Sunday Telegraph 6/10/02
http://www.telegraph.co.uk/news/main.jhtml?xml=/news/2002/10/06/nmmr06.xml&s
Sheet=/news/2002/10/06/ixhome.html
Measles virus is found in boy's brain after MMR
By Lorraine Fraser, Medical Correspondent
(Filed: 06/10/2002)
A child who developed severe epilepsy after receiving the MMR jab has been found
to have measles virus from the vaccine in his brain. The results of tests
conducted recently have been revealed by the
13-year-old boy's mother. She says that she has decided to go public in order to
push the Government to take the plight of children allegedly damaged by the
three-in-one measles, mumps and rubella vaccination more seriously.
Scientists say that the implications of the discovery are difficult to assess
without further research. However, it raises new questions about the triple
inoculation, which has been dogged by controversy since Andrew Wakefield, a
former consultant at the Royal Free Hospital in London, linked it with a new
syndrome of bowel disease and autism in children. The boy's mother, who has
asked to remain anonymous, told The Telegraph yesterday that her son had
developed an allergic rash eight days after he received the MMR vaccination when
he was 15 months old. He then progressed to have 10 to 12 seizures every month.
In the summer of 1998, however, he descended into "status epilepticus"
-continuous convulsions - and surgeons at a London hospital decided that he
needed emergency brain surgery to save his life. It was at this point that a
brain biopsy was taken. The woman, who is suing the manufacturers of the MMR
vaccine on behalf of her son, declined to say where the biopsy had been tested
for the measles virus but indicated that this had been done in a reputable
laboratory.
She had been shocked to receive the test results indicating that vaccine-strain
measles virus had been found, she said. She had also learnt that samples from
her son's bowel, taken in 1997 because he had digestive problems, had tested
positive for vaccine-strain virus. After the operation when he was nine, her son
had had to relearn "virtually everything", she said. His personality changed and
he was no longer able to attend mainstream school, although he had very recently
been free of seizures.
"Now with this new information I am very concerned," the boy's mother said. "Is
it over for him or not? No one knows and this is why all these children - not
just my son - need to be acknowledged rather than have the continuous stream of
blanket denials that have been issued by the Department of Health." British
specialists investigating MMR were reluctant to comment publicly on the case
last night. One cautioned that it was theoretically possible that the boy had
developed a vaccine-related condition that was more commonly caused by a natural
measles virus infection.
If this was the case, he said, then MMR would actually help to protect the wider
population from similar infections. However, he added: "We do not know what this
result means." The Department of Health has told parents they have no need to be
concerned about MMR - a position supported by leading medical bodies worldwide.
New Study Supports Possible Link Between MMR Vaccine and
Autism
Virus Detected in Spinal Fluid of Children with Autism, But Not Controls
JUNE 9, 2004 (c)ICDRC Melbourne FL
These data published today in the most recent Journal of American Physicians
and Surgeons, represent the second in a series of direct observations of
Measles Virus (MV) persistence in children with
Autistic Regression. All
children had been vaccinated shortly prior to the development of autistic
symptoms. While all of the controls had also been vaccinated - they were all
negative for viral persistence. Taken together with the finding of MV in the
intestinal tract of these and other children previously reported by Uhlmann,
this represents evidence of active replication of virus and further indicates
either failure of the vaccine to protect these children from natural
infection or more likely, given the lack of any history of MV apart form the
vaccine, this represent vaccine strain persistence.
Presently there is no proven intervention for viral persistence and it is the
hope of the authors that these observations will stimulate additional reearch
into the nature of the viral persistence and means of assisting the children
in completely clearing the virus.
While MMR vaccine is generally considered safe, we propose a subset of
genetically vulnerable children lack the ability to clear the vaccine strain
of the virus and that this is - on the balance of the available biological
data - a direct cause of their symptoms. We recognize the failure of
epidemiology to validate these observations, and beleive this specific
hypothesis has never been adequately tested with any previous epidemiological
study.
Jeff Bradstreet MD FAAFP
Director ICDRC
Professor of Child Development Southwest College of Naturopathic Medicine and
Adjunct Professor Stetson University
321-953-0278
This study is the latest in a series that examines the relationship between
persistent measles virus infection and regressive autism. While the Institute
of Medicine were made aware of these findings, and indeed similar findings in
a larger group of autistic children, they chose to ignore them in their
latest report. This situation is quite unacceptable.
Dr Andrew Wakefield MB.BS., FRCS., FRCPath
Thoughtful House, Austin Tx and
Director of Research ICDRC, Melbourne Fl.
Evidence of MMR Risk Is 'Compelling'
[From the Daily Mail; London (UK).
http://infobrix.yellowbrix.com/pages/infobrix/Story.nsp?story_id=42342181&ID
=infobrix&scategory=The+Iraq+Situation&
Compelling evidence of a link between MMR, autism and bowel disease has
emerged in research carried out for a landmark legal battle. Experts say
children suffering autism and gut disorders have the same strain of the measles
virus in their bowel, blood and spinal fluid as the one used in the triple jab.
The findings are the closest scientists have come to proving a causal link
between the jab, autism and painful gut disorders. But campaigners claim
authorities are trying to prevent the evidence being made public after legal aid
was withdrawn from more than 1,000 families suing vaccine manufacturers.
It means their case - seen as a crucial test of whether MMR is safe - is
unlikely to go ahead because the families will probably not be able to afford to
continue their fight against drug firms GlaxoSmithKline, Merck and Co and
Aventis Pasteur MSD.
Legal aid bosses said yesterday that they were 'mistaken' to have backed
the families' case, which has already received 15million of taxpayers' money to
help fund the research. Richard Miles, whose 14-year-old autistic son
Robert is involved in the case, said: 'It seems incredible that the scientists
can come this far and then the powers that be decide that we should not take the
case to court.' Seven children involved in the legal battle had their spinal
fluid tested by pathologist Professor John O'Leary, of Trinity College in
Dublin. The measles virus was found in three samples of spinal fluid. One
of these was an MMR strain but doctors were unable to identify the other two.
'No measles should have been there in the first place but for the MMR
strain to be found in spinal fluid is unheard of,' a source said yesterday. 'It
is extremely supportive of a causal link between MMR and autism and bowel
disorders.' Around 100 bowel tissue and blood samples taken from autistic
children by the Royal Free Hospital in London were also tested.
DID MMR GIVE MY SON EPILEPSY?
Daily Mail April 6, 2004
As the campaign to prow MMR is safe intensifies, one mother claims the jab
left her son suffering over 60 epileptic fits a day and says she has
compelling scientific evidence to back it up NO ONE knows precisely how Lewis
Pickering's life might have prospered had he not been inoculated with the MMR
vaccine. But his mother Wendy has memories, sharpened by regret, of the
child he once was.
