MUST READ: THE VACCINE / AUTISM LINK COURT DOCUMENTS

Health Lover, Ilena Rosenthal, applauds David Kirby and thanks him
for helping expose this covered-up document and bringing it to life.

The breast implant / vaccinations industires have long forced "gag"
orders on losing cases such as this. This stayed covered up only
around 4 months ... despite their best efforts.

May God protect him and all the rest of us exposing the real
Snake-oil ... Vaccinations.
http://ilenarose.blogspot.com

www.BreastImplantAwareness.org/Snake-oil.htm
Partial List of Vaccination Propagandists seen thoughout the net ...

EXCERPT: In sum, DVIC has concluded that the facts of this case meet
the statutory criteria for demonstrating that the vaccinations CHILD
received on July 19, 2000, significantly aggravated an underlying
mitochondrial disorder, which predisposed her to deficits in cellular
energy metabolism, and manifested as a regressive encephalopathy with
features of autism spectrum disorder. Therefore, respondent recommends
that compensation be awarded to petitioners in accordance with 42
U.S.C. § 300aa-11(c)(1)(C)(ii).


http://www.huffingtonpost.com/david-...-_b_88558.html

Below is a verbatim copy of the US Government concession filed last
November in a vaccine-autism case in the Court of Federal Claims, with
the names of the family redacted. It is the subject of my post
yesterday.


Every American should read this document, and interpret for themselves
what they think their government is trying to say about the
relationship, if any, between immunizations and a diagnosis of autism
spectrum disorder.

If you feel this document suggests that some kind of link may be
possible, you might consider forwarding it to your elected
representatives for further investigation.

But, of course, if you feel that this document in no way implicates
vaccines, then let's just keep going about our business as usual and
not pay any attention to all those sick kids behind the curtain.


IN THE UNITED STATES COURT OF FEDERAL CLAIMS
OFFICE OF SPECIAL MASTERS


CHILD, a minor,

by her Parents and Natural Guardians,

Petitioners,

v.

SECRETARY OF HEALTH AND HUMAN SERVICES,

Respondent.

RESPONDENT'S RULE 4(c) REPORT

In accordance with RCFC, Appendix B, Vaccine Rule 4(c), the
Secretary of Health and Human Services submits the following response
to the petition for compensation filed in this case.

FACTS

CHILD ("CHILD") was born on December --, 1998, and weighed eight
pounds, ten ounces. Petitioners' Exhibit ("Pet. Ex.") 54 at 13. The
pregnancy was complicated by gestational diabetes. Id. at 13. CHILD
received her first Hepatitis B immunization on December 27, 1998. Pet.
Ex. 31 at 2.

From January 26, 1999 through June 28, 1999, CHILD visited the
Pediatric Center, in Catonsville, Maryland, for well-child
examinations and minor complaints, including fever and eczema. Pet.
Ex. 31 at 5-10, 19. During this time period, she received the
following pediatric vaccinations, without incident:

Vaccine Dates Administered

Hep B 12/27/98; 1/26/99

IPV 3/12/99; 4/27/99

Hib 3/12/99; 4/27/99; 6/28/99

DTaP 3/12/99; 4/27/99; 6/28/99

Id. at 2.

At seven months of age, CHILD was diagnosed with bilateral otitis
media. Pet. Ex. 31 at 20. In the subsequent months between July 1999
and January 2000, she had frequent bouts of otitis media, which
doctors treated with multiple antibiotics. Pet. Ex. 2 at 4. On
December 3,1999, CHILD was seen by Karl Diehn, M.D., at Ear, Nose, and
Throat Associates of the Greater Baltimore Medical Center ("ENT
Associates"). Pet. Ex. 31 at 44. Dr. Diehn recommend that CHILD
receive PE tubes for her "recurrent otitis media and serious otitis."
Id. CHILD received PE tubes in January 2000. Pet. Ex. 24 at 7. Due to
CHILD's otitis media, her mother did not allow CHILD to receive the
standard 12 and 15 month childhood immunizations. Pet. Ex. 2 at 4.

