The RICO Lawsuit (filed 171110 in Texas)

This lawsuit (links below) neglects the FRAUD aspect of the cryme, and also the “Deprivation of Rights under Color of Law” (because CDC officers Barbour, Steere, probably Wormser, and Barbara Johnson were involved) with all the slander and libel as shown here:
http://www.actionlyme.org/2017_Criminal_Charges_Sheets_All.pdf

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I dont see how the Plaintiffs can win without showing fraud, and that was the same reason Blumenthal’s lawsuit against these crooks failed.

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Frighteningly, these Plaintiffs *KNEW* OspA alone caused the disease, so killing spirochetes with antibiotics (or not, the False Dichotomy) is not what the disease and the controversy are all about.  Therefore, not only it is false that the bad guys denied them the opportunity for a cure with their lies about the case definition (you’re screwed in like the first week after a tick bite – Baumgarth), it is false that antibiotics would cure them even as little as month after a tick bite, because Lyme is not about antibiotics-and-spirochetes.  OspA or triacyl lipopeptide (TLR2/1-agonists) injections alone caused the post-sepsis syndrome we call Chronic NeuroLyme.
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Read more here about how fungal antigens INHIBIT APOPTOSIS:
https://crymedisease.wordpress.com/2016/08/02/inhibition-of-apoptosis/
So that you understand the primary mechanism of disease, and so that when you read what Nicole Baumgarth has to say, here, about the early collapse of the germinal centers perhaps because none of the immune cells are “presenting antigen” you’ll understand this all more clearly.

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I am not even sure how long it takes for anti-flagellar antibodies show up.  I think no sooner than a week.  It is quite likely none of these claimants can prove exactly when they were bitten by a tick and when they first went to a doctor for a Lyme test.
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These Plaintiffs all lied to their law firms regarding what the disease was about.  Many if not most of them knew me and about OspA-disease (fungal endotoxin induced immunosuppression and sepsis), since I been screaming about it for over a decade.
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We cant use the Fallon and Klempner long term treatment studies since both of those were invalid – because they were both based on Dearborn as a “case” and Dearborn excludes NeuroLyme.  We know Chronic NeuroLyme does not test HLA-linked-, hypersensitivity-, “Bad Knee Only-“, Case definition-, Dearborn-Lyme positive.  So those 2 grants of 4.7 million dollars were wasted.  Also, here is a recent data-summary of the efficacy of antibiotics in neuroLyme (post-sepsis):
https://www.ncbi.nlm.nih.gov/pubmed/27931077

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They dont work.  Therefore, there is no harm in denying them.

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Since antibiotics dont work for viral infections, the Plaintiffs do not have a case for harm caused by perjury and other lies about Lyme and early treatment.

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This lawsuit makes the case for how it is wrong and selfish to make Lyme “All About Meeee!!”

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The Case:

https://www.courthousenews.com/wp-content/uploads/2017/11/LymeDisease.pdf

https://www.courthousenews.com/insurers-accused-conspiring-deny-lyme-disease-coverage/

 

Okay, so what really happened was this:

It was known basically WHY treatment failed before the year 1990, when the ALDF.com was founded (Dattwyler and Bb Osp-/glycolipid-induced immunosuppression, Steere, Duray, sepsis and EBV), and the fact that the NIH (Dorward, Martin and Marques) thinks this is about the shed blebs (containing Osps) causing global immunosuppression and reactivating EBV. 
In 2016, Chiu found early treatment fails in half the cases of even EARLY treatment (same as in 1989);
in Dec 2016, the crooks Wormser and Steere reported that TLR2 agonism (immunosuppression was the more important driver of disease – basically admitting the truth);
and just this month, November 2017, Linden Hu (partner with Klempner in the bogus study that became the essence of the “IDSA Guidelines”) reported that the shed blebs were indeed causing the immunosuppression disease, “Chronic Lyme,” to look exactly like LYMErix disease (post-sepsis syndrome), because it is.

 

And learned from Baumgarth and Barthold that spirochetes go after the lymph nodes and destroy immunity within days:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3358496/

“Thus, it is of interest to consider potential roles for the inhibition of the CP beyond protection from complement-mediated attack. For example, upon colonizing lymph tissue Bburgdorferi disrupts the normal formation of germinal centers (GC) [60,61]. Lack of normal GC development ultimately results in reduced antibody titers against Bburgdorferi in experimental infection [60]. Local complement C4 deposition on follicular dendritic cells (FDC) is significantly reduced in Bburgdorferi infected lymph nodes and this is speculated to be responsible for the premature collapse of GC responses due to diminished antigen presentation by FDCs [60].”

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4725857/#ppat.1005404.ref060

 

“Local complement C4 deposition on follicular dendritic cells (FDC) is significantly reduced in Bburgdorferi infected lymph nodes and ***this is speculated to be responsible for the premature collapse of GC responses due to diminished antigen presentation by FDCs. ***…”

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If the shed blebs are FUNGAL-ish, bearing Osps or Vmps or glycolipids (anything that is a TLR2/1 agonist, or a fungal endotoxin, stops “presenting antigen” according Clifford Harding and others) the HLA molecules do not “present antigen;” if antigen is not “presented,” no antibodies are made.  See the “Occam’s Razor” criminal charge sheet in truthcures.org/charge-sheets for more of this science, or in the one pdf of all the charges:
http://www.actionlyme.org/2017_Criminal_Charges_Sheets_All.pdf

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Here is what Baumgarth said, most recently:

“By decreasing the capacity of the host to produce effective antibodies against B. burgdorferi, the GC collapse may help B. burgdorferi evade clearance. The signals and mechanisms leading to the collapse, however, are unknown. One possible mechanism is the interference of B. burgdorferi with the complement system. Continued antigen presentation is crucial for hyperaffinity maturation, and components of the complement system are known to be involved in this process. Specifically, activated C3 and C4 fragments bound to antigen and adhere to complement receptors 1 and 2 (CR1 and CR2). These receptors are present on the major antigen-presenting cells in the GC, the FDC, and on GC B cells. It was shown previously that GCs will form normally in mice lacking CR1 and CR2, but collapse prematurely, before GCs can perform their important functions (120). This phenotype is strikingly similar to that seen in wild-type mice infected with B. burgdorferi. Interestingly, in B. burgdorferi-infected mice, although CR1 and CR2 are present on FDCs and GC B cells, C4 is not detectable (69). C4 is typically deposited on the surface of FDCs supporting antigen presentation. Interference with C4 deposition could inhibit antigen presentation by FDCs to GC B cells and thereby lead to GC collapse. B. burgdorferi interference with activation of complement could also have various indirect effects on GCs: changing the cytokine milieu, reducing antigen presentation to naïve B cells via CR1 on APCs outside the GC, reducing naïve B cell activation viaco-stimulation with CR2, and reducing opsonization (and thus uptake) of antigens. Exploring the role of complement and complement inhibition by B. burgdorferi during infection are important subjects for future studies.”

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5316537/

And

“Furthermore, the appearance of culturable B. burgdorferi and its visible presence in cortical sinuses in the lymph nodes is correlated with the disruption of the usually well-demarcated T and B cell areas and an expansion of the lymph node cortex by day 10 of infection (37). ”
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3993384/

You’re effed, before you ever knew what hit you.

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1986, Steere with Duray, describing Lyme as if it is post-sepsis with reactivated EBV and with deformed, immature B cells
http://www.actionlyme.org/clinical-pathologic-correlations-of-lyme-disease-by-stage-Steere-Duray.pdf

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1990, Feb, NIH’s Dave Dorward and the shed blebs:

“The invention relates to novel antigens associated with Borrelia burgdorferi which are exported (or shed) in vivo and whose detection is a means of diagnosing Lyme disease. The antigens are extracellular membrane vesicles and other bioproducts including the major extracellular protein antigen. Another object of the invention is to provide antibodies, monoclonal and/or polyclonal, labeled and/or unlabeled, that are raised against the antigens. A further object of the invention is to provide a method of diagnosing Lyme disease by detecting the antigens in a biological sample taken from a host using the antibodies in conventional immunoassay formats. Another object of the invention is to provide kits, for the diagnosis of Lyme disease, comprising the antibodies and ancillary reagents. The advantage of the antibodies used in the invention is that they react with the antigens from geographically diverse strains of Borrelia burgdorferi, but do not react with antigens from related Borrelia spirochetes.”
http://patft.uspto.gov/netacgi/nph-Parser?Sect1=PTO1&Sect2=HITOFF&d=PALL&p=1&u=%2Fnetahtml%2FPTO%2Fsrchnum.htm&r=1&f=G&l=50&s1=5,217,872.PN.&OS=PN/5,217,872&RS=PN/5,217,872

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2016, December,  Crooks Wormser and Steere reporting that Lyme and LYMErix diseases are diseases of global immunosuppression (due to the antigens of spirochetes being fungal-ish):

161219_STEERE_WORMSER_IMMUNOSUPPRESSION

Abstract (published Dec 15, 2016):  https://www.ncbi.nlm.nih.gov/pubmed/27976670

Full Text:  http://www.actionlyme.org/Steere_Wormser_Admit_Immunosuppression.2016_Dec_15.pdf

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2017, November, Hu and the shed blebs containing TLR2 agonists [Osps (and glycolipids, I assume)]:
171102_HU_BLEBS_OSPS

 

 

Dattwyler on Bb hydrophobic antigens (supernatant) inhibiting NK cell activity (1988):
http://www.actionlyme.org/1988_DattwylerGolightly_NK_cells.pdf

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2013, NIH’s Martin and Marques on the shed TLR2 agonist Osps, blebs and glycolipids causing global immunosuppression with an inflammed brain (the opposite):
https://www.ncbi.nlm.nih.gov/pubmed/?term=Martin+and+Marques+and+TLR2

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NIH’s Adrianna Marques in the NYT saying EBV may be the real culprit:
https://well.blogs.nytimes.com/2013/07/08/when-lyme-disease-lasts-and-lasts/

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It’s basically settled.  Yes there is a RICO, but treatment fails in half the cases regardless:

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1989, Dattwyler and Luft, saying so in IDSA’s own journal:
http://www.actionlyme.org/IDSA_IMMUNO_DATTWYLER.htm

161130_DATT_50_FAIL

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2016, Chiu:

“… Researchers examined 29 patients before and after they received a three-week course of antibiotic treatment and also six months later. Compared to patients with other active bacterial or viral infections, the Lyme disease patients had distinctive gene signatures that persisted for at least three weeks, even after they had taken the antibiotics. Some differences in the transcriptome lingered for six months.

“To our knowledge, this study is the first to document changes in gene expression occurring even after a bacterial infection has been treated with appropriate antibiotics,” said John Aucott, MD, assistant professor of medicine at the Johns Hopkins University School of Medicine and a senior investigator on the study.

Six months after treatment, 15 of the 29 patients in the study had fully recovered, while 13 had persistent symptoms, and one had dropped out. Despite the stark differences in how the patients reported feeling, the researchers could not detect transcriptional differences between the two groups. They said larger studies are needed to confirm this finding.”
https://www.ucsf.edu/news/2016/02/401581/gene-signature-could-lead-new-way-diagnosing-lyme

13 out of 29 were not cured with early treatment.  Same as in 1989.

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