'Lewis was just joyous: a lively, lovely little boy who was bright and
healthy and met all his milestones at the right time,' she says. Yet today
her adored only son is an adolescent imprisoned in a child's mind; bewildered
by memory loss, prone to violent mood swings; sweet, sullen, aggressive and
affectionate by turns. His mind skitters and races, then drifts off into
abstraction. He has no grasp of social behaviour, no sense of time or place,
and no hope of independence.
But more than that, his young life is blighted by the severe epileptic fits
that have assailed him since he had the triple vaccine for measles, mumps and
rubella at 15 months. The safety of the triple vaccine - or MMR-was first
questioned in 1998 in a report by Dr Andrew Wakefield which suggested a
possible link between the jab and bowel disease and autism in children. Since
then, hundreds of parents have come forward claiming that their children have
suffered autism as a result of having had the vaccine. Others have told of
epilepsy and learning difficulties.
Wendy, who has always striven to preserve her son's privacy, now feels driven
to tell Lewis's story. Stung by the Government's obdurate refusal to engage
in a debate over MMR, and devastated by the collapse last month of the
parents' appeal for legal aid to fight for compensation from the vaccine
manufacturers, she feels her only recourse is to speak out. For Wendy
believes she has compelling evidence of a link between the MMR vaccine and
the onset of her son's epilepsy which would otherwise be suppressed.
Five-and-a-half years ago. Lewis, now 15, underwent emergency life-saving
neuro-surgery to arrest potentially fatal epileptic fits. It was then that
tissue from the frontal lobe of his brain was found to contain a strain of
the measles virus that could only have originated in the MMR vaccine.
'Lewis has never had measles,' says Wendy. 'It could only have come from the
vaccine. My son is a case study. I have watched him suffer this vicious
assault from epilepsy. 'His anguish continues, and he dreads and hates the
fits. I am 100 per cent convinced that the MMR vaccine precipitated the
epilepsy. It has blighted not just Lewis's life, but hundreds of others.'
WENDY Pickering's grief for the bright boy she lost and the changed and
diminished son who usurped him is compounded by anger. She reserves equal
fury for the health authorities and the Government, who have failed to
address her concerns.
'It's criminal,' she says. 'I am just asking for a proper investigation so
the parents involved can know the truth. 'But all we hear is the same mantra:
there is no link between MMR and epilepsy or autism - despite experts who
claim to the contrary. 'All I've had is a letter from the health authority
telling me they sympathise with the plight of my son. I don't want their
sympathy. I want them to look at the evidence and ask some searching
questions. 'To get this vital issue into the public domain, I have to expose
my son to the glare of publicity. I don't want to do so, but I do it out of
necessity.
'Our Prime Minister, Tony Blair, has declined to say whether his son Leo has
had the MMB jab. He says he wants such personal information to remain
private. Sadly, if I want this vital subject addressed, I have to compromise
my own son's privacy. 'The pertinent question is: what does the Prime
Minister know about MMR? What information does the Department of Health have?
And when, particularly, are they going to investigate the measles virus found
in my son's brain?'
While the Government conveniently absolves itself of responsibility, Wendy,
48, and her 55-year-old husband Brian, a production supervisor, live daily
with the heavy weight of their son's dependency. 'Lewis cannot be left at
home unsupervised,' says Wendy. 'We cannot let him walk into town alone
because he has the vulnerability of a child. We worry so much about the
future. When we're no longer around, how on earth will he cope?' Lewis
Pickering's personal tragedy began in September 1990, a month after he had
the MMR vaccination. He was born in May 1989; a happy, responsive
and bright baby who scored highly in all the standard health tests.
Then eight days after he was vaccinated, he suffered an allergic reaction:
the raised itchy rash that covered his body was treated with antihistamine.
Four weeks later came the first seizure. 'I started to feed Lewis and he
became vacant, still and unresponsive,' recalls Wendy. 'He just stared,
completely blankly, and I was terrified. I phoned for an ambulance. I thought
he was dying. 'At hospital they took brain X-rays, but they couldn't find
any-thing wrong. Lewis fell asleep in my arms, then he just seemed to
recover.' The fits that ensued did not follow this pattern. "There were other
seizures where he was vomiting, convulsing and turning blue,' says Wendy.
'The feeling of nausea persisted. Whenever Lewis had fits he complained of
stomach pains.'
THE tyranny of epilepsy escalated. Lewis began to attend the mainstream
school a short walk from the family home at Shoreham-by-Sea, West Sussex,
when he was five. Almost every night subsequently he was jolted into
terrifying wakefulness by a seizure. 'He would suddenly sit up, eyes wide and
shout out for Brian or me,' says Wendy. 'His hands would jerk uncontrollably.
His face and mouth were contorted. The fits were so frequent we logged them
in a diary.' Wendy, a former legal secretary, has kept meticulous records of
her son's seizures. She pulls out a huge file: 1993 was a bad year - almost
every day is circled.
Lewis shuttled back and forth from hospital as efforts were made to control
his fits with drugs. There were assorted combinations and cocktails. The
drugs seemed to fog his mind and subdue his vitality. But they didn't
suppress the fits. On one awful day he suffered 62. 'It was like
madness,' says Wendy. 'We had barely finished writing down the details of one
fit when another happened. 'I remember Lewis yelling: "Help me! I want my
Dad! I love him so much. Where am I?" His awful bewilderment brought us to
the brink of tears.' In 1997, because of the severe gastric pain that
accompanied Lewis's fits, he was admitted to the Royal Free Hospital,
Lon-don, where Dr Andrew Wake-field's team carried out a colonoscopy.
A virus found in Lewis's gut matched one discovered in autistic children
whose parents had made a link with their condition and MMR. This association
triggered fresh fears and convinced Wendy that further investigation was
vital. She says: 'Just the thought of there being a connection with the
measles virus was scary. 'I wondered what harm it was doing and what was
likely to happen in the future. And we went on to experience just how much
more awful it could get.' What ensued was a waking nightmare in which Wendy
and Brian came perilously close to losing Lewis. In July 1998, he suffered
132 epileptic seizures. The fits were escalating in intensity and frequency
and within a month Lewis was in intensive care.
His epilepsy had failed to respond to every drug that had been administered and
his body was convulsed by almost continuous fits. The succession of
potentially fatal seizures had to be broken.
'The neurologist said he had another course of action left,' recalls Wendy.