According to the medical records, CHILD consistently met her
developmental milestones during the first eighteen months of her life.
The record of an October 5, 1999 visit to the Pediatric Center notes
that CHILD was mimicking sounds, crawling, and sitting. Pet. Ex. 31 at
9. The record of her 12-month pediatric examination notes that she was
using the words "Mom" and "Dad," pulling herself up, and cruising. Id.
at 10.

At a July 19, 2000 pediatric visit, the pediatrician observed that
CHILD "spoke well" and was "alert and active." Pet. Ex. 31 at 11.
CHILD's mother reported that CHILD had regular bowel movements and
slept through the night. Id. At the July 19, 2000 examination, CHILD
received five vaccinations - DTaP, Hib, MMR, Varivax, and IPV. Id. at
2, 11.

According to her mother's affidavit, CHILD developed a fever of
102.3 degrees two days after her immunizations and was lethargic,
irritable, and cried for long periods of time. Pet. Ex. 2 at 6. She
exhibited intermittent, high-pitched screaming and a decreased
response to stimuli. Id. MOM spoke with the pediatrician, who told her
that CHILD was having a normal reaction to her immunizations. Id.
According to CHILD's mother, this behavior continued over the next ten
days, and CHILD also began to arch her back when she cried. Id.

On July 31, 2000, CHILD presented to the Pediatric Center with a
101-102 degree temperature, a diminished appetite, and small red dots
on her chest. Pet. Ex. 31 at 28. The nurse practitioner recorded that
CHILD was extremely irritable and inconsolable. Id. She was diagnosed
with a post-varicella vaccination rash. Id. at 29.

Two months later, on September 26, 2000, CHILD returned to the
Pediatric Center with a temperature of 102 degrees, diarrhea, nasal
discharge, a reduced appetite, and pulling at her left ear. Id. at 29.
Two days later, on September 28, 2000, CHILD was again seen at the
Pediatric Center because her diarrhea continued, she was congested,
and her mother reported that CHILD was crying during urination. Id. at
32. On November 1, 2000, CHILD received bilateral PE tubes. Id. at 38.
On November 13, 2000, a physician at ENT Associates noted that CHILD
was "obviously hearing better" and her audiogram was normal. Id. at
38. On November 27, 2000, CHILD was seen at the Pediatric Center with
complaints of diarrhea, vomiting, diminished energy, fever, and a rash
on her cheek. Id. at 33. At a follow-up visit, on December 14, 2000,
the doctor noted that CHILD had a possible speech delay. Id.

CHILD was evaluated at the Howard County Infants and Toddlers
Program, on November 17, 2000, and November 28, 2000, due to concerns
about her language development. Pet. Ex. 19 at 2, 7. The assessment
team observed deficits in CHILD's communication and social
development. Id. at 6. CHILD's mother reported that CHILD had become
less responsive to verbal direction in the previous four months and
had lost some language skills. Id. At 2.

On December 21, 2000, CHILD returned to ENT Associates because of
an obstruction in her right ear and fussiness. Pet. Ex. 31 at 39. Dr.
Grace Matesic identified a middle ear effusion and recorded that CHILD
was having some balance issues and not progressing with her speech.
Id. On December 27, 2000, CHILD visited ENT Associates, where Dr.
Grace Matesic observed that CHILD's left PE tube was obstructed with
crust. Pet. Ex. 14 at 6. The tube was replaced on January 17, 2001.
Id.

Dr. Andrew Zimmerman, a pediatric neurologist, evaluated CHILD at
the Kennedy Krieger Children's Hospital Neurology Clinic ("Krieger
Institute"), on February 8, 2001. Pet. Ex. 25 at 1. Dr. Zimmerman
reported that after CHILD's immunizations of July 19, 2000, an
"encephalopathy progressed to persistent loss of previously acquired
language, eye contact, and relatedness." Id. He noted a disruption in
CHILD's sleep patterns, persistent screaming and arching, the
development of pica to foreign objects, and loose stools. Id. Dr.
Zimmerman observed that CHILD watched the fluorescent lights
repeatedly during the examination and

would not make eye contact. Id. He diagnosed CHILD with
"regressive encephalopathy with features consistent with an autistic
spectrum disorder, following normal development." Id. At 2. Dr.
Zimmerman ordered genetic testing, a magnetic resonance imaging test
("MRI"), and an electroencephalogram ("EEG"). Id.

