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Subject: Re Lyme Crymes; Why did Pat Coyle and Adrianna Marques Jump Ship and Turn Coats?
Date: Mar 20, 2014 8:07 AM
Note to the
Governor of Vermont,
regarding your reply to my friend
Richard [XXXXXXXX] in the UK about the
Lyme Disease crimes (below):
Greetings,
Allow me to introduce myself, first:
My name is Kathleen Dickson, a
former Pfizer analytical
methods development (and
VALIDATIONS!!) chemist. So this
area of bogus testing for Lyme would be
my bailiwick. I am the whistleblower for
the crime and you can verify
independently by googling: Kathleen
Dickson Yves Lobet
and find mine and Yves Lobet's
(SmithKline, Belgium) testimony at the
FDA re the LYMErix fiasco from Jan 31,
2001. I recommend reading both
contributions to that hearing on LYMErix
adverse events since Lobet slams
Allen Steere :)
I spoke about the falsified case
definition (we call it "Dearborn") and
how LYMErix caused immunosuppression
rather than, "was a vaccine." The
science has since born that out, as the
NIH admits, and I will show you.
Now, bear in mind, Yale et al, said
LYMErix was a vaccine. If it was
not, it must have been falsified.
You can follow this logic.
Per numerous requests into "What Is This
Disease Exactly, and why does it call
for antiviral and the mab treatments
against Epstein-Barr?" I wrote a little
note that is well-referenced, and you,
yourselves can contact to the authors of
these reports and ask if they,
themselves, are actually the authors of
those reports? Then you will
obviously determine that this is not MY
science, but the NIH's.
Here is that report - it is a report via
an explainer to my friends who have Lyme
and of course are not cured by
antibiotics, because Lyme is like AIDS -
it is the Great Initiator, as the
science, below, will bear out. We
discovered this phenomenon by the
astounding situation where the (fake)
OspA/LYMERix vaccine produced the same
"chronic multi-isystem disease" as
"Chronic Lyme."
??? A recombinant antigen caused
"Chronic Lyme?"
Crazy, right?
Well it's true because it was a fungal
antigen and all along it was known
fungal antigens are immune-suppressors.
https://www.facebook.com/notes/kathleen-dickson/why-did-pat-coyle-suny-and-adrianna-marques-nih-jump-ship-and-turn-coats/723862150979341
====================
TEXT, transferred to email:
---------------------------------
Why Did Pat Coyle (SUNY) and Adrianna
Marques (NIH) Jump Ship and Turn Coats?
March 19, 2014 at 7:05am
Importantly, let me start from the
beginning:
Coyle and Marques used to be on our
side, but then they both discovered
LYMErix was also the cause of the MS
outcome of Lyme. Coyle turned into
an angry snot back in 2004 or 2005 (to
my friend, the late Barb Fitzmaurice, in
person, at a conference Coyle was giving
on MS,... and Barb asked her about Lyme,
whereupon Coyle detonated). And
Marques, we always thought was on our
side, but when I called her office,
looking to speak to Roland Martin about
his OspA experiments (cited below), she
turned into a snotty beeech (whereas she
used to be the Miracle Girl of Lyme-MS,
we thought, and came to LDF conferences
(2000-2001) and everyone adored her; I
think she is from Brazil or Argentina or
something).
So, Coyle jumped ship and only talks
about MS, now. And Marques is
angry about OspA being the cause of the
MS version of Lyme. Roland Martin,
her former boss, quit and went home to
Germany some time after 2006 when he
published this data (below) about OspA
or TLR2-agonists being the cause of the
MS outcomes of Lyme.
==============================================
I am producing this Note because of a
dialog started by my friend Sharon,
which I decided to keep and expand.
Sharon: "... a women came in and stated
they would have a cure for lyme 2019 I
said I wanted the proof what do you
think?"
Kathleen Dickson: "We could cure Lyme
now, in most cases. Alemtuzumab or
Rituximab and antivirals. It's already
worked for MS and transplant patients.
And CFIDS patients." (This is
after 3 months of IV cef as shown by
Fallon and Dattwyler; and don't ask me
how you can get it without becoming a
Lyme fighter and knowing what to say;
that's what this is all about- training
you allins)
Ross: "Kathleen Dickson, just
curious. How was it discerned that these
cocktails worked? Symptom improvement,
blood testing or what?"
Ann-Marie: "Yes, Kathleen Dickson any
links I can send my doc? And which
antivirals?
Kathleen: "Sure I will get links:
http://www.ncbi.nlm.nih.gov/pubmed/?term=alemtuzumab+and+ebv
http://www.ncbi.nlm.nih.gov/pubmed/?term=rituximab+and+chronic+fatigue
Kathleen: "Yeah, the NIH finally
admitted last summer (NYT, Adrianna
Marques. NINDS) that this was about EBV.
