned in 1995, obviously, about the three cases that occurred in young people. I remember very well the occasions when they were brought to my attention. There was extreme concern in my team in Tolworth: Kevin Taylor, myself, Danny Matthews, Tom Eddy and Richard Carden; we were all extremely concerned about these cases.

We were keeping in close touch with the Department of Health and also with SEAC and listening to the advice which they gave us. ¹

7.118 He explained that it was because of his continuing concern about CJD in farmers and in young people that he asked Mr Eddy to send him a note of SEAC's discussions on 5 January. ²

7.119 Mr Meldrum also told us:

What I would like to point out is that in that report Dr Will said that he considered there was a very high chance that one of the 29 year olds and the 30 year old were genetic and he reminded SEAC that if this was the case then the figures were perhaps not so worrying at that stage, given the fact that there had been two cases in France although over a 15 year period, and two in Japan and other cases reported in the Netherlands and Australia under 30. ³ Also, I would like to refer to the minute I received from Mr Eddy of 8th January, 1996 ⁴ which summarised the meeting of SEAC on 5th January, 1996 ⁵ and which indicated that there was no additional reason for concern. So at this point in time, although I was concerned at the number of cases occurring in young persons, there was no advice emanating from SEAC that further protection measures for either animals or humans was likely to be necessary. ⁶

7.120 We consider that Mr Meldrum's reaction to Mr Eddy's minute was reasonable. While the minute described the concern of Dr Will about the cases in young people, it also recorded the likelihood that the cause for concern would be diminished by the diagnosis of two of the cases as being the familial variety of the disease.

Reaction to Dr Wight's minute of 9 January

7.121 Dr Wight's minute was sent to Dr Harvey, Sir Kenneth Calman's Private Secretary, and copied to Dr Metters and Dr Rubery, among others.

7.122 Sir Kenneth was already aware of Professor Collinge's concern about the cases in young people, for he had spoken of this to Sir Kenneth on 31 October 1995. ⁷ Sir Kenneth was asked, when giving evidence, whether it would have made a difference to his reaction if Dr Wight had included in her minute the concerns expressed at the SEAC meeting of Dr Will and Professor Collinge. He thought that it would have made a difference, ⁸ but added that if SEAC had concluded that the number of young cases suggested a link with BSE, he would have expected their Chairman or one of their number to raise this with him directly. ⁹

7.123 Sir Kenneth added that Dr Wight's statement that 'it is not without precedent world wide' as:

. . . reflected the world literature at the time. It could have happened and therefore was not anything particularly significant at the time, especially with the two that might just have been genetic . . .

But of course the minute itself is one which I noted and waited for further information on. ¹⁰

7.124 It seems to us that Sir Kenneth failed to appreciate from Dr Wight's minute the extent of the concern felt by Dr Will and Professor Collinge about the young cases of CJD. Had he appreciated this, we feel that he would have taken a more personal interest in events over the next months than in fact he did. Having regard to the terms of Dr Wight's minute, we do not find Sir Kenneth's reaction surprising or a matter for criticism.

7.125 Dr Metters, like Sir Kenneth, was not alerted by Dr Wight's minute of 9 January to the concerns that the young cases of CJD were generating. In a written statement he commented:

Up to the date of the SEAC meeting on 1 February 1996, ¹¹ the expert advice which DH had been receiving was that the risk posed by BSE to human health was remote and that there was no evidence of a link between BSE and CJD. SEAC had specifically considered the cases of CJD in teenagers (at its meeting on 8 September 1995) and advised that it was not possible to draw any conclusions from them. ¹²

The latest factual developments on BSE and the experts' advice thereon were constantly considered and re-evaluated by officials within DH, ¹³ especially when SEAC had something new to say, and, as part of that process, consideration was given to whether any specific contingency plans needed to be made. However, in the light of the facts set out above, the position as at 1 February 1996 was that DH had no reason to make any such plans. ¹⁴

7.126 Just as in the case of Sir Kenneth, we do not consider that Dr Metters is open to criticism for not being alerted by Dr Wight's minute.

