STRICTLY EMBARGOED UNTIL 10.30 A.M. ON
TUESDAY 28TH JANUARY 2003
IN THE COURT OF APPEAL (CRIMINAL DIVISION)
2002/3824/Y3
IN THE MATTER OF A REFERENCE BY THE CRIMINAL CASES REVIEW
COMMISSION
THE QUEEN
v.
SALLY CLARK
Appellant
_____________________________
SKELETON ARGUMENT ON
BEHALF OF SALLY CLARK
_____________________________
1.
For nearly three years after the death of Harry Clark, his mother Sally Clark, her
lawyers and their medical advisers believed that there was not any evidence of infection
or any possible natural explanation of his death. The cause of his death was mysterious
and, in the language of the medical profession, “unascertained”.
2.
At the end of 2000 it emerged, for the first time, that there was clear evidence of an
infection with staphylococcus aureus that had spread as far as Harry’s cerebral spinal
fluid (CSF). This fluid should be sterile in a healthy child, protected from harmful
substances in the blood by the blood brain barrier. The evidence of this infection had
been known to the prosecution pathologist, Dr Williams, since February 1998. He had
kept the results secret from Sally Clark and her advisers.
3.
This is a clear case of non disclosure by the prosecution. This non disclosure has caused
a serious miscarriage of justice. The microbiological test results on Harry Clark
demonstrate that, in all likelihood, he died suddenly, in reaction to the staphylococcus
aureus bacteria with which his stomach, lungs and CSF were riddled.
4.
It requires no degree of expertise to realise that the test results should have been
revealed by Dr Williams and not kept secret. It is obvious that, if the results been made
known at trial, Sally Clark would not have been convicted of murdering Harry or his
dead brother, Christopher.
5.
It is a matter of regret that the prosecution has failed to accept that there has been any
material non disclosure in this case. Instead an attempt has been made to minimise the
importance of the microbiological test results. This has wholly failed. It is plain even
from the statements made by the prosecution expert witnesses, that the results were
material, in the sense described in R v. Judith Ward1, in that they might arguably have
assisted the defence at trial.
6.
Each of the prosecution experts has conceded that it is possible that Harry died of acute
staphylococcal infection. The area of disagreement between the prosecution and
defence experts is the degree of likelihood to be attached to that possibility.
7.
Dr Keeling’s conclusion is; “The concept of an infectious cause of death was not
considered by any of the experts at the original trial. Now that the concept of infection
has been introduced it is important to appreciate that the case for infection is being
made on the basis of positive cultures. Positive cultures alone are not sufficient
evidence of the presence of disease; they can be artefactual as the result of
contamination.2” (Emphasis added).
8.
Dr Klein’s opinion is that; “While there is no doubt that the sequence of events as
described [by Dr Morris of an infection and toxic reaction causing bleeding] could
occur in an infant of Harry’s age it would be exceedingly rare in an otherwise healthy
individual.3 ”
9.
Dr Wilson concludes that, in his view, the staphylococcus must have spread in the
blood stream before Harry’s death. The absence of toxins does not exclude the
organism being contributory to death. The white cell response in the CSF is probably
1
(1993) 56 Cr App R 1
Keeling Pros A/3A/12
3
Klein Pros A/3C/12
2
2
related to a bleed but the presence of early meningitis is not excluded. “S. aureus and/or
its toxin is suspected to be a cause of SIDS but the mechanism has not been elucidated.
It can cause petechial haemorrhages secondary to circulatory failure and toxin release.4”
10.
An attempt has also been made by the prosecution, in the alternative, to say that the
biochemical tests were so obviously flagged that they were effectively disclosed and it
is the fault of the defence that the results were not discovered.
11.
Finally and bizarrely it is suggested that the results were known to the defence but were
discounted or disregarded because they were irrelevant.
12.
The last two suggestions may be rapidly disposed of. In his second affidavit, Michael
Mackay has confirmed that none of the defence lawyers were made aware of the
results5. This mirrors the position of the CPS which asserts that none of the prosecution
lawyers knew of the results6.
13.
The assertion by the CPS is accepted, subject to the caveat that any prosecution lawyer
who inspected file 89 at court (in which the results were probably stored7) may have
become aware of the results and should then have disclosed them.
14.
The prosecution skeleton disingenuously suggests that the test results “were always
available for inspection”8. This is not true. The results may, as it transpires, have been
available for inspection by the prosecution in police file 89. However that was not a file
that was ever listed in the prosecution list of used and unused material. It was not
“available” to be inspected by the defence lawyers in any meaningful sense of the word.
4
Wilson Pros A/3D/9
This has now been accepted. Pros A/1/148B
6
Pros A/1/40 “The prosecution did not have a copy of the microbiological reports that were significant in
triggering the Commissions decision.” Pros A/1/142 “The results were not at any stage within the possession of
the police. It follows that the results of those tests were not supplied to the prosecution.”
7
Pros A/1/68 see also A/1/226
8
Prosecution skeleton 1.4(b)
5
3
15.
The prosecution also suggest there was disclosure because the fact of testing was
revealed, even if the results were not9. This suggestion is wrong. Disclosure is not
meant to be a game where the defence guess what may be relevant with the benefit of
hints dropped by the prosecution. Unless and until the existence of positive
microbiological results are made known to the defence and copies of those results are
supplied or inspection invited, they cannot be said to have been disclosed.
16.
The prosecution argument appears to have overlooked the fact that the professional and
legal obligation to effect disclosure by providing copies or inviting inspection has been
clear for more than 20 years. The old Attorney General’s Guidelines10 required
disclosure to be effected by provision of a copy, either by post, by hand, or via the
police. If the unused material exceeded about 50 pages or was unsuitable for copying,
the defence solicitor had to be given an opportunity to inspect it at a convenient police
station or, alternatively, at the prosecuting solicitor's office. The House of Lords has
held (in overturning the rule in Bryant and Dixon)11 that the common law requires the
physical disclosure of police witness statements by the provision of a copy. The
Criminal Procedure and Investigations Act 1998 (the CPIA) requires disclosure to be
effected by copying the information to the defendant or, if that is not practicable or
desirable, allowing the defendant to inspect it12. The decision in R. v. X Justices ex
parte J13 has made it clear that there is in all criminal cases a strong presumption in
favour of the provision to the defence in good time of copies of all copiable exhibits. It
is for the prosecution to displace that presumption. No factors justifying the
displacement of that presumption have been identified.
17.
So far as the defence medical experts are concerned, all bar Professor Emery (who died
before the results were disclosed) have been contacted. Each has confirmed that results
were not disclosed by Dr Williams or seen by them in the course of the case.
9
Prosecution skeleton 4.30 (a)
(1982) 74 Cr. App. R. 302 Paras. 4 & 5
11
R. v. Mills and Poole [1998] AC 382
12
CPIA ss 3(3)-(5), 7(4), 9(7)
13
[2000] 1 All ER 183
10
4
18.