And that explains LYMErix Disease, too.
We have an AIDS like disease, not just
spirochetes.
ADDED IN A DAY LATER:
"Complicating the picture is the fact
that some people with PTLDS symptoms
apparently never had
Lyme disease in the first place,
Dr. Marques said in an interview. There
are other infectious organisms —
Epstein-Barr virus, for example — that
can produce similar symptoms and may be
the real culprits."
http://well.blogs.nytimes.com/2013/07/08/when-lyme-disease-lasts-and-lasts/
ADDED IN A DAY LATER:
Pat Coyle on "Seronegative Chronic
Relapsing Neuroborreliosis"
http://www.ncbi.nlm.nih.gov/pubmed/7796837
ADDED IN A DAY LATER:
Adrianna Marques and Germany's Roland
Martin (NIH or NINDS) on LYMErix or
exposure to OspA blebbing as the source
of the MS version of Lyme and LYMErix
Disease (2 reports, the second one shows
you might not even have antibodies to
flagellin as a result of exposure to
OspA/TLR2-agonists/fungal antigens):
"Borrelia burgdorferi Induces TLR1 and
TLR2 in human microglia and peripheral
blood monocytes but differentially
regulates HLA-class II expression."
http://www.ncbi.nlm.nih.gov/pubmed/16783164
AND
"Borrelia burgdorferi
lipoprotein-mediated TLR2 stimulation
causes the down-regulation of TLR5 in
human monocytes."
http://www.ncbi.nlm.nih.gov/pubmed/16479520
ADDED IN A DAY LATER, RE the reports
from the early 2000s to the present by
Clifford Harding and Justin Radolf
explaining why most people (those
without Steere's RA HLAs) exposed to
fungal antigens do not produce
antibodies, and how those who do have
Steere's HLAs produce auto-reacting
antibodies.
http://www.jimmunol.org/cgi/content/full/167/2/910
Toll-like receptor 2-dependent
inhibition of macrophage class II MHC
expression and antigen processing by
19-kDa lipoprotein of Mycobacterium
tuberculosis.
Department of Pathology, Case
Western Reserve University and
University Hospitals of Cleveland,
Cleveland, OH 44106, USA. Noss EH, Pai
RK, Sellati TJ, Radolf JD, Belisle J,
Golenbock DT, Boom WH, Harding CV.
Mycobacterium tuberculosis (MTB)
induces vigorous immune responses, yet
persists inside macrophages, evading
host immunity. MTB bacilli or lysate was
found to inhibit macrophage expression
of class II MHC (MHC-II) molecules and
MHC-II Ag processing. This report
characterizes and identifies a specific
component of MTB that mediates these
inhibitory effects. The inhibitor was
extracted from MTB lysate with Triton
X-114, isolated by gel electroelution,
and identified with Abs to be MTB 19-kDa
lipoprotein. Electroelution- or
immunoaffinity-purified MTB 19-kDa
lipoprotein inhibited MHC-II expression
and processing of both soluble Ags and
Ag 85B from intact MTB bacilli.
Inhibition of MHC-II Ag processing by
either MTB bacilli or purified MTB
19-kDa lipoprotein was dependent on
Toll-like receptor (TLR) 2 and
independent of TLR 4. Synthetic analogs
of lipopeptides from Treponema pallidum
also inhibited Ag processing. Despite
the ability of MTB 19-kDa lipoprotein to
activate microbicidal and innate immune
functions early in infection, TLR
2-dependent inhibition of MHC-II
expression and Ag processing by MTB
19-kDa lipoprotein during later phases
of macrophage infection may prevent
presentation of MTB Ags and decrease
recognition by T cells. This mechanism
may allow intracellular MTB to evade
immune surveillance and maintain chronic
infection.
AND NOW I WILL SHOW THE MECHANISM
REVEALED BY CLIFFORD HARDING AND OTHERS
ON THE CONNECTION BETWEEN TLR2-AGONISTS
LIKE OSP-A or spirochetal blebbing of
TLR2/1 agonists and HLAs or why some
people have "autoimmunity":
http://www.ncbi.nlm.nih.gov/pubmed/?term=harding+cv+and+MHC
See Item Number 4, above, or the
following report:
"Mycobacterium tuberculosis
synergizes with ATP to induce release of
microvesicles and exosomes containing
major histocompatibility complex class
II molecules capable of antigen
presentation."
"Major histocompatibility complex
class II (MHC-II) molecules are released
by murine macrophages upon
lipopolysaccharide (LPS) stimulation and
ATP signaling through the P2X7 receptor.
These studies show that infection of
macrophages with Mycobacterium
tuberculosis or M. bovis strain BCG
enhances MHC-II release in synergy with
ATP.
