“Chronic Lyme:” It’s a Coin Toss

It has been known almost from the very beginning that treatment for “Lyme disease” is as good as a coin toss. Here are three separate reports on the topic, spanning 34 years: Allen Steere in 1983, Dattwyler and Luft in IDSA’s journal in 1989, and Chiu/Soloski of UCSF and Johns Hopkins, respectively, in 2016.

Allen Steere observed, in his 1983 report “The Clinical Spectrum and Treatment of Lyme Disease” in the Yale Journal of Biology and Medicine,

“Regardless of the antibiotic agent given, nearly half of patients still experienced minor late complications-recurrent episodes of headache or pain in joints, tendons, bursae, or muscles, often accompanied by lethargy [19].”

Here is what Luft and Dattwyler said in IDSA’s journal in 1989 about how treatment fails, and how this may be due to “pathological changes that occur prior to treatment” confirmed by Baumgarth when she showed infection with Borrelia damaged B cell germinal centers and rendered victims unable to deal with a common viral infection like influenza.

Rheum Dis Clin North Am. 1989 Nov;15(4):747-55. Treatment of Lyme borreliosis.

Luft BJ1, Dattwyler RJ. https://www.ncbi.nlm.nih.gov/pubmed/2555849

“FAILURE RATES OF >50% ARE BEING REPORTED….CLEARLY, ALTERNATIVE THERAPIES ARE NEEDED.” Clearly.

Then we had a UCSF/Johns Hopkins group (Chiu, Soloski, et al) report, in 2016:

“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.”

Here is the PR version of the story; you can link to the published report from there.

So, for 34 years, it has been known, and confirmed and reconfirmed, that treatment fails half the time, and there are long term, chronic consequences.

All of us victims know that, for sure, and I’d venture to guess that the true rate of chronic illness from tick bite post-sepsis is even higher.

The fact of the matter is that “chronic Lyme,” the outcome that was eliminated from the case definition at Dearborn in 1994, is tick bite post-sepsis AIDS, an immunosuppression disease. Many different scientific groups agree on this matter, including the crooks who sought to capitalize on our suffering.

Who says it’s an immunosuppression disease?

Here are the two reports by Martin and Marques at the NIH’s NINDS’ *Lyme and MS Division* that say OspA is responsible for causing nearly complete immunosuppression, in the end:

J Neuropathol Exp Neurol. 2006 Jun;65(6):540-8. Borrelia burgdorferi Induces TLR1 and TLR2 in human microglia and peripheral blood monocytes but differentially regulates HLA-class II expression.

https://www.ncbi.nlm.nih.gov/pubmed/16783164

J Infect Dis. 2006 Mar 15;193(6):849-59. Epub 2006 Feb 8. Borrelia burgdorferi lipoprotein-mediated TLR2 stimulation causes the down-regulation of TLR5 in human monocytes. Cabral ES1, Gelderblom H, Hornung RL, Munson PJ, Martin R, Marques AR.

https://www.ncbi.nlm.nih.gov/pubmed/16479520

Gary Wormser, 2010:

Modulation of lymphocyte proliferative responses by a canine Lyme disease vaccine of recombinant outer surface protein A (OspA). Chiao JW1, Villalon P, Schwartz I, Wormser GP.

https://www.ncbi.nlm.nih.gov/pubmed/10865170

“The modulation of human lymphocyte proliferative responses was demonstrated with a recombinant outer surface protein A (OspA) vaccine preparation for the prevention of Borrelia burgdorferi infection. After exposure to either the unaltered vaccine preparation or OspA prepared in saline, normal lymphocyte responses to the mitogens concanavalin A, phytohemagglutinin-M or pokeweed mitogen, or the antigen BCG were consistently reduced. Whole cell extracts of B. burgdorferi also modulated immune responses but required a much greater quantity of protein than needed for the OspA preparation. The magnitude of modulation was directly dependent on the quantity of OspA. OspA interferes with the response of lymphocytes to proliferative stimuli including a blocking of cell cycle phase progression . Future studies designed to delete the particular region or component of the OspA molecule responsible for this effect may lead to improved vaccine preparations.”