Professor Berry has said in terms he was never told about the results. Indeed he seems
to have been misled into believing that there was a negative result in relation to the
microbiology tests performed on Harry. In his report dated 3.9.99, he stated that neither
Harry nor Christopher “showed any symptoms in life, nor was the mode of their death
compatible with infection. All tests for infection were negative with the exception of the
unremarkable finding of Staph. aureus in the respiratory tract of Christopher.”
19.
Contrary to the suggestion by the prosecution that his opinion would have been
unaffected by knowledge of the results14, Professor Berry has made it clear that the
results were “very unusual” and would have had a significant impact on his opinion as
to the cause of Harry’s death15.
20.
Dr Rushton is equally confident that he was not made aware of the results at the time of
the trial. Had he been he; “would certainly have investigated the significance of the
isolation of the staphylococcus by consulting my microbiological colleagues”. He has
concluded on the basis of the reports now available from the defence micro biologists
that the death of Harry was due to staphylococcal infection16.
21.
Professor Luthert has also confirmed that he was not aware of the results. He described
the situation on non disclosure to Mike Mackey as “blood chilling”17. He has also stated
that he would have no difficulty in reconciling the episcleral haemorrhages at the back
of Harry Clark’s eyes with death arising from septicaemia.
22.
Professor Whitwell has confirmed that she was not told of the results18. She understood
Dr Williams assertion to the effect that there was no evidence of disease to be a
confirmation that the microbiological results were negative.
23.
Each of these experts has also confirmed that they relied upon the prosecution doctors
to disclose all relevant results. This is obviously the proper approach, both as a matter
14
Prosecution skeleton argument 1.4(c)
Berry Defence Disclosure bundle item 37
16
Rushton Defence Disclosure bundle item 34
17
Mike Mackey second affidavit para 33
18
Mike Mackey second affidavit para 34
15
5
of law and as a matter of common sense. The only contrary suggestion comes from Dr
Keeling who herself failed to seek the results. She excuses that omission by reference to
her late involvement19. This is not an issue that needs to be resolved for the reasons set
out in the Defence Note of November 2002. If this is not a case of prosecution non
disclosure, it is a fresh evidence case in which relevant and credible fresh evidence is
now available.
24.
Professor David (the court appointed expert who gave evidence for the defence with the
leave of the family court judge) has been contacted by prosecution counsel. Following
that contact prosecuting counsel has suggested that the results may have been disclosed
to Professor David because “it is still not known for sure whether the microbiology
results were in fact in the papers supplied to Professor David 20.” Given Professor
David’s response in his letter dated 6th December 200221 this seems a far fetched basis
on which to claim the tests results were disclosed.
25.
Professor David has been explicitly dismissive of the prosecution suggestion that the
results may have been disclosed to him, but ignored, because he regarded them as
irrelevant. His letter states:
“What is so extraordinary is that these results were obviously of special interest to the pathology
department to the extent that the samples were actually sent away to the headquarters of the public health
laboratory service for further testing and yet, despite this step being taken, none of the results were
disclosed. The PHLS in Colindale is the national reference laboratory for microbiology and I am at a loss
to understand how all these results and laboratory data did not come to be passed into the care
proceedings papers. There is no doubt that had these results been available, I would have referred to them
in my report and I would have investigated their possible significance further not only in relation to the
death of Harry but also the death of Christopher.”
19
Keeling ProsA/3A/11, see also A/1/125
Prosecution skeleton argument 3.36-3.38
21
Defence Disclosure bundle p. 35 “… [I]t is inconceivable that I could have seen all these [microbiology]
results and then totally forgotten all about them.”
20
6
Non disclosure
26.
Unfortunately this case demonstrates that the lessons that should have been learned, as a
result of the decision of the Court of Appeal in Ward22, have not been. The duties of the
prosecution and of the forensic experts instructed by the Crown were spelt out in clear
and uncompromising terms in Ward. The scope of that duty has not been affected by the
coming into force of the CPIA since the CPIA does not affect the common law duty of
disclosure of expert witnesses, see Archbold 10-68.
27.
The Court in Ward dealt with the critical importance of ensuring that there is a proper
understanding of the nature and scope of the prosecution's duty of disclosure in relation
to expert scientific witnesses. The prosecution barrister in that case had suggested that
the problem was solved by the Crown Court (Advance Notice of Expert Evidence)
Rules 1987 that enable the legal representatives of a defendant in a Crown Court
criminal case to require the prosecution by notice in writing to provide in respect of
scientific evidence a copy of (or an opportunity to inspect) “the record of any
observation, test, calculation or other procedure on which (any) finding or opinion is
based.” The Court observed: “The new rules are helpful. But it is a misconception to
regard them as exhaustive: they do not in any way supplant or detract from the
prosecution's general duty of disclosure in respect of scientific evidence. That duty
exists irrespective of any request by the defence. It is also not limited to documentation
on which the opinion or findings of an expert is based. It extends to anything which
may arguably assist the defence. It is therefore wider in scope than the rule. Moreover,
it is a positive duty, which in the context of scientific evidence obliges the prosecution
to make full and proper enquiries from forensic scientists in order to ascertain whether
there is discoverable material. Given the undoubted inequality as between prosecution
and defence in access to forensic scientists, we regard it as of paramount importance
that the common law duty of disclosure, as we have explained it, should be appreciated
by those who prosecute and defend in criminal cases. And, if difficulties arise in a
particular case, the court must be the final judge.23”
22
23
(1993) 56 Cr App R 1
pp 52-53
7
28.
Even for a layman it should have been readily apparent that the microbiology tests
results might raise two or more medical issues in connection with the death of Harry
Clark. The first obvious issue was whether the results indicated staphylococcus aureus
infection. The second issue was, assuming that there was an infection, what effect might
that have had on Harry’s condition.
29.
In Keane24 the Lord Chief Justice made it clear that the documents that must be
disclosed as 'material' are those that can be seen; “on a sensible appraisal by the
prosecution: (1) to be relevant or possibly relevant to an issue in the case; (2) to raise or
possibly raise a new issue whose existence is not apparent from the evidence the
prosecution proposes to use; (3) to hold out a real (as opposed to fanciful) prospect of
providing a lead on evidence which goes to (1) or (2).25”
30.
Any qualified medical practitioner or prosecutor who was shown the microbiology
results ought to have appreciated that they might possibly raise issues in the case of
Sally Clark, whose existence would not be apparent from the evidence the prosecution
proposed to use.
Good faith?
31.
It is submitted that the non disclosure must have been deliberate, since it is to be
assumed that the prosecution asked appropriate questions to ascertain whether there was
discoverable material in Harry’s case. Questions such as: “Are there any test results
relating to Harry Clark that have not already been disclosed?” must have been posed.
The prosecution must have been told, wrongly, that there were not.
32.
This appears to be the explanation for the assurance given by the solicitor to the Police
Authority (following discussions with the CPS and DI Gardiner) in April 1999 that
there were no further autopsy reports other than those already disclosed26.
24
Keane [1994] 1 W.L.R. 746
pp 751-752
26
Defence Disclosure bundle pp. 19-29 “I confirm that in respect of paragraph 6 [request for any autopsy report
not already disclosed] you have been informed and accept that there are no further reports.”
25
8
33.
