US Govt’s Spirochete Crymes (vs. Baumgarth)

Update (170717):

“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].”


“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 ***…”


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.”


Of course there is another reason antigen is not presented – it could be OspA, or Pam3Cys, which downregulates that function.




Previously, (posted Dec 2016):

HOW could it be surprising that the U.S. Govt. is lying about “Lyme disease,” if everyone knows they’ve already done this?


White people are known to be more susceptible to dementia from borrelia or syphilis – and this was the reason for the Tuskegee and Guatemala syphilis crimes:

Toll-like Receptor Polymorphisms Are Associated with Increased Neurosyphilis Risk

“Clinicians in the early 20th century posited that race influenced susceptibility to neurosyphilis, citing a decreased risk in African Americans compared to Caucasians (7). Subsequent work suggested a genetic basis for such differences, with an increased risk of syphilitic dementia, but not other forms of neurosyphilis, in patients with certain HLA types (8) that differed in African Americans compared to Caucasians (9). While more recent reports suggest that there may be genetic contributions to syphilis susceptibility (10-13), to the best of our knowledge there have been no recent investigations of genetic susceptibility to neurosyphilis.”

Spirochetes ruin your immune system by “stealth bombing” (Barthold and Barbour) it with blebs that have fungal lipoproteins on them and DNA in them (Dorward, discussed around 1990, and also discussed at the LDF conferences in NYC in the late 1990s which I attended). The reactivation of latent viruses, basically is what drives the chronic fatiguing disease (opportunistics, or the result of TOLERANCE and cross-tolerance).

See for yourselves, Dorward, NIH, RML:

What is the process by which spirochetes damage B cell germinal centers (Baumgarth, Barthold would be what we want to know next. Is it the shed blebs that contain DNA, or is it like Steere (HLA connection), Paul Duray, & Dave Persing (“Target Imbalance”) describe what they see in “bad knees” (shed exosomes outnumber spirochetes, sticking to everything)?





Here we have a report that ties in the relatedness of several diseases (Occam’s Razor, below), and what is the official Govt spin (Victim-Blaming) But the head of NIAID owns a patent for this very-, officially-denied-, condition we call Lyme or CFIDS or Fibro. There is no OPPOSITE of “ALLERGY” or HLA-linked hypersensitvity or autoimmunity “National Institute of…”.

If you dont know what “HLA-linked autoimmunity” means, look that up now.

The U.S. Govt does not recognize chronic illnesses that are not-HLA-linked – which includes the majority of vaccine-autism cases as well as is the very foundation of the science of “stealth disablers” (fungal-ish animal diseases that leave no antibody trace of the original infection, but which “overwhelm the immune system”).

The U.S. Govt. has clearly twice before experimented with spirochetes as disablers of the immune system: Tuskegee and Guatemala (native Americans). China also claims USA dropped Borrelia on them, too, found in bugs suddenly appearing in the winter, on the snow, which would not be expected. Therefore what Korea claimed about Americans’ war crimes may have been true.

When the US Navy descended upon Unit 731 in Manchuria at the end of World War II, among the organisms they found and brought back home was Brucella, a “lameness” causing illness that bears LYMErix-like antigens. So much for the “phage-vectored DNA” or “Lateral Gene Transfer” (plasmids) that I have been talking about since at least 2001 (Albany Lyme hearing, November).

Edward McSweegan worked for the US Navy and stole their vector- borne diseases funding via a fake whistleblower letter to Senator Goldwater in 1986, the DNA patenting era (Dole-Bayh Act). Then he was put in charge of the NIAID TBDs grants, funneling them into his own particular criminal outlaw gang, including Durland Fish and CDC officers Johnson and Barbour, called the ALDF, which ws founded in 1990, a year after Pat Smith’s LDA.

This criminal racketeering enterprise,, changed the Lyme case definition to exclude the fungal-related immunosuppression outcomes to spirochetes because they could not otherwise sell vaccines and test kits based on their own patented DNA.

But here you see…



The most serious form of Lyme, neurologic or chronic neurologic, will have no antibodies against the Outer Surface Proteins, since they’re fungal, TLR2/1 agonists and cause tolerance which is a form of immunosuppression.  Above, you see Allen Steere say all this plainly.  The people with the chronic neurological outcome of Lyme, will not test positive to the arthritis-only case definition, we refer to as “Dearborn.”

They, this criminal ALDF RICO organisation, at the same time proceeded to attack MDs like Joe Burrascano and others (many activists, including the LDF) who claim spirochetal diseases were long term infections and not cured with short term antibiotics. Finally in early 1999 when their fake OspA vaccine hit the market, it was giving people “Lyme again.” This was overwhelmingly puzzling… since it was a recombinant ANTIGEN, and not whole spirochetes.  Some of the ALDF members were CDC officers.  Such aggression is known as “Color of Law” abuses.

That there are Lyme disease “guidelines” based on this fraud, published by, based on the Dearborn case definition, means this federal charge is still viable against all the signers of the “guidelines.”