'He said they would anaesthetize Lewis to stop all brain activity and try to
break the cycle of fits. 'He said there was a chance that all his organs
would pack up and he would die. I asked what the risk was. He said: It does
not go into double figures." They agreed to go ahead.
'We would have given anything to have spared Lewis the suffering. As he was
taken to intensive care, he said to me, in that straight-speaking way
children have: "I'm not going to die, am I Mum?"'
Although Lewis survived the anaesthesia, it did not stop the fits. Wave after
wave of them racked his body. There was one drastic mea-sure left. Lewis was
rushed to Great Ormond Street Hospital in London for life-saving brain
surgery. It was the last hope. 'It was as if we were in a disaster film,
confronting one mountainous tragedy after another,' says Wendy. 'The anxiety
was almost unbearable. 'I was told Lewis might become paralysed down his
right side by the surgery. I could not envisage my lively son in a
wheelchair. They said he might lose the power of speech. We did not know how
he would emerge from the operation.'
In fact, the surgery to remove part of the left frontal lobe of Lewis's brain
saved his life. He remained in hospital for six months but when he returned
home he was a different child. Mercifully, he did not lose his mobility, but
he had to learn from scratch and with slow deliberation how to walk again. He
did not forfeit the power of speech, but he had to re-acquire the process of
stringing isolated words into conversation. Lewis suffers from frontal lobe
syndrome. The condition is characterised by emotional volatility, problems
with concentration, inattention and inappropriate behaviour.
Sufferers are bereft of the social skills that allow them to interpret body
language or read mood. Their short-term memory is poor. 'Since 1998, Lewis's
life has diminished,' says Wendy. 'We used to have so much fun. The changes
since his operation have been dramatic and marked. My heart lifts now when he
remem-bers someone's name, because he cannot even keep track of what happened
earlier in the day. HE DOES not know if it is morning or afternoon; whether
he has had breakfast or lunch. I read to him every night, but I do not
know how much pleasure he takes in it. His mind seems to drift.
'We have been through hell and so has Lewis. He is not the child we started
out with. I remember the day he asked me: "Are you my mummy?" It was when he
was making the slow recovery after surgery. 'Such moments are like snap-shots
that stick in the memory. I can still hear the tone of his voice and feel the
turmoil of loss and confusion in his mind.' Lewis attends a special school
now. He is popular boy, both with teachers and pupils, and his beseeching
brown eyes have a puppy-like appeal. He is Wendy's only child, although Brian
- a widower when he and Wendy met - has a daughter, Holly, 26, whom they both
regard as their own.
After school, Lewis bounds into the house. He shows me first his Lego models,
then his pet hamster, then his remote control car and X-Box. The house is
rendered chaotic by the sheer force of his energy. Lewis also suffers from
Attention Deficit Hyperactivity Disorder. And you understand at once the
scope and scale of his parents' exhaustion. 'Sometimes I feel worn down,'
says Wendy 'Lewis has no independence. I cannot leave him for an hour. So
tensions can run quite high. He still
suffers from fits. They are more prolonged now and he says he hates living
with the epilepsy.
'We have been through so much. It has been a mighty climb and it still is. We
dare not look too far into the future. We have had to adjust to the boy Lewis
has become. It has been like a bereavement and we are grief-stricken for him.
'As if we had not endured enough, we are now being denied our day in court.
The health authorities are trying to bury any link between Lewis's epilepsy
and the MMR. So my only recourse is to speak out. Other parents must be
warned. Right and justice have to prevail.'
http://pediatrics.aappublications.org/cgi/content/abstract/114/5/e657
A New Complication of Stem Cell Transplantation: Measles Inclusion Body
Encephalitis
Measles inclusion body encephalitis (MIBE) is a disease of the
immunocompromised host and typically occurs within 1 year of acute measles
infection or vaccination. We report a 13-year-old boy who had chronic
granulomatous disease and presented 38 days after stem cell transplantation
with afebrile focal seizures that progressed despite multiple
anticonvulsants. After an extensive diagnostic evaluation, brain biopsy was
performed, revealing numerous intranuclear inclusion bodies consistent with
paramyxovirus nucleocapsids. Measles studies including reverse
transcriptase-polymerase chain reaction and viral growth confirmed measles
virus, genotype D3.
Immunohistochemistry was positive for measles nucleoprotein. Despite
intravenous ribavirin therapy, the patient died. MIBE has not been described
in stem cell recipients but is a disease of immunocompromised hosts and
typically occurs within 1 year of measles infection, exposure, or
vaccination. Our case is unusual as neither the patient nor the stem cell
donor had apparent recent measles exposure or vaccination, and neither had
recent travel to measles-endemic regions. The patient had an erythematous
rash several weeks before the neurologic symptoms; however, skin biopsy was
consistent with graft-versus-host disease, and immunohistochemistry studies
for measles nucleoprotein were negative. As measles genotype D3 has not been
seen in areas where the child lived since his early childhood, the
possibility of an unusually long latency period between initial measles
infection and MIBE is raised.
In addition, this case demonstrates the utility of brain biopsy in the
diagnosis of encephalitis of unknown cause in the immunocompromised host.
Alexandra F. Freeman, MD*, David A. Jacobsohn, MD, ScM, Stanford T. Shulman,
MD*,William J. Bellini, PhD, Preeti Jaggi, MD*, Guillermo de Leon, MD||,
Gesina F. Keating, MD¶, Francine Kim, MD#, Lauren M. Pachman, MD*, Morris
Kletzel, MD and Reggie E. Duerst, MD
Regressive Autism, Ileal-Lymphoid Nodular Hyperplasia,
Measles Virus and MMR Vaccine
Summary of Published Studies Offering Evidence for Linkages
By
David Thrower
(download pdf)
This note summarizes:
• clinical evidence for the link between autism and a novel form of inflammatory
bowel disease
• clinical evidence for the link between inflammatory bowel disease and measles
virus
• clinical evidence for the link between measles virus and vaccination with MMR
• some of the other wider safety concerns over MMR
(A) The Link Between Autism and a Novel Form of Inflammatory Bowel Disease
There is now ample evidence, confirmed by independent groups of researchers, of
a link between regressive autism and a novel form of inflammatory bowel disease.
Full publication references are at the end of these notes.
• The possible association between MMR vaccine, regressive autism and intestinal
symptoms was first recounted by parents to Dr. Andrew Wakefield, a UK
gastroenterologist at the Royal Free Hospital, London, in 1995. The first group
of children presenting in this way to Wakefield and colleagues at the Royal Free
were reported in The Lancet as a clinical case series in February 1998 (1).