7.127 Dr Rubery told us about her working relationship with Dr Wight:

When I became head of Health Aspects of the Environment Division (in Public Health Group of Department of Health) in April 1995, I realised that Dr Wight kept in close contact with Kenneth Calman (CMO) and Jeremy Metters (DCMO) on CJD and BSE issues. I took care not to disturb this working relationship which appeared to work well. I expected to be routinely copied into all minutes that went from Dr Wight or Mr Charles Lister to Ministers or CMO and DCMO and used these minutes plus formal and informal contacts with Dr Wight and her line manager (Dr Roger Skinner) as the mechanism for monitoring the Division's handling of these issues . . .

After a SEAC meeting it is my understanding that Dr Wight usually phoned the CMO to update him on key issues dealt with. This was routinely followed by a minute to CMO from her or one of her team confirming the key issues. The formal minutes of the SEAC meeting would not usually be finalised until a few weeks later. Dr Wight or one of her team would inform me personally or by phone of any decision likely to be of concern to Ministers or CMO. Often I would go down to their offices to ask if there was any news during the afternoon of a SEAC meeting if I was not in a meeting myself. I would expect to always be aware of the outcome of a SEAC meeting by the following morning at the latest. ¹⁵

7.128 Dr Rubery told us that she received a copy of Dr Wight's minute of 9 January. She said that she was confident that she would have discussed informally with her line manager, Dr Roger Skinner, and also with Dr Wight and her team, the nature of the data given to SEAC, how SEAC felt it should be handled and what advice should be given to Ministers and the CMO. SEAC had asked for further information from Professor Smith to help them assess the significance of the information reported by Dr Will, and Dr Rubery considered that she did not need to initiate any further action until further advice was received from SEAC. ¹⁶

Reactions outside government

7.129 On 22 January 1996, Sir Donald Acheson, former CMO, who had visited DH in November, wrote to Professor Pattison (who was Dean of the University College Medical School at which Sir Donald now worked part time ¹⁷). ¹⁸ The letter was copied to Sir Kenneth Calman. Sir Donald said he had now had a chance to study the recent reports of the CJD Surveillance Unit (August 1995), the Advisory Committee on Dangerous Pathogens (ACDP) (1994) and SEAC (1994). He had also re-read the Southwood Report. He said:

The principal point I want to make is that subsequent events have shown that the assumption made in the summary of the Southwood Report in 1989... that the BSE epidemic is due to the presence of the scrapie agent in meat and bone meal fed to cattle is now less secure than it was then. ¹⁹

7.130 Sir Donald then quoted from the Southwood Report:

The epidemiological evidence suggests this new disease has appeared as a result of contamination of meat and bone meal derived from sheep offal and fed to British cattle from the early 1980s. Contamination has arisen because modern rendering practices failed to destroy the agent of scrapie, the endemic Spongiform Encephalopathy of sheep. ²⁰

7.131 He continued his letter:

At that time the basis for the reassurance that we gave the public ('beef is safe') rested on the analogy with scrapie. Thus, this condition, although it had been endemic in sheep in Britain since 1732 and sheeps' brain and offal had been freely available for human consumption; had not led to spongiform encephalopathies in man. Nor did the global distribution of scrapie bear any relation to the distribution of CJD.

In the interim, however, it has become clear that the agent of BSE either did not originate from scrapie material in sheep or, if it did, changed in passage through cattle. Two lines of evidence point in this direction. In the first place, while there is no evidence of scrapie having transmitted to the domestic cat it became clear late in 1991 that BSE had transmitted by the alimentary route [ie, orally] to the domestic cat. Later, evidence emerged of transmission to various exotic cats in captivity. In other words the inter-species transmissibility pattern of BSE differs from scrapie. ²¹

The second line of evidence comes from experiments using the mouse model. These confirm that there are differences between the scrapie and BSE agents. Various experiments have shown that unlike scrapie BSE appears to act as a single strain, appears to be more heat resistant and produces a different and consistent pattern of disease and incubation period in mice. ²²

While this does not necessarily mean that BSE is any less innocuous to man than scrapie it means that much of the reassurance which the scrapie analogy afforded and on which the original policy was based has unfortunately fallen away. Happily the potentially serious implication of the successful transmission by cerebral inoculation of BSE to primates (marmoset) in 1993 is offset by the fact that scrapie has also been transmitted to marmosets.