“Since 28 January,” the telegram began, “the enemy has furiously employed continuous bacterial warfare in Korea and in our Northeast and Qingdao areas, dropping flies, mosquitoes, spiders, ants, bedbugs, fleas … thirty-odd species of bacteria-carrying insects…. They were dropped in a very wide area…. Examination confirms that the pathogenic microorganisms involved are plague bacillus, cholera, meningitis, paratyphoid, salmonella, relapsing fever, spirochaeta bacteria, typhus rickettsia, etc…. Now that the weather is turning warm, contagious disease and animal vectors will be active without restraint, and serious epidemic diseases from enemy bacterial warfare can easily occur unless we immediately intensify nationwide work on the prevention of epidemic disease.” Everyone receiving this message knew immediately that there was no room for complacency or business as usual; the high-ranking cadres in the provinces and in the localities realized that they were expected to play a leading role.


“The telegram signaled the disease-prevention targets in order of precedence: plague, cholera, smallpox, paratyphoid, relapsing fever, meningitis, encephalitis, and yellow fever. “After new laboratory results are obtained, adjustments [in this order] will be made.” District boundaries were stipulated: Korea as an epidemic disease district; northeast China as an urgent epidemic disease-prevention district; the north, east, and central South China coastal areas were observation districts; inland areas were preparatory districts. Each district was assigned its priority task, ranging from health reconnaissance, preventive vaccinations, and preparation of hospitals to receive epidemic disease patients, to controlling communication and transportation lines and keeping watch on the maneuvers of enemy planes. All personnel entering or leaving certain critical railway and highway junctions had to have certificates of vaccination; “otherwise they must receive injections from the station’s quarantine organization.”

Steere and Duray in 1988 talking about seeing the blebs:

“Using monoclonal antibodies to spirochetal antigenes and lymphoid cell surface markers, we examined the synovial lesions of 12 patients with Lyme disease, and compared them with rheumatoid synovium and tonsillar lymphoid tissue. The synovial lesions of Lyme disease patients and rheumatoid arthritis patients were similar and often consisted of the elements found in normal organized lymphoid tissue. In both diseases, T cells, predominantly of the helper/inducer subset, were distributed diffusely in subsynovial lining areas, often with nodular aggregates of tightly intermixed T and B cells. IgD-bearing B cells were scattered within the aggregates, and a few follicular dendritic cells and activated germinal center B cells were sometimes present. Outside the aggregates, many plasma cells, high endothelial venules, scattered macrophages, and a few dendritic macrophages were found. HLA-DR and DQ expression was intense throughout the lesions. In 6 of the 12 patients with Lyme arthritis, but in none of those with rheumatoid arthritis, a few spirochetes and ***globular antigen deposits*** were seen in and around blood vessels in areas of lymphocytic infiltration. Thus, in Lyme arthritis, a small number of spirochetes are probably the antigenic stimulus for chronic synovial inflammation.”

Persing finding more bleb-DNA than whole spirochetes, 1994:

Target imbalance: disparity of Borrelia burgdorferi genetic material in synovial fluid from Lyme arthritis patients.

Persing DH1, Rutledge BJ, Rys PN, Podzorski DS, Mitchell PD, Reed KD, Liu B, Fikrig E, Malawista SE.

“Lyme arthritis is a late manifestation of Lyme disease that results in episodic synovial inflammation and swelling. Although this process is thought to be driven directly by the spirochetal etiologic agent, Borrelia burgdorferi, the organism itself has been recovered by culture only twice. In contrast, polymerase chain reaction (PCR) studies are usually positive. This apparent discrepancy in 19 culture-negative synovial fluid specimens from 18 patients with Lyme arthritis was investigated. In all 19, DNA sequences characteristic of plasmid-encoded genes OspA and OspB were easily detected. However, despite equivalent or even superior analytic sensitivity for detection of cultured organisms, the reactivity of two genomic DNA targets was often weak or absent altogether in the clinical specimens. ****This apparent overrepresentation of B. burgdorferi plasmid sequences was found exclusively in clinical specimens and not in cultured organisms.*** The physiologic imbalance of genomic and plasmid DNA reactivity in B. burgdorferi infection may signal an underlying pathogenetic mechanism.

Barbour and Barthold talking about the stealth-bombering of your immune system with shed blebs or exosomes in 1996:

“Many researchers believe that the secret to B. burgdorferi’s infectivity and inflammatory capacity lies in the interaction of its surface proteins with the host’s immunological system. Yale researcher Stephen Barthold, a veterinarian and professor of comparative medicine who developed the first mouse model of Lyme disease, studies the expression of B. burgdorferi surface proteins throughout various stages of the spirochete’s life cycle. He finds that during the early stages of infection, B. burgdorferi avoids immune detection by decreasing its expression of surface proteins or cloaking its expressed surface proteins under a layer of slime. ***”It’s using some sort of stealth-bomber-type mechanism,”*** he says. Or, using another diversionary tactic called blebbing, the spirochete can pinch off bits of its membrane in order to release its surface proteins. Explains Barbour: “It’s like a bacterial Star Wars defense program,” in which released surface proteins might intercept incoming host antibodies, keeping the spirochete safe from immunological attack.”

McSweegan’s 1986 fake whistleblower letter to Goldwater and the US Navy’s FURIOUS response (I need a pdf-maker):

But Borrelia spirochetes, which are more virulent that syphilis, the US Govt says, only causes “bad knees.”  And that was because the OspA vaccines caused the very same immunosuppression disease, with the subsequent brain damage and dementia.


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