Wormser & Sellati, 2012:

Arthritis Rheum. 2012 May; 64(5):1311-5. doi: 10.1002/art.34386.

The Toll of a TLR1 polymorphism in lyme disease: a tale of mice and men. Sellati TJ, Sahay B, Wormser GP.

https://www.ncbi.nlm.nih.gov/pubmed/22246662

“Negative regulatory pathways” means exactly this post-sepsis outcome.

Medvedev talking about immunosuppression (tolerance and cross tolerance) from Post-Lyme and Post-LYMErix Sepsis (TLR2-agonists or Pam3Cys is OspA or shed borrelial antigens)

IRAK4 kinase activity is not required for induction of endotoxin tolerance but contributes to TLR2-mediated tolerance

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3714565/

“Development of endotoxin tolerance following the initial “cytokine storm” phase of sepsis is thought to protect the host from an overexuberant immune response and tissue damage but at the same time, may render the host immunocompromised and more susceptible to secondary infection [18,–20]. …

“…Notably, IRAK4 kinase activity was found to be a prerequisite for conferring inhibition of LPS-inducible JNK and p38 MAPK activation following prior exposure to Pam3Cys. These results represent the first systematic analyses of the role of IRAK4 kinase activity in TLR homo- and heterotolerance and pave the way for improved understanding of how IRAK4 kinase dysregulation may underlie immunocompromised states in late sepsis.”

Harding says the chronic agonism of TLR2/1 by these lipoproteins also inhibit TLR7/9 function (manages the viruses like EBV:

TLR2 signaling depletes IRAK1 and inhibits induction of type I IFN by TLR7/9.

http://www.ncbi.nlm.nih.gov/pubmed/22227568

“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.”

Mario Philipp (Tulane) has for years said OspA was associated with the production of the immunosuppressive cytokine, IL-10 (this was mentioned to the FDA by Dickson, Jan 31, 2001). Here he is saying so, in 2006:

Interleukin-10 anti-inflammatory response to Borrelia burgdorferi, the agent of Lyme disease: a possible role for suppressors of cytokine signaling 1 and 3.

https://www.ncbi.nlm.nih.gov/pubmed/16988256

“It has been established that interleukin-10 (IL-10) inhibits inflammatory cytokines produced by macrophages in response to Borrelia burgdorferi or its lipoproteins….Our data are evidence to suggest that expression of SOCS is part of the mechanism of IL-10-mediated inhibition of inflammatory cytokines elicited by B. burgdorferi and its lipoproteins.”

Dattwyler & Luft, Seronegative Lyme Disease, 1989 (Remember that they also reported in IDSA’s journal the very same year, that treatment fails half the time.)

http://www.nejm.org/doi/full/10.1056/NEJM198812013192203

We have Nicole Baumgarth, UC Davis, looking at various mechanisms of borrelial immunosuppression, as noted earlier: https://www.ncbi.nlm.nih.gov/pubmed/?term=Baumgarth+and+borrelia

And, last but not least (and this is NOT an exhaustive list, but simply some highlights), we have the crooks, themselves….

December 2016: Lyme Cabal members Gary Wormser, Allen Steere, “CDC officer” Paul Mead, and others admit Late Lyme and LYMErix diseases are immunosuppression outcomes, saying the “TLR2/1 agonism” (immunosuppression) is probably the “more important” driver of the disease outcome.

Nat Rev Dis Primers. 2016 Dec 15;2:16090. doi: 10.1038/nrdp.2016.90.

Lyme borreliosis

https://www.ncbi.nlm.nih.gov/pubmed/27976670

“This finding suggests that there is redundancy in the ability of the innate immune system to recognize B. burgdorferi and/or that these components can activate pathways that produce anti-inflammatory cytokines……the anti-inflammatory effects might be the more important function of TLR signaling.”

All of this begs some very serious questions:

WTF is ILADS treating?

WTF is the government hiding?



Categories: Lyme Disease

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