It is appears that responsibility for the deliberate non disclosure lies with Dr Williams.
He was the sole named recipient of Dr Wills’ reports. He is most likely to have
provided the false or misleading information that the CPS and Police Authority solicitor
relied upon.
34.
Dr Williams’ explanation for his failure to disclose the reports is wholly unsatisfactory.
His claim to the meeting of experts that there was no evidence of infection in Harry’s
case27 was, on its face, untrue. His present position is equally incredible28.
35.
On one view the question of Dr Williams’ credibility may be something of a side issue
for the reasons identified in the Defence Note of November 2002. If the Court
concludes that the microbiology results were not disclosed and that the expert opinions
now obtained, commenting on the relevance of the results, amount to credible fresh
evidence going to a relevant issue in the trial, then the appeal should be allowed.
36.
However it is submitted that the fact of a deliberate non disclosure will impact on Dr
Williams’ credibility, competence and claimed impartiality. This is of significance since
the majority of the critical points in the prosecution case depend upon disputed and
inadequately documented ‘findings’ by Dr Williams.
37.
Thus the case on Christopher in relation to the ‘nick’ in the frenulum and the presence
of abrasions or bruises depends entirely on Dr Williams’ evidence. Without that
evidence, the only relevant medical evidence relating to Christopher that was properly
recorded and capable of being independently investigated were the slides of
Christopher’s lungs showing bleeding and haemosiderin and the test results relating to
Christopher’s blood chemistry. No expert has suggested that the slides of the lungs are
capable of establishing a case of murder. At its highest, the presence of bleeding merely
Defence Disclosure bundle pp. 30 Answer 2(d) “A finding of this kind [a swelling in the cord within the dura],
could indicate injury, infection or perhaps a tumour. Dr Williams thought there was no evidence of either
infection or tumour.”
28
Pros A/1/47 “It is clearly stated in the second paragraph in my report that microbiology samples were taken.
In conclusion I mention that there is no evidence of infection this would mean that I had seen the microbiology
reports.”
27
9
requires close attention29. In the absence of any other material it is not does not
establish the cause of death.
38.
Dr Williams’ credibility is also of acute significance in Harry’s case. Much turns on Dr
Williams’ denial of the allegation that many of his findings were artefactual, caused by
his faulty post mortem technique. For example, in the original police investigation,
great significance was attached to his finding of haemorrhages in the eye. In the course
of discussions between the experts it became apparent that Dr Williams could not tell
the difference between the choroid and the retina. In the event, by the time of trial it
was accepted that there were no relevant retinal haemorrhages. However, both at trial
and on appeal, attention was given to the ‘finding’ by Dr Williams of scleral
haemorrhages. The defence case is that they are artefactual. Dr Williams’ competence
and credibility is therefore directly in issue on this point.
39.
Similar issues arise in relation to Dr Williams ‘finding’ of bleeding and swelling in
connection with Harry’s spinal cord. The claimed swelling was not detectable in the
sections taken by Dr Williams. The bleeding was likely to be post mortem in origin, in
the view of the defence experts.
40.
The suggestions that there was a dislocation between the cartilage and the bone of
Harry’s right second rib and a callus formation on his rib are similarly dependent on the
reliability of Dr Williams’ observation. There was no evidence of fracture on the X ray
and no adequate attempt was made to document the ‘finding’, either photographically
or histologically. The existence of a fracture or dislocation is also quite inconsistent
with Harry’s observed well being at all times prior to his death.
41.
Dr Williams’ claim that the biochemistry results were irrelevant does not stand up to
scrutiny. The detailed forensic attention that has been paid to the results for the
purposes of this appeal underlines the fact that it is highly unlikely that a skilled and
conscientious pathologist would have ignored the results and treated them as unworthy
of mention. For this reason alone, the defence does not accept Dr Williams’ explanation
29
Professor Byard has pointed out that it is now appreciated that bleeding in the lung may be affected by the
interval before post mortem, attempts at resuscitation and the position of the child’s body after death.
10
for not referring to the results in his reports, in his discussion with defence experts and
in his evidence at trial.
42.
Prof Berry describes the results as “very unusual”30. Dr Morris describes them “highly
significant31”. Dr Walters says they are “most unusual”32 and adds that to find
staphylococcus aureus as a contaminant with the presence of polymorphs in two sites
would be “remarkable”33. Prof Fleming confirms this. Staphylococcus aureus “is not a
common organism to be isolated from multiple deep sites at post mortem and is very
rarely isolated from the CSF”34. Even Dr Wills suggested in his original letter to Dr
Williams that: “It is somewhat unusual to find a contaminating organism so widely
spread and it may be that there was a transient or terminal bacteraemia [The presence of
viable bacteria circulating in the bloodstream].”35.
43.
For the prosecution, Dr Keeling accepts that “CESDI36 study findings (no SA cultured
from CSF) indicate that it is an unusual occurrence and its significance should be
considered most carefully. Sonnabend et al 1985 accept a pure culture of an organism in
the CSF is evidence of pathogenicity [the ability of a parasite to inflict damage on the
host].”37
44.
The standard protocol for pathologists in the investigation of sudden unexpected
deaths38 requires the “bacteriological examination of bloods, cerebrospinal fluid and
lung to rule out septicaemia, meningitis and bacterial lung infection respectively”. The
standard work on the Principle and Practice of Infectious Diseases39 emphasises the role
played in the diagnosis of bacterial meningitis by a CSF examination.
30
Berry
Morris ProsA/2A/1
32
Walters ProsA/2B/3
33
Walters ProsA/2B/6
34
Fleming
35
Wills
36
The CESDI SUDI Study, (Sudden Unexpected Death In Infancy. The CESDI SUDI Studies 1993-1996. Eds.
P.J.Fleming and others. Pub.The Stationery Office, London,. 2000. ISBN 0 11 322299 8
37
Keeling ProsA/3A/11
38
CESDI Chapter 4 page 97
39
Mandel et al
31
11
45.
For Dr Williams to dismiss the reported finding of staphylococcus aureus in the
cerebrospinal fluid (CSF) coupled with the presence of white blood cells, polymorphs,
lowered glucose and a raised protein level without any discussion or disclosure is
extraordinary.
46.
The failure by Dr Williams to refer to the test results is also a clear departure from best
practice. There is evidence that, in the context of a police investigation or a coroner’s
inquiry, a pathologist should record the outcome of all results, whether positive or
negative, in his report40. In the absence of such action by the pathologist there appears
to be no mechanism for informing the authorities, such as the police, the coroner, and
the CPS of the results41. As Dr Walters observed “an autopsy report that does not
include the results of supplementary tests is an incomplete record of the examination,
capable of misleading anyone who consults it in the future.”42
47.
Dr Keeling, for the prosecution, agrees with this. “Reports of all investigations done
outwith the pathology department are reported in full including the accession number to
facilitate any discussions at a later date.43”
48.
The best practice is in fact exemplified in Dr Williams’ own report to the coroner where
he reports his negative findings. Features that were said by Dr Williams to be irrelevant
on analysis (such as a mark on Harry’s cheek), were identified and carefully explained
in his report.
