Blowing the Whistle at the FDA, Jan 2001, exposing Dearborn and how OspA causes immunosuppression rather than, "was a vaccine."
 


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CDC "SPIDER"

Fungal Exosomes Inhibit Apoptosis

IDSA: "Vaccines serve the mfgs, not their victims"

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BlumenthalAntiTrust Lawsuit

Exosomes, Blebs

Spirochetal_Dementia


PDFs
CDC Admits Fraud, 2016
Dattwyler, 1988
Golightly, 1988
Dressler, 1994
BarbourFish, 1993
Dearborn, 1994
BarbourFishpdf.pdf
 

Pathogenic Fungi

Bush's warcrimes, Oct 2000

Trainer

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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

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