Although the interpretation put on this paper at the time was the subject of
intense controversy - particularly in the absence of corroborative clinical
research by other researchers at that time - the strong evidence of a
hitherto-unreported link between autism and a novel intestinal disease, ileal-lymphoid
nodular hyperplasia, has not been disputed, and still stands as an important
initial clue as to the causes of regressive autism.
• A group of researchers led by Horvath (2) subsequently independently reported
in 1999 upon patients with autism who had gastrointestinal symptoms, including a
study of 36 children with autism that found grade I or II reflux esophagitis in
25 (69.4%), chronic gastritis in 15 (42%) and chronic duodenitis in 24 (67%).
•
Further research published in September 2000 (3) by Wakefield, Anthony et al
confirmed that ileal-lymphoid nodular hyperplasia (ILNH) was found in 54 out of
58 (93%) children with autism or other disorders (50 with autism, 5 Aspergers, 2
disintegrative disorder, one ADHD, one schizophrenia, one dyslexia), but only 5
out of 35 (14.3%) normal controls, pointing to a very strong ILNH-autism link.
• Research published in 2001 by Furlano, Anthony et al (4) reported on
ileocolonoscopy performed on 21 consecutively-evaluated children with autistic
spectrum disorders and bowel symptoms, and made “blinded” comparisons with 8
children who had a histologically normal ileum and colon, plus 10
developmentally-normal children with ILNH, 15 with Crohn’s Disease, and 14 with
ulcerative colitis. The study confirmed a distinct lymphocytic colitis in the
children with ASD, in which the epithelium appeared particularly affected,
offering further corroboration for gut epithelial dysfunction in autism.
• Research reported in 2001 by Buie (5) reported that, as a result of over 400
gastrointestinal endoscopies with biopsies and evaluation of digestive enzyme
function, on children with autism, he had found the presence of chronic
inflammation of the intestinal tract, although the incidence was less frequent
than in the Royal Free Hospital group of patients reported by Wakefield et al,
and that biopsy results indicated the presence of chronic inflammation of the
digestive tracts, including esophagitis, gastritis and enterocolitis. Ileal
lymphoid nodular hyperplasia, as first found by the Royal Free study, had been
found in 15 of 89 children examined for it.
• A review (6) published in September 2002 by Wakefield, Anthony, Montgomery et
al noted that as early as 1986, a researcher named Soddy had noted that
recurrent gastrointestinal upsets were a constant feature of autistic children,
and that in a systematic analysis of an unselected population of 385 children on
the autistic spectrum, clinically-significant gastrointestinal symptoms occurred
in 46%, compared with 10% of 97 developmentally-normal controls, strongly
suggesting a gastrointestinal-autism link. Mucosal lesions in the small and
large intestine were consistent with an autoimmune pathology, and suggested the
possibility of an autoimmune response leading to cerebral damage.
• A June 2002 presentation (7) by Krigsman to the US Congressional Committee on
Government Reform reported that a large percentage of his autistic patients
suffered from chronic unexplained gastrointestinal symptoms. Of 43 patients, the
majority had a clear history of developmental regression, after previous normal
development, suffering gradual or precipitous decline between age 12 months and
18 months. Most regressive children also exhibited poor growth. Patients had
undergone colonoscopy. Findings were that the lymphoid nodules of the terminal
ileum were markedly enlarged, thus confirming the early work of the Royal Free
team. Evaluation of biopsy specimens confirmed that 65% had colitis, 51% had
active colitis, 40% had chronic colitis, 7% had eosinophilic colitis, 90% had
lymphoid nodular hyperplasia of the terminal ileum, and 35% had neither active
nor chronic nor eosinophilic colitis. Patterns of inflammation were patchy and
unpredictable, but findings were similar and consistent from patient to patient
within affected sub-groups.
• A November 2003 paper (8) published by Ashwood, Murch et al reported on the
examination of 52 affected autistic children, compared with 25 histologically-normal
developmentally-normal controls and a further 54 histologically-inflamed but
developmentally-normal controls. Analysis of intestinal biopsies in
regressive-autistic children indicated a novel lymphocytic enterocolitis with
autoimmune features, though the precise linkage between the finding and
cognitive functions still remained unclear. The study concluded that it provided
further evidence of a pan-enteric mucosal immunopathology in children with
regressive autism, that is distinct from other previously-known inflammatory
bowel diseases.
• An April 2004 paper (9) by Torrente, Anthony et al identified, following
earlier reports of lymphocytic colitis and small bowel enteropathy in children
with regressive autism, that the gastritis in regressive autism was clearly
distinct from that in Crohn’s and other conditions, pointing to a distinctive
form of gastritis being linked with regressive autism.
• A November 2004 paper (10) by Ashwood, Anthony et al found that molecules
(cytokines) produced by immune cells in the intestine, that cause or control
inflammation, showed an abnormal pattern in autistic children compared with
non-autistic children. The pattern was different to other forms of intestinal
inflammation, and the disease resembled a longstanding viral disease of the
intestine, not unlike the intestinal inflammation seen on patients with other
viral infections such as HIV-associated enteropathy (intestinal disease) that
often accompanies infection with HIV.
• A February 2005 paper (11) by Jyonouchi, Geng et al further confirmed the
original ileal-lymphoid nodular hyperplasia/regressive autism link first
reported by the Wakefield team in 1998. The study again found evidence of marked
inflammatory and immune abnormalities in children with autism associated with
gastrointestinal symptoms.
• An April 2005 published letter (12) by Balzola, Barbon et al, Pan-Enteric IBD-Like
Disease in a Patient with Regressive Autism Shown for the First Time by the
Wireless Capsule Enteroscopy - Another Piece in the Jigsaw of this Gut/Brain
Syndrome?, reported that a 28-year-old male with regressive autism, severe
constipation, bloating, abdomen distension and symptoms of gastroesophageal
reflux was examined. Gastroscopy under general anaesthesia revealed hemorrhagic
gastritis with inflammatory pseudopolypsthat had reached the pylorum, with a
pearl-necklace appearance, and a panenteric IBD-like disease consistent with
previously-published descriptions of autistic enterocolitis was finally
diagnosed. The wireless capsule images were the first to be obtained beyond the
limits of the duodenum and terminal ileum, and demonstrated the potential for
the entire bowel to be implicated in this inflammatory disease.