49.
Furthermore, even if Dr Williams may claim that he was entitled to regard some of the
results obtained as contamination; it is plain that some of the results were not. The
transient bacteraemia suggested by Dr Wills and the identical phage typing suggest that
there was staphylococcus aureus in Harry’s airways. This finding should have been
reported, just as it was in the case of Christopher, even if it is then dismissed as being
unexceptional.
40
See Berry [], Whitwell [] and Luthert Defence Disclosure bundle p. 36
Wills ProsA/3B/6-7 Dr Wills has confirmed that Dr Williams is the sole recipient of his reports.
42
Walters ProsA/2B/15-16
43
Keeling ProsA/3A/11
41
12
50.
If, as Professor Green claims44, Dr Williams told him about the results in Harry’s case
(although Dr Williams does not claim to have done so), that can only serve to confirm
the proposition that the results should have been disclosed in order that they could be
taken into account by others. There is no excuse for Dr Williams not providing the same
information to Professor Emery and Dr Rushton when they performed the second post
mortem. The only purpose in reporting the results to Professor Green can have been
because they were potentially relevant to anyone providing a second opinion. They
would have been equally relevant to Professor Emery and Dr Rushton.
51.
In fact Professor Green’s note does not support either Dr Williams’ claim that the
finding of staphylococcus was irrelevant, or Professor Green’s own memory that
Harry’s results were discussed.
52.
The prosecution quotation from the note in its skeleton argument is incomplete and
misleading45. The note records46:
“Christopher Clark was brought in dead to Macclesfield hospital shortly after 9.30pm. He was alone with
his mother and was allegedly being nursed in his bouncy chair. She had breast fed him a few hours
previously. Dr Williams was concerned that the child had various minor bruises and abrasions (although
the post-mortem photographs are of very poor quality). The child also had a torn frenulum, but as
resuscitation had been attempted, Dr Williams felt he should give the child “the benefit of the doubt”.
Staphylococcus aureus was grown from various swabs, and therefore although the histology showed no
convincing signs of infection, this was written off as a cot death. …
He [Dr Williams] had made no comment on the histology of the lungs of Christopher Richard Clark
except to note the presence of “focal inflammation”. Again specimens from this child grew a
staphylococcus.”
(Underlined part quoted in prosecution skeleton argument and said to be a reference to
Harry)
44
Pros A/1/110
Prosecution skeleton 3.22 (a)
46
A/1/111-2, 115-116
45
13
53.
The significance of the note (if it is accurate) from the point of view of the defence, is
that in 1998 Dr Williams was prepared to ascribe significance to the finding of
staphylococcus aureus (in Christopher), a proposition he has since been forced to ignore
in his efforts to excuse his non disclosure in the case of Harry. It will be observed that
the note provides no support for the proposition that the finding of staphylococcus in
Harry was discussed. It strongly suggests that it was not.
54.
The note also suggests that the failure to report Harry’s results was a clear departure
from Dr Williams’ own practice of reporting biochemistry results. It supports the
possibility that the non disclosure was deliberate and motivated by partisan
considerations.
55.
The partisan motives may also be evident in the fact that Dr Williams persistently failed
to correct the defence experts, all of whom proceeded on the basis that there was no
evidence of infection. For example Professor Berry in his report dated 3.9.99 stated that
neither Harry nor Christopher “showed any symptoms in life, nor was the mode of their
death compatible with infection. All tests for infection were negative with the exception
of the unremarkable finding of Staph. aureus in the respiratory tract of Christopher.”
56.
Even if Dr Williams did not supply this inaccurate information to Professor Berry, he
must have noticed Professor Berry’s error and should have corrected it.
57.
The whole trial proceeded on the basis that there was no natural explanation for nonartefactual bleeding in Harry, no evidence of natural disease and no natural explanation
for his death47. Defence experts were repeatedly forced to concede that there was no
evidence of infection or other natural causes48. Sally Clark was driven to accept that she
could not explain how Harry died or why he might have bled. Dr Williams never
volunteered the information that there was evidence of infection (even if he personally
did not believe it).
47
48
Keeling ProsA/3A/12
See analysis of trial transcripts
14
58.
When the jury asked “Are there blood tests results for Harry?” Dr Williams gave a
deliberately misleading answer. The degree of deliberation involved is confirmed by the
fact that it is now clear from the police investigation, carried out in 2002, that Dr
Williams must have consulted the files that contained toxicology, virology and
microbiology49 results for Harry before answering the question.
59.
Robin Spencer QC has devoted 16 pages of his skeleton argument50 to an attempt to
excuse and explain what was, on any view, an incomplete answer given by Dr
Williams.
“Q
Can I turn to the blood sampling for Harry? Have you been able to make enquiries and check
the records in respect of Harry?
A We’ve looked at the records as far back as we can. …
Q Was a blood sample taken from Harry at post mortem when you carried the post mortem out?
A Yes, a sample is always taken at post mortem.
Q Do you know what was done with that?
A That was submitted for toxicological examination and some of it would have been sent for viral
studies.”
60.
Whilst the explanation fashioned by Mr Spencer (in the absence of evidence tested
under cross examination from Dr Williams) might just be possible if, as he suggests, the
question was misunderstood by Dr Williams, it is not a likely explanation. It is
extraordinary that Dr Williams should choose to refer only to toxicology and viral
studies when he knew that there has also been microbiological testing. All are equally
remote from the topic of blood chemistry that Mr Spencer suggests lay behind the jury
question and Dr Williams’ answer.
The non disclosure was material/Fresh evidence
61.
As the Court will appreciate from the Defence Note of November 2002, it is submitted
that the success of this appeal is not dependent on the prosecution non disclosure. The
appeal could be allowed on the grounds of fresh evidence alone. The evidence of the
49
50
Pros A/1/68 see also A/1/226
Pages 29-45
15
defence experts is plainly capable of belief. It would have been admissible at trial.
There is a cogent explanation for the failure to call it at trial, namely that the defence
did not know that there had been a positive result obtained from the microbiological
testing.
62.
The only relevant issue in connection with the fresh evidence is whether the evidence
may afford a ground for allowing the appeal. As the House of Lords indicated in
Pendleton51, the Court is entitled to form a view on whether the evidence give rise to a
reasonable doubts about the verdict. The Court should however recognise it is at a
disadvantage in seeking to relate that evidence to the rest of the evidence which the jury
heard. “For these reasons it will usually be wise for the Court of Appeal, in a case of
any difficulty, to test their own provisional view by asking whether the evidence, if
given at the trial, might reasonably have affected the decision of the trial jury to
convict. If it might, the conviction must be thought to be unsafe.”
63.
There are three questions that may have to be answered in assessing materiality or the
safety of the conviction. The first question is whether the results may have been caused
by infection rather than contamination? The second question is what may be the effect
of staphylococcal infection? The third question is the issue canvassed above, namely
the impact on Dr Williams’ credibility and competence of the fact of deliberate non
disclosure.
1. Contamination?
64.