In the circumstances, and bearing in mind that the small number of pathogenesis experiments using tissue from cattle provide at best a weak negative, it seems appropriate for DH and MAFF to review once more its policies in relation to BSE to see whether any further steps should be taken to protect the health of the public. The elimination of calf brain and other offal and of beef liver from food permitted for human consumption including baby food would seem to be matters for reconsideration, and there may be others. ²³

7.132 Sir Kenneth Calman's Secretary sent Sir Donald a response dated 26 January 1996. This stated that Sir Kenneth had found the information contained in the letter to Professor Pattison 'very useful' and had retained it in his office for future reference. ²⁴

7.133 On 24 January 1996, at the twenty-fifth meeting of MAFF's Consumer Panel, MAFF tabled a paper called 'BSE: the Government's Perspective'. ²⁵ It presented a brief history and description of TSEs, and discussed BSE in relation to human and animal health. It included the following statement:

. . . there is no evidence of any link between beef eating and CJD. All cases of CJD in the UK are intensively studied by the CJD Surveillance Unit which publishes an annual report each summer. The number of cases fluctuates from one year to another, but the early data for 1995 shows that the number of cases will be lower than in 1994. ²⁶

7.134 The paper concluded:

This paper has been written to explain the control measures taken to protect animal and public health in the light of independent advice and a substantial ongoing research programme. Government has made it very clear that its overriding priority must be the protection of human health. Economic considerations are secondary. The control measures which have been taken are consistent with this stance. ²⁷

7.135 Dr John Godfrey of the Consumer Panel wrote a response to the MAFF paper. ²⁸ His final paragraph stated:

5. However, these cases demand most careful consideration. CJD is a disease of the old. If BSE proves to have been able to jump the species barrier to man it can be expected to present as CJD, or a CJD-like encephalopathy. May I suggest a few initial thoughts?

- These cases will probably prove to have been a cluster of no discernible significance. The history of epidemiology is, largely, a history of clusters that demanded attention, but deserved eventual dismissal.

- The putative importance of these cases has to be judged on the strength of the evidence that they are the first ones here, and among very few worldwide. If numerous cases have died without being diagnosed there is not much to worry about. This is a matter of clinical judgement, that I lack. The authors of the papers quoted write: '. . . it seems unlikely that CJD, and particularly cases with a typical clinical presentation and histology, would have been previously missed in teenagers.' It seems likely that this statement is intended to apply only to countries with an advanced health service. That all the cases have been reported from Europe and North America may well be due to failure to diagnose other cases that died unrecognised elsewhere.

- If the tiny cluster is due to people having been infected, further cases are likely, perhaps many of them. It seems best for government to plan now for this highly improbable possibility. This should include: (a) taking statistical advice on what will be taken as significant evidence, leading to action (did R. A. Fisher work on an efficient test for very small samples?); (b) what advice should be given to consumers. It should be the aim to get advice across to us before the predictable reactions to what would be major tragedy, but also a major news story; (c) what action should be taken, in this hypothetical situation, to make the beef that could be eaten by consumers in the future safe again. This would obviously cost a lot, and be technically difficult, but possible. ²⁹

7.136 It was Dr Godfrey who had earlier questioned the infectivity of dorsal root ganglia. We consider that his contributions to the Consumer Panel showed commendable perception.