• A May 2005 study (13) by Balzola, Daniela et al reported on 9 consecutive
patients (range 7-30 years) with autism and chronic intestinal symptoms
(abdominal pain, bloating, constipation and/or diahorrea). Routine blood and
stool tests and gastroscopy and colonoscopy with multiple biopsies were
performed under sedation, and wireless enteroscopy capsules were used in three
of the adult patients. Gastroscopy revealed mucosal gastritis in 4 patients,
esophagitis in 1 patient and duodenitis in 1 patient, and histological findings
showed chronic inflammation of the stomach and duodenum in 6 patients,
inconsistent with celiac disease. The authors reported that preliminary findings
were strongly consistent with previous descriptions of autistic enterocolitis,
and supported a not-coincidental occurrence. They showed for the first time a
small-intestinal involvement, suggesting a pan-enteric localization of this new
inflammatory bowel disease.
• Also in 2005, a further paper (14) by Wakefield, Ashwood et al was published,
assessing ileocolonic lymphoid nodular hyperplasia in ASD and normal control
children. Some 148 consecutive children with ASD, with gastrointestinal
symptoms, were investigated by ileocolonoscopy, with 74 ASD children and 23
normal controls undergoing upper gastrointestinal endoscopy. The presence of
lymphoid nodular hyperplasia was significantly greater in ASD children compared
with controls, in the ileum (129 out of 144, compared with 8 out of 27
controls), and in the colon (88 out of 148, compared with 7 out of 30 controls).
Comparative percentages were 90% vs 30% and 59% vs 23%. This was whether or not
controls had co-existent colonic inflammation. The severity of ILNH was
significantly greater in ASD children compared with controls, with
moderate-to-severe ILNH present in 98 out of 144 ASD children compared with 4
out of 27 controls; percentages were 68% and 15%. On histopathological
examination, hyperplasic lymphoid follicles were significantly more prevalent in
the ileum of ASD children (84 out of 138, or 61%) compared with normal controls
(2 out of 23, or 9%). The data thus further corroborated the finding that ileal
lymphoid nodular hyperplasia is a significant pathological finding in autistic
children.
• Additionally in 2005, a study (15) was published by Gonzalez, Lopez et al,
seeking evidence of immunological alterations in 68 autistic children ages 22
months to 11 years and presenting with digestive systems, and examining biopsies
from their digestive tracts. Endoscopies and colosopies were undertaken, with
biopsies of the esophagus, stomach, duodenum and colon, with verification of
presence of inflammation, eosiophil infiltration, lymphoid nodular hyperplasia
and CD-4 and CD-8 cells. The results were that lymphoid nodular hyperplasia was
discovered in 2/68 esophagus, 6/68 stomachs, 8/68 duodenums and 36/68 (53%) of
colons. Eosiophil infiltration with more than 20 eosiphils per field were found
in 3/68 eosphagus, 1/68 stomach, 8/68 duodenum and 24/68 (35%) colons.
Inflammatory reactions were found in 56/68 (82%) esophogitis, 64/68 (94%)
gastritis, and all (100%) presented with duodenitis and colitis. CD-4/CD-8
relationship existed of >3 in 42/68 (62%) and <1 in 16/68. The authors concluded
that the children presented immunological and immunohistochemical alterations of
the biopsies of their digestive tracts, and that there was a significant finding
of lymphoid nodular hyperplasia, eosiophilinfiltration, and that prevalence of
greater CD-4 than CD-8 cells in the inflammation of the intestinal wall
demonstrated in favour of a Th2 type allergic reaction.
Taken together, the above now provide very convincing evidence from a number of
wholly-independent groups of researchers of a link between the novel
inflammatory bowel disease of ileal lymphoid nodular hyperplasia and regressive
autism.
(B) The Link Between Inflammatory Bowel Disease and Measles Virus
These autism/inflammatory bowel disease findings were followed by findings that
linked the novel form of inflammatory bowel disease with persistent measles
virus in the gut of affected children:
• A paper (16) by Uhlmann, Sheils et al, noting that measles virus nucleoprotein
(N antigen) had been detected in association with follicular dendritic cells (FDC)
in patients, and seeking molecular confirmation of this result, found that
:solution phase RT PCR yielded specific measles virus N gene amplification in
affected children (10/10), and identified distinct measles virus genome in FDC
reactive follicular centres by in-cell RNA amplification. None of the normal
controls showed any evidence of measles virus genome. The data highlighted a
possible causal link between measles virus infection and ileo-colonic lymphoid
nodular hyperplasia in affected children.
• A paper (17) presented in the year 2000 by Singh to the US House of
Representatives Committee on Government Reform reported a hyperimmune response
to the measles virus, with an association between measles virus antibody levels
and incidence of brain autoantibody.
• An April 2000 paper (18) presented by O’Leary to the Committee on Government
Reform reported the investigation whether measles virus was present n the gut
biopsies of autistic children, and if so, where and how much. The paper reported
that the biopsies of 24 out of 25 (96%) of the autistic children examined were
positive for measles virus, and that amongst normal (non-autistic) controls,
only 1 out of 15 children (6.6%) were positive, strongly suggesting a connection
between measles virus and autism.
• A February 2002 paper (19) by Uhlmann, Wakefield, O’Leary et al investigated
the presence of persistent measles virus in the intestinal tissue of 91 autistic
patients with new-variant inflammatory bowel disease (ileal-lymphoid nodular
hyperplasia, or ILNH). Patient samples were provided by the Royal Free Hospital,
London. The patients were ages 3-14, and 77 out of 91 were male. There were 70
developmentally-normal controls ages 0-17 years, 47 out of 70 being boys. Of
these, 19 had normal ileal biopsies, 13 had mild non-specific chronic
inflammatory changes, 3 had ILNH and had been investigated for abdominal pain, 8
had Crohn’s Disease, one had ulcerative colitis, and 26 had undergone
appendicectomy for abdominal pain including appendicitis. The results were that
75 out of 91 patients with a histologically-confirmed diagnosis of ileal-lymphoid
nodular hyperplasia and enterocolitis were positive for measles virus in their
intestinal tissue, compared with 5 out of 70 controls. Using TaqMan RT-PCR
techniques, 70 out of 91 affected children were positive for measles virus,
compared with 4 out of 70 controls. Of the controls, measles virus was not
detected in normal children or children with isolated ileal-lymphoid nodular
hyperplasia. However, 4 out of 26 appendicectomy samples harboured measles virus
genome; the study suggested that the prevalence of measles virus in the general
population warranted further investigation. The study concluded that the data
confirmed an association between the presence of gut pathology and of measles
virus in children with developmental disorder. The study did not exclude the
presence of alternative infections to measles virus.