Dr. Zimmerman referred CHILD to the Krieger Institute's
Occupational Therapy Clinic and the Center for Autism and Related
Disorders ("CARDS"). Pet. Ex. 25 at 40. She was evaluated at the
Occupational Therapy Clinic by Stacey Merenstein, OTR/L, on February
23, 2001. Id. The evaluation report summarized that CHILD had deficits
in "many areas of sensory processing which decrease[d] her ability to
interpret sensory input and influence[d] her motor performance as a
result." Id. at 45. CHILD was evaluated by Alice Kau and Kelley Duff,
on May 16, 2001, at CARDS. Pet. Ex. 25 at 17. The clinicians concluded
that CHILD was developmentally delayed and demonstrated features of
autistic disorder. Id. at 22.

CHILD returned to Dr. Zimmerman, on May 17, 2001, for a follow-up
consultation. Pet. Ex. 25 at 4. An overnight EEG, performed on April
6, 2001, showed no seizure discharges. Id. at 16. An MRI, performed on
March 14, 2001, was normal. Pet. Ex. 24 at 16. A G-band test revealed
a normal karyotype. Pet. Ex. 25 at 16. Laboratory studies, however,
strongly indicated an underlying mitochondrial disorder. Id. at 4.

Dr. Zimmerman referred CHILD for a neurogenetics consultation to
evaluate her abnormal metabolic test results. Pet. Ex. 25 at 8. CHILD
met with Dr. Richard Kelley, a specialist in neurogenetics, on May 22,
2001, at the Krieger Institute. Id. In his assessment, Dr. Kelley
affirmed that CHILD's history and lab results were consistent with "an
etiologically unexplained metabolic disorder that appear[ed] to be a
common cause of developmental regression." Id. at 7. He continued to
note that children with biochemical profiles similar to CHILD's
develop normally until sometime between the first and second year of
life when their metabolic pattern becomes apparent, at which time they
developmentally regress. Id. Dr. Kelley described this condition as
"mitochondrial PPD." Id.

On October 4, 2001, Dr. John Schoffner, at Horizon Molecular
Medicine in Norcross, Georgia, examined CHILD to assess whether her
clinical manifestations were related to a defect in cellular
energetics. Pet. Ex. 16 at 26. After reviewing her history, Dr.
Schoffner agreed that the previous metabolic testing was "suggestive
of a defect in cellular energetics." Id. Dr. Schoffner recommended a
muscle biopsy, genetic testing, metabolic testing, and cell culture
based testing. Id. at 36. A CSF organic acids test, on January 8,
2002, displayed an increased lactate to pyruvate ratio of 28,1 which
can be seen in disorders of mitochondrial oxidative phosphorylation.
Id. at 22. A muscle biopsy test for oxidative phosphorylation disease
revealed abnormal results for Type One and Three. Id. at 3. The most
prominent findings were scattered atrophic myofibers that were mostly
type one oxidative phosphorylation dependent myofibers, mild increase
in lipid in selected myofibers, and occasional myofiber with reduced
cytochrome c oxidase activity. Id. at 7. After reviewing these
laboratory results, Dr. Schoffner diagnosed CHILD with oxidative
phosphorylation disease. Id. at 3. In February 2004, a mitochondrial
DNA ("mtDNA") point mutation analysis revealed a single nucleotide
change in the 16S ribosomal RNA gene (T2387C). Id. at 11.

CHILD returned to the Krieger Institute, on July 7, 2004, for a
follow-up evaluation with Dr. Zimmerman. Pet. Ex. 57 at 9. He reported
CHILD "had done very well" with treatment for a mitochondrial
dysfunction. Dr. Zimmerman concluded that CHILD would continue to
require services in speech, occupational, physical, and behavioral
therapy. Id.

On April 14, 2006, CHILD was brought by ambulance to Athens
Regional Hospital and developed a tonic seizure en route. Pet. Ex. 10
at 38. An EEG showed diffuse slowing. Id. At 40. She was diagnosed
with having experienced a prolonged complex partial seizure and
transferred to Scottish Rite Hospital. Id. at 39, 44. She experienced
no more seizures while at Scottish Rite Hospital and was discharged on
the medications Trileptal and Diastal. Id. at 44. A follow-up MRI of
the brain, on June 16, 2006, was normal with evidence of a left
mastoiditis manifested by distortion of the air cells. Id. at 36. An
EEG, performed on August 15, 2006,

showed "rhythmic epileptiform discharges in the right temporal
region and then focal slowing during a witnessed clinical seizure."
Id. At 37. CHILD continues to suffer from a seizure disorder.