7.137 On 29 January 1996 Miss Jill Wordley (MAFF Consumers and Nutrition Policy Division) minuted Mr Eddy with her thoughts on 'groups to be briefed on BSE'. She mentioned consumer organisations and the MAFF Consumer Panel, and the disadvantages of relying 'too heavily on the MLC': 'It seems to me that as far as the general consumer is concerned, the MLC are perceived as being in the "save the meat industry" camp. A better impression of impartiality might be given if MAFF organised as much as possible itself.' She also mentioned scientists, food and health writers, the internet and schools. ³⁰

7.138 Mr Eddy said in a written statement, 'I don't recall this exercise [ie, publicity] progressing further and believe that it was simply overtaken by the aftermath of the nvCJD announcement.' ³¹

SEAC meeting: 1 February 1996

7.139 We now turn to the second SEAC meeting in 1996 (the twenty-fourth in all), at which the findings of the CJD Surveillance Unit were discussed. SEAC was given a further update by Dr Will. ³² The developments which had occurred in the Unit's consideration of recent cases of CJD in young people are described in detail in vol. 8: Variant CJD. Things had moved on since SEAC was updated on 5 January. Dr Will told the Inquiry that by the end of January the Unit had identified 'what we believed might be a common clinical phenotype' in the young cases. He stressed that the identification of this possibly novel phenotype was 'tentative' at this stage and the possibility that some of the cases might have been genetic had not been ruled out. ³³ Dr Will summarised the views he held at the end of January 1996:

I had become increasingly concerned about the young cases of CJD, but there was insufficient scientific evidence to reach a conclusion about the novelty of these cases, nor to reach a judgement about whether these cases might be causally linked to BSE. The interpretation of the neuropathological findings was of critical importance and I asked Dr Ironside [CJD Surveillance Unit] for his opinion. Dr Ironside said that there clearly were very unusual pathological features in these cases, but that it would be premature to conclude that these cases were linked to BSE on the basis of the neuropathological findings alone. ³⁴

7.140 As a result of these developments, Dr Will explained in his statement that by 1 February 1996 his assessment of the extent to which some of the scientific criteria were met (in relation to judging the significance of the cases) had changed from the position at 5 January:

i. (a) is there a novel clinical phenotype?: possible (compared with 'not identified' on 5 January)

(b) is there a novel pathological phenotype?: possible (compared with 'not identified' on 5 January)

(c) are these cases linked to PRNP mutations?: no mutation identified in three cases

(d) is there ascertainment bias or increased efficiency of surveillance?: probable

ii. (a) are these cases in the UK distinct from previous experience?: possible (compared with 'not identified' on 5 January)

(b) are these cases only occurring in the UK?: unknown ³⁵

7.141 It was in the light of these developments that Dr Will provided SEAC with an update of CJDSU findings at the meeting in February. The minutes of SEAC's meeting recorded that:

Dr Will referred to the suspect CJD case in a 52-year-old who had worked in an abattoir for 18 months from 1989, and who was reported to have sustained an injury while working. He had in fact been kicked by a steer and had received no hospital treatment.

Dr Will reported that he had been advised of one possible case of CJD in a German who had worked in an abattoir for 10 years, 30 years prior to death, and of one confirmed case in France in 1995 in a man aged 59 who had worked for 36 years in an abattoir.

He reported that the 1995 UK incidence of CJD appears to be about 20% down on the 1994 level and updated SEAC on the now 5 pathologically confirmed individuals under 30 years of age. Three of these patients have died and 2 remain alive. Genotyping is incomplete. Dr Will confirmed that [name not specified] is not one of these 5 cases. Two cases of CJD have been confirmed by pathology in 30-39 year olds and a further patient in this age group has pathology suggestive of GSS. Dr Will also reported a further confirmed case of CJD in a 41-year-old.

In all of the cases mentioned above (except the GSS case and one case where results are incomplete) there was extensive plaque formation in the cerebral cortex, cerebellum and spinal cord. An extensive and unusual pattern of PrP deposition was an unexpected finding. Dr Will reported Dr Ironside's view that it is premature to decide that these cases are linked with BSE . . .

. . .