• A February 2004 paper (20) presented by Singh to the US Institute of Medicine,
Washington DC, measured antibodies in autistic children to five viruses,
measles, mumps, rubella, CMV and human herpes virus 6. Researchers found that
the antibody level of the measles virus alone, and not the other four, was
significantly higher in autistic children than in normal children. The research
also found a correlation between measles antibody and brain autoimmunity, which
was marked by myelin basic protein antibodies. The two markers correlated in
over 90% of the autistic children tested for them, suggesting a causal link
between measles virus and autoimmunity in autism. The serology to other viruses
and other brain autoantibodies did not show this correlation. This suggested a
temporal link of measles virus in the etiology of autism.
An early-report presentation by Walker, Hepner et al, at the International
Meeting for Autism Research, Montreal, June 2006, reported that PCR analysis on
terminal ileum biopsy tissue from an initial 82 patients found 70 (85%) positive
for measles virus f-gene amplicon. These preliminary results confirm earlier
findings of measles virus RNA in the terminal ileum. Full publication of this
study is anticipated.
The above studies provide significant evidence for a link between measles virus
and ileal lymphoid nodular hyperplasia, with the latter’s earlier-demonstrated
onward link with regressive autism.
(C) The Link Between Measles Virus and Vaccination with MMR
• A July 2002 paper (21) presented by O’Leary reported that the strain of
measles virus used in MMR had been detected in the gut tissue of 12 autistic
children. Medical histories had indicated that each of the children had
developed autism after the date of receipt of MMR, and none had exhibited
outward signs of measles infection before becoming autistic.
• An April 2000 study (22) by Kawashima, Takayuki et al confirmed that, amongst
8 patients with Crohn’s Disease, 3 patients with ulcerative colitis and 9
patients with autistic enterocolitis, and 8 children who were either healthy or
who had SSPE, SLE or HIV-1, 1 out of 8 patients with CD, 1 out of 3 patients
with UC and 3 out of 9 patients with autism were positive for measles virus.
Controls were all negative. The sequences from patients with CD shared the
characteristics of wild-strain measles virus. The sequences from patients with
UC and from patients with autism were consistent with vaccine strain measles
virus. These results were consistent with patients’ medical histories, and point
to a connection between autism and vaccine-strain measles virus.
• A May 2002 paper (23) by Singh, Nelson, Jensen and Bradstreet found that a
significant percentage of autistic children examined had antibodies to myelin
basic protein (up to 88% positive) and to MMR (up to 65% positive). Normal
children did not exhibit these antibodies. The analysis of paired samples (serum
and cerebral spinal fluid from 7 autistic children also revealed a high degree
of serological association between MMR and myelin basic protein. Some 50% of CSF
had MMR antibodies, 86% of CSF had MBP antibodies, 75% of sera had MMR
antibodies and 100% of sera had MBP antibodies. Therefore there was a strong
correlation between MMR antibodies and myelin basic protein antibodies. By using
monoclonal antibodies, the authors characterized that the MMR antibodies were
due to the measles sub-unit, but not to the mumps or rubella sub-units, of MMR.
In the light of this, the authors suggested that in some cases of autism, MMR
might cause autoimmunity, and it might be doing so by bringing on an atypical
measles infection that manifests neurological symptoms.
• An earlier 1999 paper (24) by Bitnun has previously and independently
confirmed the presence of measles virus in the brain tissue of a
previously-healthy child following exposure to MMR, when the child had no
history of wild measles infection.
• A February 2004 paper (25) by Bradstreet, O’Leary, Sheils et al to the US
Institute of Medicine, and subsequently published later that year, reported that
three children with regressive autism had undergone cerebrospinal fluid
assessment, including for measles virus. All three had had concomitant onset of
gastrointestinal symptoms and had already had measles virus genomic RNA detected
in biopsies of ileal-lymphoid nodular hyperplasia. None of the cases nor
non-autistic controls had any history of measles exposure other than possibly
via MMR. Serum and cerebrospinal fluid samples were also evaluated for
antibodies to measles virus and myelin basic protein. The result was that
measles virus f-gene was present in the cerebrospinal fluid of all three
autistic cases but not in non-autistic controls. Further, serum anti-myelin
basic protein autoantibodies were detected in all children with autistic
encephalopathy. Anti-MBP and measles virus antibodies were detected in the CSF
of two cases, but the third had neither. The study concluded that the findings
were consistent with a measles-virus etiology for autistic encephalopathy,
indicating the possibility of a virally-driven cerebral immunopathology in some
cases of regressive autism. The virus genome found in the autistic children was
“exclusively consistent with vaccine strain”.
• A May 2006 study (26) by Wakefield, Stott and Limb investigated the hypothesis
as to whether a dose-response effect of measles-containing vaccine on intestinal
pathology existed. If it did exist, this would constitute evidence of a causal
association. In the study, children with normal early development and
autistic-like developmental regression were divided into two groups. Children
were divided into two groups: some 23 re-exposed children, i.e. those who had
received more than one dose of a measles-containing vaccine (MCV), and 23
children who had received only one dose of MCV. The groups were matched for sex,
age and time that had elapsed from first exposure to time of endoscopy.
Comparisons made included secondary gastrointestinal (GI) and related physical
symptoms, and “observer-blinded” scores of endoscopic and histological disease.
The results were that re-exposed children scored significantly higher than
only-once-exposed for secondary physical symptoms, including incontinence,
presence of severe ileal-lymphoid nodular hyperplasia, the number of biopsies
with epithelial damage, and number of children with acute inflammation. Markers
of acute inflammation include number of children affected, and proportion of
biopsies affect. The conclusion of the study was that the data confirmed a
re-challenge effect (i.e. a double-hit effect) of measles-containing vaccines on
symptoms, and also confirmed a biological gradient effect upon intestinal
pathology. These findings thus link exposure to measles-containing vaccines to
autistic-like regression and enterocolitis. (Note: it was stated in April 2001
by the Vaccine Safety Committee of the US Institute of Medicine that in the
context of MMR and autism “challenge re-challenge would constitute strong
evidence of an association”.)
Taken together, with the Walker, Hepner et al study, the above points to MMR as
the means by which measles virus enters and persists in the gut, leading to
ileal-lymphoid nodular hyperplasia, and in turn leading to regressive autism.
The evidence to fully explain the complete causational mechanism by which this
occurs is still emerging, and clearly requires further urgent research.
The intestinal disease has the features of a viral disease. Measles virus is
known to infect the intestine, and produces the features described originally by
Wakefield and colleagues in 1998.
All the findings described in the 1998 Lancet report by the Wakefield team -
including the discovery of a possible new type of inflammatory bowel disease,
have therefore been subsequently independently confirmed by other researchers in
the US, in Italy and in Venezuela.