There is no plausible basis for assuming contamination. The finding of staphylococcus
aureus in the CSF is highly unusual52. In studies53 of hundreds of sudden infant deaths,
there has been only 1 case in which the CSF was found to be infected with
staphylococcus aureus and 7 where staphylococcus aureus was found in the blood.
Since it is common and unremarkable for such infants to have staphylococcus aureus in
51
R. v. Pendleton [2002] 1 Cr.App.R. 441 at 454
Morris ProsA/2A/3; Walters ProsA/2B/3
53
The CESDI SUDI Study; The Avon study, RE Gilbert and others. Combined effect of infection and heavy
wrapping on the risk of sudden infant death. Arch. Dis. Child 1992;67:272-277 and OAR Sonnabend and others.
Continuous microbiological and pathological study of 70 sudden and unexpected infant deaths. The Lancet 2nd
February 1985
52
16
their airways54, it is astonishing if the mechanism of contamination favoured by Dr
Keeling is possible or even likely, that staphylococcus aureus has not been found more
widely in the blood and CSF of dead infants.
65.
In addition, the absence of staphylococcus aureus in the blood suggests that any
contamination did not occur during resuscitation or after death. The only physical
medium in which staphylococcus aureus in the airways, lungs or stomach could be
transferred so as to contaminate the CSF is the blood55. The absence of staphylococcus
aureus in the post mortem blood sample suggests that contamination did not happen at
the point of death or resuscitation since there would be no mechanism for the
staphylococcus aureus to disappear from the blood and yet remain in the CSF.
66.
The absence of staphylococcus aureus in the blood sample taken by A&E has no
significance either way since the sample may not have been large enough 56 In any event
a negative culture does not exclude infection57.
67.
Overall the absence of staphylococcus aureus in the blood argues strongly in favour of a
infection in life that Harry’s defences may have cleared from his blood but whose
presence elsewhere had not be cleared and killed him. This appears to be a possibility
accepted by Dr Wilson for the prosecution58.
68.
The fact that the finding is of a single pure organism also suggests there is no
contamination. Contamination caused by intubation or resuscitation might be expected
to spread a variety of organisms, not a single organism59.
69.
The case for contamination is undermined by the levels of red blood cells and
leukocytes (white blood cells) plus polymorphs in the CSF60. The presence of
54
Morris ProsA/2A/2-3, Keeling ProsA/3A/3, Klein ProsA/3C/1, Wilson Pros A/3D/4
Keeling ProsA/3A/9
56
Blackwell, Wilson Pros A/3D/8
57
Morris
58
Wilson Pros A/3D/5-8
59
Morris ProsA/2A/4, Walters ProsA/2B/41, Keeling ProsA/3A/3, see also Nolan and Beatty. Staphylococcus
aureus bacteraemia April 1976 The American Journal of Medicine vol 60 p 496-7.
60
Walters
55
17
polymorphs can only be explained by a reaction to infection or irritation in life61. This is
conceded by Dr Keeling62. Dr Wills for the prosecution agrees that the presence of
white blood cells indicates an inflammatory reaction.63 Dr Wills also concedes that:
“The polymorph cells [in the CSF] are suggestive of a bacterial infection,64” although
he goes on to says that the response is too low for meningitis. Dr Wilson states that
“polymorphs in the CSF do suggest a reaction to inflammation before death, as the ratio
of red to white cells is not what would be expected from a simple leak of blood into the
CSF.65”
70.
The attempt to explain the polymorphs and white blood cells by reference to a
prosecution theory that Harry had been shaken and had bled into his CSF in the last 2 to
3 hours of his life does not stand up to scrutiny.
71.
Not only is the number of red cells minute (no more than a pin head of blood) and
insufficient to cause irritation, but the reaction to the presence of that blood in the CSF
would account for only 1 of the 80 leukocytes plus polymorphs observed66. Dr Wills
has conceded this, albeit at a late stage67. The only available and plausible explanation
for the remaining 79 leukocytes is the presence of the staphylococcus aureus.
72.
The blood irritation theory also provides no explanation for the presence of
staphylococcus aureus and polymorphs in the stomach68. No one has suggested bleeding
at that site or the presence of any other irritant69. Dr Wilson considers that this also
points towards an infection during life70. His conclusion is “that it is not possible to
exclude meningitis in addition to bleeding into the CSF”.
61
Walters ProsA/2B/3
Keeling ProsA/3A/10
63
Wills ProsA/3B/13
64
Wills ProsA/3B/11
65
Wilson Pros A/3D/5
66
Morris ProsA/2A/4-5 and [] Walters ProsA/2B/8 and [] see also Byard and Fleming
67
Wills ProsA/3B/16 “The white cells cannot be solely accounted for by the leakage of blood”.
68
Wills ProsA/3B/3
69
Walters ProsA/2B/3
7070
Wilson Pros A/3D/5
62
18
73.
The presence of staphylococcus aureus, in life, for several hours is also supported by
the presence of polymorphs71 coupled with the raised protein levels, the reduced
glucose levels72 and the colour of the CSF.
74.
At a late stage the prosecution experts appear to have abandoned the attempt to make
the microbiological facts fit the theory advanced by Mr Spencer that “Harry had been
subjected to some trauma two to three hours prior to death, by shaking or otherwise
…73.”
75.
It is now suggested by the prosecution, in yet another attempt to make the facts fit a
murder charge, that the microbiological results are the result of much older bleeding.
This is unacceptable for a number of reasons.
76.
First it is noteworthy that the shift of ground seems to be justified by reference to the
disputed finding by Dr Williams of a rib fracture and haemosiderin around Harry’s
cord. Second the suggested early bleeding makes no sense. It would take a considerable
and significant bleed to raise the protein to 3.24gms/litre. This must have occurred at
least 10 days prior to death as it would take at least that time to clear the red cells (only
230 per microlitre remained at the time of death). Any such bleed would have caused
Harry to be extremely ill. This would have been obvious to all concerned and he would
have required admission to hospital and intensive care.
77.
In fact at all times up to 4 hours prior to his death Harry was seen by a series of
independent witnesses to be healthy and well. He exhibited no signs of distress. He was
handled daily by health care workers who noticed no physical discomfort and saw no
signs of injury. At that time Harry’s CSF protein must have been normal and he could
not have been suffering from meningitis. He cannot have suffered physical trauma.
78.
The elevated CSF protein must therefore be due to events in the last four hours of his
life. If it is not a consequence of a recent bleed, the only plausible explanation is
cytokine release due to staphylococcal infection.
71
Morris ProsA/2A/8
Blackwell
73
Wills Pros A/3B/15, Wilson Pros A/3D/7
72
19
79.
The suggestion that the turbidity of the CSF and its xanthachromatic (yellow) colour
indicate bleeding has also been demonstrably destroyed74.
80.
So far as turbidity is concerned, the growth of staphylococcus aureus post mortem
would be limited for the reasons explained by Professor Blackwell75. The Avon study
confirms this. “There is no correlation between the length of time taken before post
mortem and the finding of bacterial samples.” The CESDI study also confirmed this.
“There was no clear relationship between mixed growth in blood samples and
increasing post-mortem intervals.” The contrary view expressed by Dr Klein is based
on little more than guess work76.