Dr Will reiterated that the crucial issue is not simply the young age or pathology of recent cases but the short time scale in which 5 cases in individuals under 30 years of age had occurred. The dates of onset of symptoms of the cases were February 94, May 94, June 94, January 95 and April 95 although they were not reported to the [CJDSU] in that order. He advised the Committee that definitive genetic data on these 5 cases would soon be available and that he intended to publish the clinico/pathological data together with that of cases under 40 years of age. Details of the third young case will also soon be published. ³⁶

7.142 The minutes also recorded that:

Professor Pattison [Chairman] said that information given to the media to date indicates that 1994 was not the start of a major rise in the incidence of CJD. He concluded that the unusual data on young cases is of greater concern than the cases in farmers which appeared to be classical sporadic cases with typical pathology. He repeated the need to look at young cases in other countries. If these cases shared the unusual pathology it would be comforting. It could be that CJD in young cases was different because of the age of the patient.

. . .

Professor Collinge was of the opinion that 5 cases in people under 30 years old in little over a year must be very significant in statistical terms. Professor Smith agreed. ³⁷

7.143 Professor Collinge told us that his understanding of the information provided to the February meeting was that:

. . . these young cases showed a unique and remarkably uniform disease pattern. This would be consistent with their being exposed to the same prion strain. I again reiterated my concerns that this was likely to represent BSE transmission to humans. ³⁸

7.144 In a statement to the Inquiry Professor Will stated:

The short time scale in which five young cases of CJD aged less than 30 years had been identified was clearly a matter of concern, but I did not at that time believe there was sufficient clinical, pathological or epidemiological evidence to indicate that we had identified a novel clinicopathological phenotype of CJD. ³⁹

7.145 In oral evidence to the Inquiry, Professor Will was asked why the meeting was considering only five cases under the age of 30 when there had been seven under 40 to date. Professor Will stated:

I gave a very full report of what was happening. And these minutes are not a full record, I think, of what I said. But I did talk about all the cases that we had, I am sure. ⁴⁰

7.146 When Professor Will was also asked whether he had communicated the shift from the January meeting, where it was 'not identified' whether the UK cases were distinct from previous experience, to the position in February, when the answer was that this was 'possible', he stated:

Yes, I think that they understood, I hope, that there was a concern about what was happening. But the level of that concern, of course, would have varied enormously from person to person within the committee. I cannot make a judgment about what everyone else felt . . . But as I have said before, I think in relation to making a judgment about whether this was truly new or truly signified any relationship with BSE could not be suggested at that time. ⁴¹

7.147 In a statement Professor Collinge told us that at SEAC's meeting on 1 February 1996 he repeated his concerns that the findings were likely to represent the transmission of BSE to humans. ⁴²

Communication of concerns expressed at SEAC meeting on 1 February 1996

7.148 As with the January meeting of SEAC, Mr Eddy and Dr Wight circulated details of the February meeting within their respective Departments.

7.149 On 6 February 1996, Mr Eddy circulated a summary of the meeting to Mr Hogg, Mrs Browning, Mr Packer, Mr Carden and Mr Meldrum. ⁴³ He reported that the meeting had 'mainly focused on research priorities and the answers to the Minister's questions'. ⁴⁴ Mr Eddy added:

I also need to alert the Minister to the fact that Dr Will, the Deputy Chairman of SEAC and Head of the CJD Surveillance Unit, is preparing two scientific papers. Both are potentially tricky and will need careful handling. He is aware of our interest and of the need to alert us in good time before they are published. He does not yet know when they will be published.

7.150 The minute went on to outline the contents of the two papers. It reported that the first paper, which was in an advanced stage, described the identification of two distinct subsets of CJD and that:

In one form the disease appears restricted to specific parts of the brain. In the other form disease is more widespread and is found in the spinal column, and shows similarities to CJD in recipients of growth hormones. The conclusion which some of our critics will draw, although there is no evidence, is that the form of CJD with the widespread spongiform appearance represents the kind of disease which can be 'caught' and that those who have this form of disease and have not had any form of medical intervention may have caught it from cattle. Dr Will's paper will not say that but others will try to interpret it in that way. ⁴⁵

7.151 He stated that the second paper, which had not yet been drafted, looked at the five confirmed cases of CJD in patients aged under 30 and that:

All five cases look the same under the microscope, with extensive plaques in both the cortex and cerebellar parts of the brain and in the spinal cord, which is an unexpected finding, and may relate to age of onset. Again, the analogy will be drawn by our critics between these cases and those described in the first paper with more extensive spongy appearance in the spinal cord and the suggestion is likely to be made that the five young cases again represent a new form of the disease which, by extension, can be 'caught' and was no doubt caught from cattle. These are major leaps of logic but cannot be ruled out on the basis of the available evidence. It is far too premature to draw any conclusions and much work needs to be done on previous cases in the UK and on cases from abroad . . . ⁴⁶

Discussion

Was Mr Eddy's minute adequate?

7.152 At the meeting Dr Will repeated Dr Ironside's view that it was premature to decide that the identified subset of CJD in young people was linked with BSE. This statement, of itself, indicated that it was a real possibility that the link would be subsequently made out.

7.153 We were concerned that Mr Eddy's minute did not record the concern about the implications of the young cases expressed by Professor Pattison, as recorded in the minutes, ⁴⁷ the concern on this subject expressed by Professor Collinge, as recorded in the minutes, ⁴⁸ or Professor Collinge's equal concern that the findings were likely to represent the transmission of BSE to humans. ⁴⁹ Although it is not minuted, we accept his evidence that he had expressed this concern, for we have no doubt that it was one that he felt.

7.154 On our reading of Mr Eddy's minute, he was setting out to warn Ministers and senior officials that the two papers to be published by Dr Will were likely to result in presentational problems. The reference to the need for 'careful handling' suggests to us careful handling of the media.

7.155 Mr Eddy told us that he believed that he intended to alert Ministers and officials to the problems of handling the situation generally; his comments were not intended to be restricted to media handling. When we come to consider the reaction to Mr Eddy's minute we shall see that Mr Hogg probably read it in the same way that we did. Others, and in particular Mrs Browning, told us they regarded the minute as a more general warning.

7.156 Mr Eddy very frankly told us that he had some difficulty in following the implications of the discussion at the SEAC meeting. He did not understand that there was a 'real possibility' as opposed to a 'possibility' that SEAC would conclude that BSE had transmitted to humans. ⁵⁰ Because of the difficulty he had with the subject matter of his minute, he sent a draft of it to Dr Wight, raising various queries and asking for her assistance to ensure that he had got everything right. Dr Wight made extensive amendments. Mr Eddy commented in evidence:

I think that reflects the point which came out, I think, in Professor Will's evidence this morning, that CJD was a complex area; that it was a human health issue; that it was Department of Health, and the CJD Unit which was financed by the Department of Health, where the expertise lay; that we in MAFF had to really just follow what we were told by the Department of Health and what was said at SEAC meetings. We had no in-house expertise. Quite frankly we found some of it rather difficult to follow.

I am sure the Committee sailed through this morning with flying colours, but I can assure you that as someone who is not trained in epidemiology and neuropathology and histopathology, that some of us find it rather difficult to follow. I was very concerned that although I wanted to let the Minister know that there were potential papers being published, I was very concerned to make sure I got it right, because I really did not think I had. I was finding it very difficult to understand, which is why I wanted to make sure that the advice I put to Ministers reflected the Department of Health's analysis of where we had got to; and that in a particular area where I was not clear, and that if they were in doubt they should go back and check with the unit themselves. ⁵¹

7.157 Mr Eddy may not have been able to follow all the details of the two papers that Professor Will intended to publish. We feel, however, that he must have appreciated the nature of the concerns expressed by Professor Pattison and Professor Collinge and that, although it was premature to draw conclusions, there was real concern that the five young cases, which showed an unusual pathology, might prove to be linked with BSE. Had he reported those concerns, it would have been plain that there was more than presentation to be worried about. We consider that he should have done so.

7.158 In a written statement Mr Eddy told us:

As far as I was concerned, in my minute of 6 February 1996 I had very clearly pressed the fire bell and those who needed to know in the senior management chain were clearly alert to the problem.