The studies suggest that in some children, brain damage leading to autism may be
secondary to, or occur in parallel with, a disease in the intestine, and that
vaccine strain measles virus has become the prime suspect in this complex
investigation.
The findings to date have important implications for our understanding and
treatment of the complex disorder of regressive autism.
(D) Wider Safety Concerns Over MMR:
It is also instructive to examine the original, and any subsequent, safety
studies of MMR.
• An authoritative independent review by the Cochrane Collaboration (27) of the
safety studies of MMR vaccine concluded that “the design and reporting of safety
outcomes in MMR vaccine studies, both pre- and post-marketing, are largely
inadequate”. It further confirmed that neither before nor after the introduction
of the MMR vaccine were proper safety trials carried out.
• A more recent review (28) from the same organization identified that safety
studies for the single measles vaccine were better than those conducted for MMR:
“We found only limited evidence of safety of MMR compared to the single
component vaccines, that had a low risk of bias”. The authors of the Cochrane
reviews were highly critical of the safety studies of MMR, which they stated
“need to be improved”. Cochrane mentioned a specific concern that safety studies
followed up the children involved for no more than three weeks, except for one
study that lasted just six weeks.
• Concern over MMR’s safety has been expressed (29) by a key former scientific
adviser to the UK licensing authorities. Dr. Peter Fletcher, former Principal
Medical Officer in the (then) UK Medicines Division, who was medical assessor to
the Committee on Safety of Medicines, commented: “Evidence on safety was very
thin”, and “Too few children were followed for a sufficient time... Big numbers
were necessary, and computerised databases were already in place to permit this,
but it was not done... Caution should have ruled the day... There should have
been strong encouragement to conduct a 12-month observational study on
10,000-15,000 children...” (this was not done) "The granting of a product
licence was premature.”
• A year-2000 review (30 by Wakefield & Montgomery examined early safety studies
of MMR, by Buynak et al 1969, Stokes et al 1971, Minekawa et al 1974, Schwartz
et al 1975, Crawford and Gremillion 1981, and Miller et al 1987. The Buynak
study identified viral “interference”, but the follow-up period was only 12
days. The Stokes study revealed persistent gastrointestinal problems in the US
trial children, but the follow-up was only 28 days. Stokes compared 228 MMR
children with 106 unvaccinated controls. Data, from Philadelphia and Costa Rica
and San Salvador, was merged - a major methodological error. Gastroenteritis was
found to be significantly more common in the Philadelphia vaccines (24%)
compared with the unvaccinated Philadelphia controls (5.6%). No significant
difference was found between the vaccinated and the unvaccinated in Costa Rica
and San Salvador because of high ambient levels of gastroenteritis anyway (50%
in vaccines, 44% in controls). Combining all the data masked these instructive
differences. There was also significant “unrelated” illness in 39% of
Philadelphia vaccines (otitis, allergy, viral infection, abdominal pain),
compared with 12.2% in controls. The potential relevance of this was not seen at
time. The Minekawa study confirmed viral interference. The follow-up period was
only 15 days. The Schwartz study also merged its data, so provided insufficient
insight, and again follow-up was only 21 days. The study looked at two different
populations, 282 children in Ohio and 926 children in Santo Domingo, Dominican
Republic. Again, the merging of data from different countries was a serious
error. No data was provided to permit analysis of adverse events. Crawford and
Gremillion’s study of USAF recruits confirmed viral interference, but the
follow-up period was only 19 days. Some 512 vaccines were compared with 835
unvaccinated controls. The study noted increased fever and diarrhoea in those
that received measles and rubella vaccines simultaneously. But the potential
effect of trivalent vaccine was only seen as additive instead of potentially
synergistic - a key point. The Eddes study (a small UK study) in 1991 compared
reactions to MMR with monovalent measles vaccine. High rates of gastrointestinal
disorders (41.9% and 37.8%) were found, but the authors dismissed these as
normal background illness. The Dr. Elizabeth Miller study noted that diarrhoea
was common (26% of vaccinees), but the follow-up again was only 21 days. This
was a major missed opportunity to follow up a large cohort. The Stokes,
Schwartz, Miller and Eddes studies were therefore all too small or too
superficial to pick up uncommon adverse events. The Plesner et al study of gait
disturbance following MMR (Acta Paediatrica, 2000, 89, 58-63) confirmed an
association, and indicated that more severe cerebellar ataxias following MMR may
be associated with residual cognitive deficits.
Cochrane was forced to conclude that “the safety record of MMR is probably best
attested by its almost universal use.” Or to put it another way, “the best
evidence of MMR’s safety we can find is that fact that it’s being widely used” -
hardly a scientific test of a product’s actual safety, particularly when the
evidence of problems is through a hitherto-unsuspected link between MMR and
autism, that would not have been monitored prior to 1998.