ANALYSIS

Medical personnel at the Division of Vaccine Injury Compensation,
Department of Health and Human Services (DVIC) have reviewed the facts
of this case, as presented by the petition, medical records, and
affidavits. After a thorough review, DVIC has concluded that
compensation is appropriate in this case.

In sum, DVIC has concluded that the facts of this case meet the
statutory criteria for demonstrating that the vaccinations CHILD
received on July 19, 2000, significantly aggravated an underlying
mitochondrial disorder, which predisposed her to deficits in cellular
energy metabolism, and manifested as a regressive encephalopathy with
features of autism spectrum disorder. Therefore, respondent recommends
that compensation be awarded to petitioners in accordance with 42
U.S.C. § 300aa-11(c)(1)(C)(ii).

DVIC has concluded that CHILD's complex partial seizure disorder,
with an onset of almost six years after her July 19, 2000
vaccinations, is not related to a vaccine-injury.

Respectfully submitted,

PETER D. KEISLER
Assistant Attorney General

TIMOTHY P. GARREN
Director
Torts Branch, Civil Division

MARK W. ROGERS
Deputy Director
Torts Branch, Civil Division

VINCENT J. MATANOSKI
Assistant Director
Torts Branch, Civil Division

s/ Linda S. Renzi by s/ Lynn E. Ricciardella
LINDA S. RENZI
Senior Trial Counsel
Torts Branch, Civil Division
U.S. Department of Justice
P.O. Box 146
Benjamin Franklin Station
Washington, D.C. 20044
(202) 616-4133


DATE: November 9, 2007

For an excellent analysis of the medical considerations regarding the
recent decision by the US Government see:

http://www.theness.com/neurologicablog/index.php?p=203

Kirby is wrong. Period.

Has the Government Conceded Vaccines Cause Autism?

No. But David Kirby and other anti-vaccinationist ideologues and
members of the so-called mercury militia would like you to think so.
For background, the Autism Omnibus refers to a set of hearings before
the Vaccine Injury Compensation Program regarding claims by about 5000
parents that their childrens' autism was caused by vaccines. These
claims are primarily based upon the various hypotheses that the MMR
vaccine, or thimerosal in some vaccines (but not MMR), or the
combination of both, is a cause of autism.

So far there have been hearings, but only one final decision. In
November the US government settled one case in favor of the
petitioner. This is the case those who have supported the failed
hypothesis that vaccines cause autism now point to as admission that
they were right all along (or at least as a means of stoking the
flames of fear about vaccines.) But the US government did not admit
vaccines cause autism - they conceded one case that is highly complex
and not necessarily representative of any other case and cannot be
reasonably used to support the vaccine/autism connection.


David Kirby, author of Evidence of Harm, wrote a highly misleading
article the other day in the Huffington Post on this issue. Orac has
already done an excellent job of tearing down Kirby's claims. He
points out that legal cases are often decided for legal - not
necessarily scientific - reasons. That the government only conceded
that "compensation is appropriate." That is all - they conceded
nothing about the larger question of vaccines and autism. Orac also
points out that if this case were a concession of a connection why
would the petitioner's lawyers settle and give away a case that could
win them all their other cases?

David Kirby has also written a follow up article, where he publishes
verbatim the US government's decision. Kirby asks his readers:

If you feel this document suggests that some kind of link may be
possible, you might consider forwarding it to your elected
representatives for further investigation.

But, of course, if you feel that this document in no way implicates
vaccines, then let's just keep going about our business as usual and
not pay any attention to all those sick kids behind the curtain.

I think Kirby is hoping that most people will not have the patience or
medical background to read and understand the entire document, and
that they will come away with a vague notion that there must be
something to all this vaccine fear-mongering. What does the document
really tell us?

