Gary Wormser - Lyme is Immunosuppression

The lead author of the IDSA Lyme disease guidelines Gary Wormser says Chronic Lyme disease doesn't exist while his published scientific research says different, that it's a disease of Immunosuppression. Wormser doesn't deny that the symptoms Lyme victims complain of are real, he refers to them as lingering effects or "post-Lyme syndrome". When what he really should be saying and what the National institutes of health (NIH) calls it, Post-Sepsis Syndrome. Much more serious and deadly than just a persistent bacterial infection or lingering symptoms. In his own published scientific research he says OspA (outer surface protein A) a triacyl endotoxin, the antigen used in the Lymerix vaccine and shed from Borrelia spirochetes outer surface does in fact cause Post-Sepsis Syndrome. All the while Wormser and his criminal cabal continue slandering, libeling and labeling their victims as Psychiatric or Hypochondriacs.

1996: U.S. Patent 6,045,804. Dave Persing here says you cannot tell the difference between a Lymerix injured or late neurological Lyme patient. 
"Vaccinated patients with multisystem complaints characteristic of later presentations of Lyme disease may be difficult to distinguish from patients with vaccine failure."

2000: Wormser publishing that the amount of OspA via tick bite or vaccine injection determines how sick you will get. Modulation of lymphocyte proliferative responses by a canine Lyme disease vaccine of recombinant outer surface protein A (OspA).
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.

He's right about persisters and that long-term antibiotic therapy doesn't work in majority. Antibiotics can't fix Post-Sepsis Syndrome, b-cell mutation, an AIDS-like illness from OspA. It's not about a persistent bacterial infection, biofilms or lingering symptoms, it's the outcome of a fungal hijacked and a permanently wrecked immune system.
"There's been no evidence that this persister phenomenon has any relevance for animals or humans. First, lab studies of B. Burgdorferi cannot account for the potential effects of the body’s immune system, which might be to eliminate persisters once the brunt of the infection is cleared. Second. Labs have yet to grow B. Burgdorferi isolated from people treated with antibiotics, and that raises questions about whether the persisters are even viable and capable of making someone sick."   

Wormser says there's no evidence of victims having Lyme disease, of course. They made their victims undectable in 1994 by falsifying the case definition and testing by changing it to a high antibody concentration and dropping antigens OspA and OspB from the diagnostics. The new diagnostics only detects 15% of the entire population that produce high antibodies and aren't sick. The other 85% who produce no to little antibodies that end up with Post-Sepsis Syndrome were excluded from the testing. In analytical testing you look for low antibody concentration, the CDC criminals did the exact opposite. The whole fraud was done to qualify Yale's crippling immune suppressing vaccine with an intended monopoly off of vaccines and test kits. Changing the testing hid that the vaccine was causing the very same disease it was "intended" to prevent .

"The majority of people I see who have been diagnosed with chronic Lyme have similar symptoms but don't have any evidence of ever having had Lyme disease."    -- Gary Wormser.

2006: Wormser again publishing chronic Lyme or post-Lyme syndrome is really immunosuppression.
“We have previously demonstrated that proteins of B. burgdorferi are capable of modulating human cellular immune responses [7]. Suppression of in vitro mitogen- or antigen-mediated proliferative responses of lymphocytes and reduced production of interleukin-2 (IL-2) from lymphocytes were demonstrated using protein extracts of B. burgdorferi. These early studies were confirmed by a report of de Souza et al. [8], who observed that B. burgdorferi infection in mice resulted in impaired T and B cell proliferation to mitogens and reduced IL-2 and IL-4 production. The nature of the B. burgdorferi proteins responsible for suppression of cellular immunity has not been defined. In this study we examined the modulating activity of a recombinant outer surface protein A (OspA) vaccine preparation on cellular immune responses.”

2012: Wormser again, the outcome is post-sespsis or Immunosuppression. The Toll of a TLR1 Polymorphism in Lyme disease: a tale of mice and men.
"During natural infection, initiation of the host response begins with CD14 recognition of triacylated borrelial lipoproteins and subsequent activation of TLR-2 in partnership with TLR-1. Such bacterial recognition activates the NF-κB, phosphatidylinositol 3-kinase/Akt, and p38 MAPK pathways. The ensuing signaling cascades initiate inflammation-associated gene activities responsible for host defense, as well as negative regulatory pathways intended to mitigate the severity and duration of the inflammatory response to spirochetes. The latter goal is achieved, in part, through the action of p38 MAPK–induced suppressors of cytokine signaling (SOCS), which down-regulate inflammation by targeting various points in the NF-κB pathway."

2005: Wormser reporting there's 2 different disease outcomes, HLA (high antibodies) and HLA restricted (low antibodies) the immunosuppression outcome who were deliberately excluded from getting a positive test.
A Case Study To Examine HLA Haplotype Associations in Patients With Posttreatment Chronic Lyme disease.

Post-Lyme syndrome is actually post-sepsis syndrome or neurological Immunosuppression, a B-cell AIDS. The CDC crooks even admit it while ILADS refuses to talk about it while treating Immunosuppression, viral infections and wrecked b-cell germinal centers with longterm antibiotic therapy. 


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