References
(on the link between autism and a novel form of inflammatory bowel disease)
(1) Wakefield et al, Inflammatory Bowel Disease Study Group, Royal Free Hospital
London, Ileal Lymphoid Nodular Hyperplasia, Non Specific Colitis and Pervasive
Development Disorder in Children, Lancet, 28th February 1998
(2) Horvath, Papadimitiou et al, Department of Pediatrics, University of
Maryland School of Medicine, Baltimore, Gastrointestinal Abnormalities in
Children With Autistic Disorder, Journal of Pediatrics, 1999 November, Vol 135
(5), pp559-563
(3) Wakefield, Anthony et al, Enterocolitis in Children with Developmental
Disorders, American Journal of Gastroenterology, Sept 2000, Vol 95, No. 9,
pp2285-2295
(4) Furlano, Anthony et al, Colonic CD8 and T-Cell Infiltration With Epithelial
Damage in Children with Autism, Journal of Pediatrics, 2001; 138; No. 3, 366-372
(5) Paper by Dr. Timothy Buie, Harvard Massachusetts General Hospital, presented
to the Oasis 2001 Conference for Autism, Portland, Oregon, November 2001
(6) Wakefield, Anthony, Montgomery et al, Inflammatory Bowel disease Study
Group, Royal Free Hospital, University College Medical School, London, and
Coombe Women’s Hospital and Trinity College Dublin, The Concept of Enterocolonic
Encepalopathy, Autism and Opioid Receptor Ligands, Aliment Pharmacological Ther,
16: pp663-674
(7) Presentation by Krigsman to the US Congressional Committee on Government
Reform’s June 2002 hearing, The Status of Research into Vaccine Safety and
Autism, held in Washington DC
(8) Ashwood, Murch et al, Royal Free Hospital, London, Intestinal Lymphocyte
Populations in Children with Regressive Autism: Evidence for Extensive Mucosal
Immunopathology, Journal of Clinical Immunology, Vol 23 No. 6 Nov 2003 pp504-517
(9) Torrente, Anthony et al, Centre for Pediatric Gastroenterology, Royal Free
Hospital and University College Medical School, London, Focal-Enhanced Gastritis
in Regressive Autism, With Features Distinct from Crohn’s and Helicobacter
Pylori Gastritis, American Journal of Gastroenterology, Vol 99, Issue 4, p598,
April 2004
(10) Ashwood, Anthony et al, Spontaneous Mucosal Lymphocyte Cytokine Profiles in
Children with Autism and Gastrointestinal Symptoms: Mucosal Immune Activation
and Reduced Counter-Regulatory Interleukin-10, Journal of Clinical Immunology,
Vol 24, No. 6, November 2004
(11) Jyonouchi, Geng et al, Department of Pediatrics, New Jersey Medical School,
Dysregulated Innate Immune Responses in Young Children with Autistic Spectrum
Disorders - Their Relationship in Gastrointestinal Symptoms and Dietary
Intervention, Neuropsychobiology, February 2005, 51 (2) pp77-85
(12) Letter by Balzola, Barbon et al, Department of Gastroenterology, Department
of Neuropsychiatry for Children, Department of Pediatric Gastroenterology and
Department of Biomedical Sciences and Human Oncology, University of Turin,
Pan-Enteric IBD-Like Disease in a Patient with Regressive Autism Shown for the
First Time by the Wireless Capsule Enteroscopy - Another Piece in the Jigsaw of
this Gut/Brain Syndrome?, American Journal of Gastroenterology, 2005; 100 (4)
p979
(13) Balzola, Daniela et al, Department of Gastroenterology, Department of
Neuropsychiatry for Children, Department of Pediatric Gastroenterology and
Department of Biomedical Science and Human Oncology, University of Turin,
Autistic Enterocolitis - Autistic Enterocolitis: Confirmation of a New
Inflammatory Bowel Disease in an Italian Cohort of Patients, paper presented to
the American Gastroenterological Association, May 2005 and published in
Gastroenterology 2005: 128 Suppl 2, A-303
(14) Wakefield, Ashwood et al, The Significance of Ileo-Colonic Lymphoid Nodular
Hyperplasia in Children with Autistic Spectrum Disorder, European Journal of
Gastroenterology and Hepatology, 2005, Vol 17 No. 8
(15) Gonzalez, Lopez et al, Endoscopic and Histological Characteristics of the
Digestive Mucosa in Autistic Children with Gastrointestinal Symptoms:
Preliminary Report, G.E.N. Suplemento Especial de Pediatria, no. 1, 2005;
pp41-47
(on the link between inflammatory bowel disease and measles virus)
(16) Uhlmann, Sheils et al, Department of Pathology, Coombe Women’s Hospital
Dublin, Trinity College Dublin and Royal Free Hospital London, Measles Virus in
Reactive Lympho-Nodular Hyperplasia and Ileo-colitis of Children
(17) Paper presented by Dr. Vijendra Singh, University of Michigan College of
Pharmacy, to the US House of Representatives Committee on Government Reform,
Washington DC, 2000
(18) Paper presented by Professor John O’Leary, Dublin Women’s Hospital, to the
US House of Representatives Committee on Government Reform, Washington DC, April
2000
(19) Paper By Uhlmann, Wakefield, O’Leary et al, Potential Viral Pathogenic
Mechanism For New Variant Inflammatory Bowel Disease, Journal of Clinical
Pathology, Molecular Pathology, 2002, 55, 0-6, published 6th February 2002
(20) Paper by Singh, Department of Biology Center for Integrated Biosystems,
Utah State University, Logan, Autism, Vaccines and Immune Reactions, presented
to the Institute of Medicine, Washington DC, February 2004
(on the link between measles virus and vaccination with MMR)
(21) Paper presented by O’Leary, Coombe Women’s Hospital and Trinity College
Dublin to the Pathological Society of Great Britain and Ireland, July 2002
(22) Kawashima, Takayuki et al, Detection and Sequencing of Measles Virus from
Peripheral Mononuclear Cells from Patients with Inflammatory Bowel Disease and
Autism, Digestive Diseases & Science, Vol 45, No. 4, April 2000, pp723-729
(23) Singh, Nelson, Jensen and Bradstreet, Abnormal Measles Serology and
Autoimmunity in Autistic Children, Journal of Allergy and Clinical Immunology
109 (1) S232, January 2002, and also presented to the 102nd General Meeting of
the American Society for Microbiology, Salt Lake City, Utah, May 2002
(24) Bitnun et al, Measles Inclusion-Body Encephalitis Caused by the Vaccine
Strain of Measles Virus, Clinical Infectious Diseases Journal, 1999, 29 855-61
(October)
(25) Bradstreet, O’Leary, Sheils et al, Detection of Measles Virus Genomic RNA
in Cerebrospinal Fluid in Children with Regressive Autism by TaqMan RT-PCR: A
Report of Three Cases, summarized at the Institute of Medicine, February 2004
and subsequently published as Bradstreet, Dahr et al, Detection of Measles Virus
Genomic RNA in Cerebrospinal Fluid of Children with Regressive Autism: A Report
of Three Cases, Journal of American Physicians and Surgeons, Vol 9, No. 2 Summer
2004
(26) Wakefield, Stott and Limb, Gastrointestinal Comorbidity, Autistic
Regression and Measles-Containing Vaccines; Positive Re-challenge and Biological
Gradient, Medical Veritas 3 (2006) 796-802
Again, taken with the latest study by Walker, Hepner et al, this now provides
evidence that it is highly likely that MMR vaccine is the source of the measles
virus that is in turn linked via significant evidence with ileal lymphoid
nodular hyperplasia, which in turn is strongly and convincingly linked with
regressive autism.
(on wider safety concerns over MMR vaccine)
(27) Jefferson, Price et al, Unintended Events Following Immunisation with MMR;
A Systematic Review, Vaccine, 2003; 21: pp3954-3960
(28) Demicheli, Jefferson et al, Vaccine For Measles, Mumps and Rubella in
Children (Review), The Cochrane Collaboration, published Wiley & Sons, UK, from
The Cochrane Library, 2005, Issue 4, art. No. CD004407
(29) Commentary by Dr. Peter Fletcher, Journal of Adverse Drug Reactions &
Toxicology, 2001, 20 (1), 47 63 Oxford University
(30) Wakefield & Montgomery Through A Glass Darkly (A Look Back At MMR’s Safety
Trials), Journal of Adverse Drug Reactions, 2000 19(4), 265-283
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