To summarize the case history, the child in the case appeared normal
and healthy, except for chronic otitis media, until about 20 months of
age at which time he had a series of vaccines according to the routine
vaccination schedule. Two days later the child had a fever to 102.3,
was lethargic, irritable, and would arch his back when he cried. The
child then developed a rash. It was later determined that the child
had: "encephalopathy progressed to persistent loss of previously
acquired language, eye contact, and relatedness." The child regressed
and developed symptoms similar to those of autism spectrum disorder.
However, the child does not have autism - he has a regressive
neurological disorder that includes blood and muscle abnormalities not
seen in autism, and any clinical resemblance to autism is not a
reflection of a common cause.

Six years after symptoms began the child also developed partial
temporal lobe epilepsy that required treatment.

During this time the child also had an extensive workup, which
discovered:

A CSF organic acids test, on January 8, 2002, displayed an increased
lactate to pyruvate ratio of 28,1 which can be seen in disorders of
mitochondrial oxidative phosphorylation.

A muscle biopsy test for oxidative phosphorylation disease revealed
abnormal results for Type One and Three.

In February 2004, a mitochondrial DNA ("mtDNA") point mutation
analysis revealed a single nucleotide change in the 16S ribosomal RNA
gene (T2387C)

It if often difficult or impossible to draw firm conclusions from a
single case, so I will lay out what I see as all the possible
alternative hypotheses to explain this information.

1) One possibility is that the child was perfectly normal prior to the
vaccines, which caused an encephalitis (inflammation of the brain)
which caused brain damage, including the later seizures. The metabolic
disorder and mutation may be a red herring and have no bearing on the
child's clinical condition.

2) The mitochondrial disorder predisposed the child to have a reaction
from the vaccines, resulting in encephalitis. The subsequent
neurological regression was due to some combination of the vaccine-
induced encephalitis and the underlying mitochondrial disorder.

3) The child's mitochondrial mutation is the primary cause of their
neurological regression, but that this regression was exacerbated by
the vaccine-induced encephalitis (this seems to be the US government's
conclusion).

4) The child has a mitochondrial encephalopathy which is the sole
cause of all of the child's neurological signs and symptoms. The
reaction to the vaccines may have played no role at all in the
subsequent regression, and the child's current neurological condition
is exactly what it would have been had they never been vaccinated. It
is even possible that the encephalitis was merely the first
manifestation of the mitochondrial disorder and the timing after the
vaccines was merely coincidental.

That lays out the spectrum of possibilities in this case. At this
point in time we do not have (or at least I am not privy to)
sufficient scientific information to say definitively where along this
spectrum the truth lies. The US government's decision was based partly
on this uncertainty - erring on the side of compensating the child and
family.

But we can discuss the plausibility of each scenario. Kirby dismisses
anything resembling option 4, but his dismissal is naive and
unjustified. In fact the patient's clinical syndrome resembles what is
called a mitochondrial encephalopathy - with increased lactic acid,
abnormal muscle biopsy, neurological regression, appropriate age of
onset, even seizures. It is probably not a coincidence that the child
has a point mutation in a gene that has been previously linked to
these very mitochondrial disorders. Kirby incorrectly argues:

While it's true that some inherited forms of Mt disease can manifest
as developmental delays, (and even ASD in the form of Rhett Syndrome)
these forms are linked to identified genetic mutations, of which
T2387C is not involved. In fact little, if anything, is known about
the function of this particular gene.

This is misleading. Kirby refers to "this particular gene" which makes
me think that he believes T2387C is a gene. It's not - it describes a
point mutation (at location 2387 a thymidine has replaced a cytosine).
The gene is the 16S ribosomal RNA gene. Mutations in this gene have
been identified to cause mitochondrial encephalopathy. So Kirby is
just wrong. It is true that I could not find that this specific
mutation has been identified before, but that is common in genetics -
a disease is linked to point mutations in a specific gene (or perhaps
specific regions of a gene) but most or all families identified have
their own specific mutation.

This makes option 4 very plausible - it would be an incredible
coincidence if this child just happened to have a mutation in a gene
that was known to cause their exact constellation of neurological
signs and symptoms and yet the mutation was not the sole or primary
cause of those symptoms.

But it does not rule out option 3 - that the mitochondrial disorder
was the primary cause of the child's neurological disorder but that a
reaction to the vaccines worsened the ultimate symptoms. Therefore the
government's decision was reasonable - but is absolutely not a
concession about any claim made by the petitioners concerning a link
between vaccines an autism.