Shed
MHC-II was contained in two distinct
organelles, exosomes and plasma
membrane-derived microvesicles, which
were both able to present exogenous
antigenic peptide to T hybridoma cells.
Furthermore, microvesicles from
mycobacterium-infected macrophages were
able to directly present M. tuberculosis
antigen (Ag) 85B(241-256)-I-A(b)
complexes that were generated by the
processing of M. tuberculosis Ag 85B in
infected cells to both M.
tuberculosis-specific T hybridoma cells
and naïve P25 M. tuberculosis T-cell
receptor (TCR)-transgenic T cells. In
the presence of prefixed macrophages,
exosomes from mycobacterium-infected
macrophages provided weak stimulation to
M. tuberculosis-specific T hybridoma
cells but not naïve P25 T cells. Thus,
infection with M. tuberculosis primes
macrophages for the increased release of
exosomes and microvesicles bearing M.
tuberculosis peptide-MHC-II complexes
that may generate antimicrobial T-cell
responses.
http://www.ncbi.nlm.nih.gov/pubmed/20837713
ADDED IN, NEXT DAY:
And here is Clifford Harding Explaining
how OspA helps EBV:
"TLR2 signaling depletes IRAK1 and
inhibits induction of type I IFN by
TLR7/9."
Liu YC1, Simmons DP, Li X,
Abbott DW, Boom WH, Harding CV.Author
information
Abstract
"Pathogens may signal through
multiple TLRs with synergistic or
antagonistic effects on the induction of
cytokines, including type I IFN (IFN-I).
IFN-I is typically induced by TLR9, but
not TLR2. Moreover, we previously
reported that TLR2 signaling by
Mycobacterium tuberculosis or other TLR2
agonists inhibited TLR9 induction of IFN-I
and IFN-I-dependent MHC-I Ag cross
processing. The current studies revealed
that lipopeptide-induced TLR2 signaling
inhibited induction of first-wave IFN-α
and IFN-β mRNA by TLR9, whereas
induction of second-wave IFN-I mRNA was
not inhibited. TLR2 also inhibited
induction of IFN-I by TLR7, another
MyD88-dependent IFN-I-inducing receptor,
but did not inhibit IFN-I induction by
TLR3 or TLR4 (both Toll/IL-1R
domain-containing adapter-inducing IFN-β
dependent, MyD88 independent). The
inhibitory effect of TLR2 was not
dependent on new protein synthesis or
intercellular signaling.
IL-1R-associated kinase 1 (IRAK1) was
depleted rapidly (within 10 min) by TLR2
agonist, but not until later (e.g., 2 h)
by TLR9 agonist. Because IRAK1 is
required for TLR7/9-induced IFN-I
production, we propose that TLR2
signaling induces rapid depletion of
IRAK1, which impairs IFN-I induction by
TLR7/9. This novel mechanism, whereby
TLR2 inhibits IFN-I induction by TLR7/9,
may shape immune responses to microbes
that express ligands for both TLR2 and
TLR7/TLR9, or responses to
bacteria/virus coinfection."
http://www.ncbi.nlm.nih.gov/pubmed/22227568
Ann-Marie: "So, treating EBV is the key?
That would explain why I did the best
while on Immunovir an antiviral for EBV
you can only get from Canada. But it was
seriously expensive and had to stop."
Kathleen: "It's more EBV *and* B cell
and T cell mutations and anergy (Follow
all of Dattwyler's reports from the late
1980s, here:
http://www.actionlyme.prg/101016.htm
).
And the fatigue returns - I mean, it's
TLR2-agonist tolerance from exposure to
shed OspA. Exposure to shed OspA-like
molecules caused a leukemia-like outcome
without the proliferation.
Kathleen: "So it seems after 3 months of
IV, people should go on to these other
treatments. The NIH knows this. They've
apparently known it at least since 2005
when Pat Coyle suddenly dropped Lyme and
went into only MS (EBV).
"We're trying to find out how far back
all the crooks knew this was more about
EBV. Pat Coyle, we know when she turned
coats and dropped the "seronegative,
relapsing neuroborreliosis" schtick."
Kathleen: "2001, Steve Schutzer
spoke about how we can't change the
standard for Lyme back to one or 2 bands
because CFIDS people, he said, also had
some Lyme bands. Makes sense only from
the perspective that they knew Lyme was
EBV back then."
Kathleen: Schutzer worked with
Coyle and produced this book:
http://www.actionlyme.org/Duray.htm
"These look like EBV-transformed cells
in the CSF of Chronic Lyme victims" -
1989, Duray."
It was based on a conference summary in
1992. In 1989, NIH/US Army scientist
Paul Duray said this about the EBV--like
transformed lymphocytes in IDSA's
special journal on Lyme and spirochetes.