I believe the minute of 6 February 1996 gave a reasonable summary of the overall tone of the meeting and left senior management in no doubt of the issues. ⁵²

7.159 We do not consider that Mr Eddy's minute 'pressed a fire bell', nor do we believe that he intended it to have this effect. Had he referred to the concerns expressed by Professor Pattison and Professor Collinge, this would have drawn the reader's attention to the implications of the subject matter of Dr Will's proposed publications. In the event the reader was left to draw his or her own conclusions. What conclusions were drawn from the minute we shall consider in due course. We turn next to consider Dr Wight's perception of the significance of the SEAC meeting.

Dr Wight's minute

7.160 On 6 February 1996, Dr Wight minuted Sir Kenneth Calman's Private Secretary. ⁵³ Dr Wight stated:

There are now 5 confirmed cases in the UK in patients under 30 years of age, all presenting in the last two years. It is likely that these will be sporadic rather than familial cases. This is clearly unusual compared with earlier data on the age distribution of disease. The course of the disease appears to be somewhat longer in those with a younger age of onset, and the pathology in these cases is distinct, with very extensive plaques in the cortex, cerebellum and also spinal cord. It appears that with newer staining techniques, a major quantitative change in plaque formation is detectable, common to young UK cases.

Comparative information on young cases in other countries is being sought. The detailed findings will be submitted for publication later in the year, and although it is premature for any conclusions to be drawn, clearly the media could make much of this in terms of BSE being responsible for a 'new' type of disease pattern.

A paper is currently in preparation by the CJD Surveillance Unit which describes variations in the degree and site of plaque formation in a subset of cases of sporadic CJD. Again, this could be interpreted by some as signalling an aetiological link with BSE.

Further, there are some loose similarities between the appearances in this subset and in the young onset cases, and that found in hGH [human growth hormone] recipients, where there is a peripheral route of exposure as would be the case if there was any link with sporadic disease to BSE. This could add to the possibility of misleading deductions being made when these various findings are published. ⁵⁴

Was Dr Wight's minute adequate?

7.161 The facts reported by Dr Wight were, on the face of it, cause for concern. Five confirmed cases of CJD in victims aged under 30 years was more than 'unusual'. It was unprecedented. A distinct pathology was further cause for concern. But the tenor of Dr Wight's minute did not acknowledge cause for concern. Statements such as:

'. . . clearly the media could make much of this . . . this could be interpreted by some . . . this could add to the possibility of misleading deductions being made . . .'

are all phrases which suggest that there was in reality no likelihood of a link between BSE and these new variant cases of CJD.

7.162 We asked Dr Wight whether at the February SEAC meeting it looked as though 'the balloon might be going to go up': that SEAC might conclude that there was a link between BSE and the young cases of CJD. ⁵⁵ She replied:

I really cannot remember what I thought at this stage. All I can do is infer what I might have been thinking from documents. I think it continued to be worrying, but I am not sure that again we were in a position to say that it was perhaps any more probable really than it had been the month before. ⁵⁶

7.163 We asked Dr Wight whether at this stage she thought that MAFF and DH were facing a very serious situation indeed. She replied:

I do not think it was, you know, possible to conclude one way or the other. I think it was important - it was very important that the data were made public, and that we were properly equipped to deal with the publication of the data, certainly. That was perhaps at that stage where the importance lay. What does all this mean? How is it going to be interpreted? How do we handle the putting of this data into the public domain? ⁵⁷

7.164 Once again we find Dr Wight's response to the situation inadequate. The information placed before SEAC by Dr Will was cause for serious concern. While it was too soon to draw conclusions, there was a real possibility that SEAC would conclude that the new cases of CJD were linked to BSE. This was to be inferred from the concerns expressed by Professor Pattison and Professor Collinge at the meeting. We consider that Dr Wight's minute should have expressed those concerns. In the event she used language that was sedative. While a careful reading of her minute should have alerted the reader to the fact that it was cause for concern, Dr Wight should have put this beyond doubt by referring to the concerns expressed by the two professors.