81.
So far as colouration is concerned, the prosecution case depends upon the proposition
that bilirubin may appear within 4 hours of a bleed into the CSF. In fact as Dr Walters
has pointed out by reference to the standard work on cerebrospinal fluid77, bilirubin
does not usually appear until 10 hours or more after the episode of bleeding. In the first
4 hours after a bleed, the CSF would be coloured pink by the process of lysis.
82.
Furthermore the presence of bilirubin would initially appear in combination with
haemoglobin and give an orange colouration. Dr Walters’ calculations have proved that
it is impossible to ascribe the colour (if correctly observed) of Harry’s CSF to the
presence of bilirubin related to bleeding78. It may be related to the increase in the
protein level79. It may more probably be related to the length of time that elapsed before
the post mortem was performed80.
83.
Any prosecution proposition that propounds that Harry must have bled into his CSF as
the result of trauma inflicted by Sally Clark is also inconsistent with two other
74
Morris []
[] See also Dr Jenkins
76
Klein Pros A/3C/16 “I have no experience of the appearance of CSF taken at post mortem. …[O]ne can only
assume that if the turbidity is due to a high concentration of organisms this was due to the growth of the
organism within the CSF [after] the removal of the fluid from Harry.”
77
Fishman: Cerebrospinal fluid in diseases of the nervous system; 2 nd Ed (1991) pp 185-187.
78
Walters []
79
Vastola. Non hemorrhagic xanthochromia of cerebrospinal fluid J Neuropath: exp.Neurol (1960) 19 296-304
at 301-304
80
Paulson and Stickney. Confin. Neurol. 33:149-162 (1971) Cerebrospinal fluid after death p159
75
20
observations. First it is impossible to postulate a form of trauma that would cause
bleeding at the site identified by Dr Williams without causing damage to other areas of
the spine. Second there is no other evidence of shaking such as would be present in a
case of shaken baby syndrome.
84.
If bleeding was present in the CSF and occurred in life it is more likely to be related to
haemorrhage caused by staphylococcus aureus toxins. It appears most likely however
that the bleeding was post mortem and caused by contamination. This proposition is
supported by the absence of any signs of haemoglobin discolouration.
2. The effect of staphylococcal infection?
85.
The second question which the court must address in connection with the issue of
materiality or safety is the effect of a staphylococcus aureus infection.
86.
It is submitted that much of what follows should be relatively uncontroversial.
Staphylococcus aureus toxins can cause bleeding81. Thus, even if it not the cause of
death, its presence is relevant to understanding the possible causes of bleeding found in
Harry. The relevant areas of bleeding were scleral haemorrhages, petechial
haemorrhages and claimed bleeding connected with the spine.
87.
Staphylococcus aureus toxins may also damage cells82. This is of importance in
connection with the changes to the cells in the temporal lobe. Dr Keeling seems to
accept this, albeit as a theoretical possibility83.
88.
Thus the existence of staphylococcus aureus infection may have helped explain all the
post-mortem findings which caused concern in Harry’s case84 (other than the disputed
evidence given by Dr Williams relating to the ribs and the finding of haemosiderosis).
This is the case even if staphylococcus aureus did not cause death.
81
Morris ProsA/2A/2 and 6; Walters ProsA/2B/3 and 2B/12-14, Keeling ProsA/3A/5, Wilson Pros A/3D/5
Morris ProsA/2A/2 and 6, Wilson Pros A/3D/5
83
Keeling ProsA/3A/12
84
Morris ProsA/2A/2
82
21
89.
It is in fact likely that staphylococcus aureus caused Harry’s death. It is not possible to
be certain of the mechanism85. All that can be said with confidence is that bacterial
toxins can kill without leaving any histological signs86. Toxic shock and septic shock87
are both possible causes of death. Staphylococcus aureus commonly causes septicaemia
without any primary focus of infection88.
90.
It is accepted by all concerned that staphylococcus aureus in the CSF can cause
meningitis, albeit infrequently89. Dr Walters’ estimate from the published data is that
staphylococcus aureus meningitis constitutes 2-10% of all cases of bacterial meningitis.
91.
If the polymorph reaction was not caused by red blood cells in the CSF then the only
possible source for the polymorphs and the raised protein is from inflammation of the
meninges. Thus, whether or not there is histological evidence of swelling in the
meninges, there must be infection in them to produce polymorphs and raise the protein
level90.
92.
The fact that the leukocyte level is above the normal limit but lower than that seen in
bacterial meningitis91 is consistent with the known delay in the rise of white cells in the
CSF after the onset of rapidly progressive meningitis92. It is also consistent with the
data that shows that cerebrospinal fluid in children shows less inflammation than for
non-infants93. Indeed children with culture proven meningitis may sometimes have
normal white cell count94.
93.
The primary reason for the rejection of the diagnosis of staphylococcus aureus
meningitis is the absence of histological change95. However it appears to be well
85
Morris []
Morris ProsA/2A/5 and [];Walters ProsA/2B/3
87
Walters
88
Tsao et al: Pulmonary manifestations of staphylococcus aureus septicaemia Chest/101/2 page 575
89
Morris ProsA/2A/5 and Morris [], Keeling ProsA/3A/9
90
Morris []
91
Smales & Rutter British Medical Journal 1979 Vol 1 588; Walters and Fleming
92
Wilson Pros A/3D/5
93
Schlesinger and others. Staphylococcus aureus meningitis: A broad based epidemiologic study Vol 66 No 2
Medicine P150
94
Fleming
95
Keeling ProsA/3A/4-5, Klein Pros A/3C/12-13
86
22
recognised that bacterial toxins can produces death or life threatening events without
any histological change, even in adults96.
94.
The likelihood of death is enhanced when, as was the case with Harry, the presence of
antibodies are at their lowest levels97. The effect of the dose of calpol given to Harry
after he was immunised may also have a role to play in suppressing inflammatory
responses98.
95.
The presence of staphylococcus aureus in cases has uncontroversially been accepted as
being related to sudden infant death even in cases where there is no histological
change99.
96.
Even the prosecution accept that death can occur very rapidly in very young children 100.
What they have failed to accept however is the logical consequence of that concession,
namely that in the case of rapid death there is unlikely to be any specific histological
change.
97.
CSF sampling is likely to be the most sensitive method of testing for the signs of early
infection and meningitis101. It is a matter of basic physiology that polymorphs will be
present before there is any histological change or visible pus on the surface of the
brain102. Dr Wilson appears to accept this proposition on behalf of the prosecution. “I
agree that the central nervous system findings would be compatible with an injury
leading to bleeding and inflammation of the meninges before death. I agree that an
illness lasting several days before death would have resulted in more striking findings at
post mortem, particularly abcesses and purulent meningitis.103” The point is made more
forcefully by Dr Wilson in the following passage: “In meningitis the usual progression
96
Morris ProsA/2A/7 See also Byard, Fleming
Morris ProsA/2A/7
98
Blackwell
99
OAR Sonnabend and others.. Continuous microbiological and pathological study of 70 sudden and
unexpected infant deaths. The Lancet 2nd February 1985
100
Keeling ProsA/3A/11, Klein Pros A/3C/14
101
Morris []
102
Walters ProsA/2B/7-11, Keeling ProsA/3A/10 accepts this point in relation to pus.