This was published by IDSA, that is.
Lyme results in EBV-like transformed
Lymphocytes."
By 2006, the NIH scientist Roland Martin
found out LYMErix was the cause of the
MS outcome of Lyme. You know what that
means. He left the USA and went back
home to Germany soon thereafter."In the
summer of 2013, the NIH finally admitted
publicly in the NYT that this was mostly
about EBV. Adrianna Marques, who worked
with Roland Martin on that report about
LYMErix and EBV and the brain being in a
state of chronic immune activation as a
result of exposure to Lyme and LYMErix."
So, 7 years after the fact, she finally
admitted this. Our question is how long
ALL of them knew. How long ago Barbour
and Steere knew? And CDC's Barbara
Johnson."
So, MS and CFIDS and Lyme are all the
same thing: Activated EBV. Cancer and
AIDS-like. Cancer and AIDS are the
complete opposite of inflammatory
diseases. They're diseases of immune
incompetence."I have a page that
explains the difference between the
Great Imitator outcomes (MS, Lupus, ALS,
etc) and the CFIDS-like,
Bioweapons-like, undefined diseases (the
ones without the associated HLAs):
http://www.actionlyme.org/130131_AMJMED_ALPERT_COMPLAINT.htm"
^^^ It ties in failed childhood immunizations and the
acquired and genetic forms of Autism. It
ties in Gulf War Illness. The answer to
the abuse of all of us reveals the truth
about kids with Autism, GWI, and
Bioweapons. "Stealth Disablers" are not
so fancy after all.
Sharon: "Hi Kathleen Dickson I asked the
question and went to work....Looks as
though you helped some others though
that's great..."
Kathleen: "I hope so. I can check back
later."
END REPORT:
-------------------------------
So, kind Governor of Vermont, I would
say the people you erroneously believe
to be "Experts" on Lyme are the very
idiots who committed the crime.
The disease is not only chronic
spirochetes. It's much, much
worse. And neatly, these criminals
exposed their own real "quality" of
expertise to be, oh, I'd say perhaps one
step above your local garbage collector.
Thanks.
Kathleen M. Dickson
http://www.actionlyme.org/index.htm
========================================
From: governorvt@state.vt.us
To: rbp588@hotmail.com
Subject: Responding to your message
Date: Wed, 19 Mar 2014 08:54:26 -0400
Dear Friend,
Thank you for contacting me regarding
Lyme disease. I know that many
Vermonters who lead active, outdoor
lifestyles are currently coping with or
are at high risk for contracting Lyme
disease. Vermonters should receive
high quality, effective treatment for
all medical conditions.
Here is what I have been told by my
Health Department: Not all doctors
believe that long term antibiotic
therapy improves the condition of Lyme
disease. Physicians in Vermont may
treat patients as they think is
appropriate. There is no specific rule
against using long-term antibiotics to
treat difficult infections and the Board
of Medical Practice has never taken
action against a doctor who prescribed
long-term antibiotic
treatment for Lyme disease.
The Board recognizes providers' rights
to make choices that they reasonably
feel to be in the best interest of their
patients.
The accepted guidelines for Lyme disease
treatment are published by the
Infectious Disease Society of America.
The recommendation for treatment is 10
days to four weeks of antibiotics,
depending on the clinical presentation.
In some cases, an additional four weeks
of antibiotics are recommended. These
guidelines are endorsed by the Centers
for Disease Control and Prevention and
the National Institutes of Health and
are consistent with treatment guidelines
in Europe and Canada. These guidelines
were also subject to an independent
review in 2008 and were found to be
appropriate. However, some people
believe that these recommendations under
treat Lyme disease.
There is no question that some people
who get Lyme disease will have ongoing
symptoms even after being treated
according to accepted treatment
guidelines. There is disagreement about
whether Lyme disease requires long-term
antibiotics to treat. Even though some
patients have ongoing symptoms, Lyme
disease is not believed to cause a
chronic infection, and clinical trials
have not found that long-term
antibiotics improve outcomes in people
with Lyme disease. However, these
treatment guidelines are not rigid
protocols or a standard of care that
must be adhered to. Any treatment plan
should match the current scientific
evidence with the individual needs of
the patient and reflect the important
doctor-patient relationship.
I am following closely the ongoing
discussion concerning Lyme disease and
am interested in hearing the opinions of
those who are dealing with Lyme disease
and the medical professionals who treat
them. Thank you again for your comments.
As we move forward with this important
issue, I will keep your thoughts in
mind. If I can be of further assistance,
please do not hesitate to reach out to
my office.
Sincerely,
Peter Shumlin
Governor
109 State Street, Pavilion
Montpelier, Vermont 05609
802-828-3333
Visit Governor Shumlin’s Online
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