It does, however, make any hypothesis resembling option 1 or 2
extremely unlikely. Further testing regarding the physiological
effects of this child's specific mutation would be helpful, and such
testing may be under way but I could find nothing published to date.
It is theoretically possible that the identified mutation does not
cause a change in the gene product or mitochondrial function, and is
therefore just a coincidence. But this is unlikely given the clinical
features in this case are a good match to known mutations of that
gene.

Kirby, however, apparently wants to wring as much fear and confusion
out of these events as he possibly can. So now he speculates wildly
that maybe children diagnosed with autism really have this
mitochondrial disorder combined with vaccines (he has to keep vaccines
in the loop). Given the rarity of such mutations, and the fact that
there were specific features in this case that would likely be
uncovered in the routine evaluation of a child with autism (like an
elevated lactic acid), it is highly unlikely that there are many
children with vaccine-triggered mitochondrial encephalopathy mimicking
autism out there.

It has been found that some children with autism have mitochondrial
dysfunction - one study found that 7.2% of subjects with autism had
"definite mitochondrial respiratory chain disorder." Poling et al, in
response to this child's case, did a retrospective study of children
with autism and with other neurological disorders and found that
"Aspartate aminotransferase was elevated in 38% of patients with
autism compared with 15% of controls." Such findings are preliminary -
the only conclusions that can be drawn is that the association between
autism and metabolic disorders requires further investigation.
However, these studies did not look at the incidence of suspicious
mitochondial mutations in autism, and these findings may not be
relevant to this case.

Kirby also wildly speculates that perhaps the evil toxins in vaccines
caused the mutation in the first place. He writes:

Use of the AIDS drug AZT, for example, can cause Mt disorders by
deleting large segments of mitochondrial DNA. If that is the case,
might other exposures to drugs or toxins (i.e., thimerosal, mercury in
fish, air pollution, pesticides, live viruses) also cause sporadic Mt
disease in certain subsets of children, through similar genotoxic
mechanisms?

Among stiff competition, this is perhaps the most absurd and
scientifically ignorant thing Kirby has every written. AZT does NOT
cause a genetic disorder. AZT blocks DNA replication (it blocks the
copying of DNA) - that is its mechanism as an anti-retroviral drug. In
patients it can also block mitochondrial DNA replication, thereby
causing mitochondrial depletion. This results in there being too few
mitochondria (the energy factories of cells) in some cell populations
and causes dysfunction in tissue that is especially susceptible to the
effects of this dearth of mitochondria. This is a side effect of AZT
and also other retrovirals because of sustained use at doses designed
to inhibit DNA replication. This does result in some effects that are
similar to mitochondrial genetic disorders - because both result in
insufficient mitochondrial activity. But that is the only similarity.
AZT does not cause a disseminated somatic mutation, which is the
incredible analogy that Kirby is making.

What Kirby is suggesting is that in infants and toddlers toxins can
cause the same point mutation in millions of different cells
throughout the body. Toxin-induced mutations do not cause genetic
diseases, unless they occur in a germ cell in which case a mother or
father can pass the mutation onto their children. If it occurs in the
womb then large cell populations may be affected (whatever cells
derive from the cell that had the mutation). But in a child a point
mutation would affect only one cell and any cells that derive from it.
A toxic mutagen would cause different random point mutations in
different cells. This could not cause the mitrochondrial
encephalopathy in this child. It can increase the risk of cancer,
because cancer can develop from a single mutation in a single cell
that causes it to become neoplastic.

Conclusion

This is a unique and idiosyncratic case that raises more questions
than it answers. In my opinion as a neurologist, with the information
provided, the child has a mitochondrial encephalopathy. The role of
the vaccines is unclear, but at worst a rare vaccine reaction
exacerbated the underlying mitochondrial disorder. This case has no
clear implication for the larger question concerning vaccines and
autism, which is likely why both sides agreed to settle.

Yet those who insist, despite the evidence, on claiming that vaccines
or mercury are linked to autism are likely to add this permanently to
their litany of misinformation and fear-mongering.

Note: I am searching for any follow up information pertinent to this
case and will post any addendum here.