The following is from the Congressional Record on Dual-Use Bioweapons exported to Iraq



The following is from the Congressional Record on Dual-Use Bioweapons exported to Iraq:

“Lyme” and OspA were time bombs or Trojan horses that detonate Epstein-Barr/similars and tolerize to fungal infections in the blood resulting in chronic fatigue.

Exposure to borrelial antigens (blebbing) turns off the antibody response, meaning “Lyme” could not possibly be an “autoimmune disease” – it’s the reverse. It belongs in the cancer and AIDS class.

Did someone day “Lyme Disease” wasn’t an accidental release from Plum Island?

1) Firstly, there is no such thing as “Lyme Disease” it’s just Relapsing Fever and officially serologically so in 1990:

Uncoordinated phylogeography of Borrelia burgdorferi and its tick vector, Ixodes scapularis.
Humphrey PT, Caporale DA, Brisson D.

Department of Biology, University of Pennsylvania, Philadelphia, PA 19104, USA.

Vector-borne microbes necessarily co-occur with their hosts and vectors, but the degree to which they share common evolutionary or biogeographic histories remains unexplored. We examine the congruity of the evolutionary and biogeographic histories of the bacterium and vector of the Lyme disease system, the most prevalent vector-borne disease in North America. In the eastern and midwestern US, Ixodes scapularis ticks are the primary vectors of Borrelia burgdorferi, the bacterium that causes Lyme disease. Our phylogeographic and demographic analyses of the 16S mitochondrial rDNA suggest that northern I. scapularis populations originated from very few migrants from the southeastern US that expanded rapidly in the Northeast and subsequently in the Midwest after the recession of the Pleistocene ice sheets. Despite this historical gene flow, current tick migration is restricted even between proximal sites within regions. In contrast, B. burgdorferi suffers no barriers to gene flow within the northeastern and midwestern regions but shows clear interregional migration barriers. Despite the intimate association of B. burgdorferi and I. scapularis, the population structure, evolutionary history, and historical biogeography of the pathogen are all contrary to its arthropod vector. In the case of Lyme disease, movements of infected vertebrate hosts may play a larger role in the contemporary expansion and homogenization of the pathogen than the movement of tick vectors whose populations continue to bear the historical signature of climate-induced range shifts.

© 2010 The Author(s). Journal compilation © 2010 The Society for the Study of Evolution.

2) We have scientific evidence that “Lyme” did not naturally evolve

Evolution of a focus of Lyme disease.
Schulze TL, Shisler JK, Bosler EM, Lakat MF, Parkin WE.

Epidemiological investigations were initiated in 1984 when significant Lyme disease activity was observed within a 5-km radius of an area previously used as a non-endemic control site for Lyme disease research in New Jersey. Through 1983, collections of Ixodes dammini from vegetation and feral rodents were infrequent and no human cases were identified within a 16-km radius of the control site. In 1984, 4 human cases and 3 serologically reactive canines (greater than or equal to 1:512) were recognized within the area and adult I. dammini populations were over 3-fold greater than those at our primary study location where Lyme disease has been endemic since 1981. Using darkfield microscopy, 53.4% of adult I. dammini were infected with Borrelia burgdorferi as compared to 50.0% of adults collected during the same period at the known endemic study site. These data indicate that a focus of Lyme disease has recently become established at the previously non-endemic control site and that the establishment of new foci may occur more rapidly than once thought.
“Despite the intimate association of B. burgdorferi and I. scapularis, the population structure, evolutionary history, and historical biogeography of the pathogen are all contrary to its arthropod vector.”

3) We have scientific evidence that the original outbreak area was indeed the area of Plum Island/Lyme

4) They happen to perform that kind of vector-pathogen competence studies on Plum Island (Durland Fish)

5) Govt Goons tried to silence Willy Burgdorfer (who was recruited from Switzerland in the first place to work at the NIH Rocky Mountains Bioweapons lab specifically because he was an expert in spirochetes)

6) No one from the NIH, CDC, Yale or IDSA will answer the question as to what OspA is and they threatened me with jail (again) if I persisted in reporting to Francis Collins that no one to whom I was referred by Collins’ office (Fauci and NIAID) could tell me what OspA was

because if anyone ever told us what OspA was, they would have to admit it could never have been a vaccine and was therefore falsely qualified (they would have to admit the Dearborn criteria was fraud). And to date, no one at MIT or Stanford or Princeton or Duke or any of the other formerly respected institutions of higher learning can tell you what OspA is either. (Because why? This is an IQ test: Why won’t anyone from or or etcetera et al report the truth about Lyme as Relapsing Fever or what OspA is/does?)

7) The “science” of “Lyme” is about attacking the victims and calling them crazy and this has been the case since 1990 when the a commercial entity supported by the likes of Mort Zuckerman (CFR) and the AIG Greenbergs (CFR) was founded at New York Medical College (
Ever since the imaginary vaccine trials, the only other so-called study performed by these crooks was Klempner’s bogus long term retreatment study of people 2/3 of whom never were treated according to the protocol before, and half of whom tested positive to the Dearborn protocol when no one knows what Dearborn means. The testing schema was research fraud committed by CDC officer/draft dodger Allen Steere alone in Europe.

None of the participants invited to the Dearborn conference in 1994 agreed with Allen Steere’s proposal:

8) The CDC deliberately falsified their mycoplasma/Chronic Fatigue Syndrome study by throwing out the red blood cells, to which the mycoplasma adhere, resulting in fatigue without the anemia:

1992; [The effect of Eperythrozoon suis infection on the osmotic fragility of erythrocytes]

Osmotic fragility of erythrocytes was tested in weaned pigs experimentally infected with Eperythrozoon (E.) suis. Acute eperythrozoonosis of splenectomized pigs led to an increase of osmotic fragility. It is supposed that E. suis infection causes a structural change in erythrocyte membrane. Possible mechanisms of this cell membrane injury are discussed.

And you can see more images of mycoplasma adhering to erythrocytes here:

The process by which people become tolerized to mycoplasma (bearing TLR2-agonists) is due to the chronic exposure of persons with Lyme Relapsing Fever to shed antigen (blebbing) as demonstrated by UConn’s Justin Radolf, here:
Blebbing, by Alan Barbour

9) Durland Fish admitted he writes “bogus articles” when planning to stalk, wiretap, and harass Karen Forschner of the Lyme Disease Foundation

10) IDSA fellas have referenced the “cysts are vi



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