103
Wilson Pros A/3D/6
97
23
would be bacteria alone, bacteria plus lymphocytes and then bacteria plus polymorphs
over a period of 3 – 5 hours.104”
98.
Once there is infection, a toxic reaction may cause death at any time. The likelihood of
death is considerably increased if there is no known focus of infection105.
99.
Although the prosecution originally suggested that the absence of any finding of the
toxins TSST and SEA-SED was conclusive to show that there had been no toxic
shock106 or other toxic effect, it is now appears to be accepted107 that staphylococcus
aureus produces a number of toxins other than the toxins tested for108, including
staphylococcal enterotoxin E (SEE)109 and F110, as well as alpha, beta, gamma and delta
toxins that damage cell membranes111. The bacterial cell wall can produce peptido
glycan toxin112. There are also other components of staphylococcus aureus that can
produce strong inflammatory responses113.
100. The argument is not illuminated by the statement of Dr Klein which contains the
unsupported assertion that there can be no meningitis without histological change. He is
not a pathologist and therefore would never have cause to examine or understand
sudden deaths where there is no sign of histological change. His assertion that there
must be symptoms and histological change is understandable given that his practice is
solely concerned with living but obviously sick children.
101. Dr Klein’s assertion cannot stand in the face of documented examples of children and
adults who have died as a result of toxins without any histological changes being
present114.
104
Wilson Pros A/3D/8
Blackwell [].
106
Keeling ProsA/3A/4-5
107
Keeling ProsA/3A/9, Wills ProsA/3B/14, Wilson Pros A/3D/5 and 7
108
Walters
109
Blackwell []; Morris
110
Waldvogel. Pt III Infectious diseases and their etologic agents Ch 183 Staphylococcus aureus 2069-2092 at
2075
111
Morris ProsA/2A/6
112
Walters and Waldvogel at 2073-5
113
Professor Blackwell
114
Moritz and Zamchek Arch Path Vol 42 459-494
105
24
102. Dr Klein’s evidence is also undermined by the fact that staphylococcus aureus is now
being identified as a possible cause of SIDS. If this identification is correct, it also
supports the proposition that death may be caused by staphylococcus aureus without
any associated histological change.
103. The proposed connection between staphylococcus aureus and SIDS also answers Dr
Keeling’s point that there cannot be a disease which either colonises (not producing
disease) or kills rapidly. If the possibility (which she has acknowledged in a paper of
which she is a co-author)115 that “pyrogenic toxins of Staphylococcus aureus are
involved in …sudden infant death” exists, then staphylococcus aureus infection may be
just such a disease.
104. The rate of infection with staphylococcus aureus fits the mathematical model for SIDS.
It occurs with greater frequency in boys, in the winter months, when babies are put to
sleep on their fronts or on old mattresses, all of which were otherwise inexplicable
epidemiological features of the incidence of SIDS116. On investigation, staphylococcus
aureus toxins have been detected in the tissues of more than 50% of SIDS victims (as
compared to a much lower level in infants who died of other causes)117.
3. The impact on Dr Williams?
105. It is not proposed to repeat the matters set out above, under the heading ‘Good Faith’. It
is clear that the fact of non disclosure raises questions about Dr Williams’ credibility
and competence. The presence of staphylococcus aureus in a pure culture, leukocytes,
polymorphs and a raised protein level ought to have suggested to Dr Williams at least
the possibility of bacterial meningitis, even if it may not have caused death 118. Dr Klein
115
Zorgani and others. Detection of pyrogenic toxins of staphylococcus aureus in sudden infant death syndrome.
FEMS immunology and medical microbiology 25(1999) 103-108
116
Harrison and others. The nasopharyngeal bacterial flora in infancy: effect of age, gender, viral upper
respiratory tract infection and sleeping position FEMS immunology and medical microbiology 25 (1999) 19-28,
Wilson Pros A/3D/4-5
117
Zorgani and others. Detection of pyrogenic toxins of staphylococcus aureus in sudden infant death syndrome.
118
Morris ProsA/2A/3
25
agrees that the CSF leukocytes is consistent with meningitis. Dr Wilson states: “It is not
possible to exclude meningitis.119”
106. On any view it was a possibility that ought to have been frankly disclosed and debated.
There are only two possibilities. Either Dr Williams is so incompetent or negligent that
he failed to recognise early signs of bacterial meningitis or he was deliberately
unwilling to acknowledge or admit that possibility, having set a murder investigation in
train.
73 million to 1
107. Despite the prosecutions claim that the 1 in 73 million statistic was and is irrelevant,
this was not the stance taken at trial. The prosecution in closing and the trial judge in
summing up both emphasised the statistic. The jury must have believed that it was
relevant.
108. If it is now conceded it was irrelevant and the Court of Appeal has determined that the
judges’ direction on the topic was inadequate to avert the danger of the ‘prosecutor’s
fallacy’120, it is necessary to evaluate the impact of the wrongly admitted evidence and
the mistaken summing up on the juries verdict.
109. In addition to this, the Court must give weight to the uncontested fresh evidence that
shows the first Court of Appeal (and the parties) were misled into thinking that,
whatever the true statistical figure might be, a cot death would still be a rare or unusual
event. This fact was highly material to the conclusion of the Court of Appeal that the
convictions were safe121.
110. However as Professor Hill has now demonstrated, in any family unlucky enough to
suffer a first SIDS, a second SIDS death is not a rare event at all. Odds of 1 in 260 have
been estimated122 or 1 in 100123.
119
Wilson Pros A/3D/7
Pros B/2/para 162-184
121
Pros B/2/para 158
122
Professor Golding
120
26
111. The figure of 73 million to 1 or any evidence of rarity would have had an effect on the
jury. It is now accepted that the evidence was inadmissible. It should therefore never
have been led. If true, the evidence was profoundly damaging. Further the damage was
exacerbated by the fact that the jury were never adequately warned about the dangers
of believing that the odds of innocence were 73 million to 1.
112. The facts must now be reconsidered in the light of the substantially diminished certainty
that can be attached to the prosecution medical case. The diminished medical evidence
also has a knock on effect on the “circumstantial evidence” relied upon. It would be
quite wrong, for example, to continue to place weight on the absence of explanations
from Sally Clark for the bleeding found in Harry, given the finding of staphylococcus.
113. Once the evidence is reassessed in this new light it is not possible to conclude that the
giving of the flawed statistic and the misdirection did not have any substantial effect
upon the jury.
The approach of the Prosecution
114. The prosecution seek to obscure the real injustice caused by their non disclosure and
misleading use of statistics by seeking to argue that nothing has changed. This is
unrealistic and wrong. The errors that have permeated this case have a widespread
ripple effect. No one aspect can be considered and dismissed in isolation. For example
the non disclosure will have affected all the evidence in relation to Harry’s case. Sally
Clark may have been regarded as less credible by the jury because she had no idea what
may have killed him. The defence experts may have suffered a similar fate.
115. The prosecution place considerable weight on the defence concessions extracted in
cross examination on the assumption that “the medical findings were genuine”124. The
concessions made by the defence experts would, in all probability, not have been made
123
124
Morris ProsA/2A/1
Prosecution skeleton 2.13, 2.17
27
if Dr Williams’ part and purpose in the non disclosure had been appreciated by those
involved.
116. Similarly little weight can be given to the prosecution list of similarities125 if the fresh
evidence is or may be credible. The critical similarities of “previous abuse” and
“deliberate injury” or “recent abuse” can only be safely relied upon if the Court is
satisfied that Dr Williams is competent and honest and that the bleeding observed
cannot have been caused by staphylococcus aureus.
117. In addition the prosecution give considerable currency to the ‘hallmark’ features of
infant killing identified by Professor Meadow. It is not accepted that such evidence is
admissible. The evidence does not qualify as expert evidence. The subject matter of the
opinion is not such as to require special assistance to be given to the jury. It consist of
no more than a list of commonplace features that a jury would not need help with 126. A
jury does not need Professor Meadow to tell them, for example, that inconsistent
accounts from parents or the previous abuse of a child or the child being well
immediately before it died may all be relevant in deciding whether a child has been
murdered by a parent.
118. Even the subject falls within the class of subjects upon which expert testimony may be
permitted, there is no sufficiently organised body of knowledge or research that ensures
that any opinion expressed on the subject is reliable. The body of knowledge relied
upon by Professor Meadow was no more than his own experience over 20 years.
However almost none of the underlying materials or data upon which Professor
Meadow’s opinion in based is now available. Access to the material was requested
before trial127. The request was denied. Professor Meadow claimed to have destroyed
the majority of the information on which his published results were based128. It is
therefore impossible to examine the claimed scientific basis for his opinions.
125
Prosecution skeleton 2.19
See Archbold 10-64 et seq especially R. v. Bonython (1984) 38 SASR 45.
127
Defence disclosure bundle Item 24
128
Defence disclosure bundle Item 25-26 and 32
126
28
119. The destruction of the material would also clearly render the admission of the opinion
unfair, even if it was strictly admissible.
Retrial
120. There is now clear and compelling evidence in favour of proposition that Harry died a
natural death. There are a series of reports (above and beyond the evidence to be called
on appeal) that demonstrate that there is a substantial and highly respectable body of
national and international medical opinion that considers Harry died as a result of
overwhelming staphylococcus aureus infection129.
121. The alternative case on shaking or smothering is substantially weakened by the
existence of an explanation for the acknowledged bleeding and petechiae observed at
post mortem. The case on shaking is further weakened by the complete absence of any
of the classic signs of shaken baby syndrome (such as axonal damage) and the inability
of any expert to describe the mechanics of the trauma suggested by the prosecution.
122. The case against Christopher is equally diminished. His cause of the death has always
been in doubt. Death was originally unequivocally ascribed to a natural cause by Dr
Williams. The prosecution experts, save for Williams, have gone no further than saying
the cause is still unascertained130. The defence have similarly concluded that the cause
is unascertained and the further experts consulted since the convictions support that
view131. Professor David, the independent court appointed expert, has suggested that
death might have been caused by acute idiopathic pulmonary haemosiderosis. Only Dr
Williams has been willing to confidently ascribe death to smothering.
123. Dr Gullino has concluded that acute idiopathic pulmonary haemosiderosis is a
reasonable possibility and has also pointed to the growing support for Professor David’s
independent diagnosis of that condition. No other diagnosis fits the findings and
explains the now accepted evidence of Stephen Clark that Christopher suffered a
spontaneous nose bleed from both nostrils whilst in his sole care in London two weeks
129
Morris ProsA/2A/2; Walters ProsA/2B/17, Byard, Fleming, Gullino, Rushton
Morris ProsA/2A/1
131
Professor Byard []; Dr Gulino [];
130
29
before his death. On the face of the totality of the medical evidence it is submitted that
the case on Christopher would not get past the close of the prosecution case. It would
certainly not end in a conviction.
124. The time has come to draw a line under these deaths. It requires no imagination to
appreciate that devastation that the deaths and these proceedings have already caused in
the Clark family. As lawyers it is easy to understand the professional disgrace that has
befallen Sally Clark (as well as the vilification of her husband for standing by her).
More poignantly it has led to (name), their surviving child, reaching the age of 4 barely
knowing his mother.
125. Sally Clark has completed 3 years of sentence of life imprisonment with a
recommended tariff of 15 years and has had to mourn the death of her children whilst
being held out to be their murderer.
126. The lives of the family have been laid waste by the seeming certainty of doctors where
certainty was not justified.
127. It is impossible to carry out further tests to determine the various hypotheses that have
now emerged as to the cause of Harry’s death. Harry was cremated after the defence
experts advised that (on the material then know to them) all the appropriate tests had
been carried. There are now only a limited range of medical samples available.
128. This situation is due to the non disclosure, coupled with the failure of Dr Williams to
undertake sufficient routine dissection and histology132. It cannot be right to have a
murder trial where the central issue, namely what caused the death of the alleged
victim, cannot be fully and properly investigated. As Professor Byard has commented:
“The Clark brothers demonstrate difficulties that may arise if cases are not fully
investigated with all the results being clearly summarised and discussed in the autopsy
reports. Trying to clarify findings diagnoses and circumstances of death at a later stage
may simply not be feasible due to the wide variety of possibilities other than inflicted
injury.”
132
Professor Byard, Gullino
30
129. The process of this appeal has also been marked by a reluctance by the Crown to make
speedy enquiries or realistic concessions.
130. In addition there has been widespread publicity given to material, introduced by the
prosecution, that could never feature in any retrial. The evidence about 73 million to 1
has, as the prosecution accepts, “attracted enormous and largely ill-informed media
comment both during and after the trial.133”
131. In addition the prosecution chose, for forensic reasons, to introduce and emphasise at
sentencing and at the first appeal the suggestion that Sally Clark was abusing alcohol.
Not only was the evidence introduced without any defence opportunity to challenge it,
but it also served no purpose other than ensuring maximum publicity (Harrison J having
ruled that alcohol had played no part in the death of the children).
132. There must be considerable doubt whether these irrelevant factors may not be so widely
imprinted on the public consciousness as to jeopardise a fair trial.
133. In the circumstances it is submitted that it would not be an appropriate case in which to
order a retrial.
CLARE MONTGOMERY QC
Matrix Chambers
Gray’s Inn
JAMES GREGORY
Lincoln House Chambers
Manchester
22nd January 2003
133
Prosecution skeleton 6.4
31
IN THE COURT OF APPEAL 2002/3824/Y3
(CRIMINAL DIVISION)
IN THE MATTER OF A REFERENCE
BY THE CRIMINAL CASES REVIEW
COMMISSION
THE QUEEN
v.
SALLY CLARK
Appellant
_____________________________
SKELETON ARGUMENT
_____________________________
Burton Copeland
Royal London House
196 Deansgate
Manchester
M3 3NE
32