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Borreliosis Basics (poster) ALDF/CDC Patents USDOJ RICO Complaint AIDS-like EBV-Borreliosis; UN Complaint (2003) Bioweapons Attributes Khan Acad of Cryme
Lyme Facts (poster) CDC's Patents w/ GSK Blumenthal (AntiTrust) Sepsis & Autism, 20 reports Antics Crazy Eddy & Durl Lyme as a bioweapon? 5 new "Axes" DSM
Persistence: Historical, IDSA's UConn Assaults Children 20 reports; Sepsis, Autism OspA / Pam3Cys Tolerance Mark Klempner's Crymes Army says Bioweapon DCF witnesses demonic
Crooks' DNA Shell Game Congenital Lyme by Yale Dattwyler: Seronegative Lyme Failed Other Fungal Vaccines Munchausen's Accusations Russians@NYMC (HLAs) 141215homepage
Steere Falsifies test Halperin: Lyme & ALS Steere: Seronegative Lyme PubMed: OspA activates EBV McSweegan Munchausen's Plum Island Evidence Cryme Trainer 2012
Yale's Lyme Vaccine Scam Steere: Lyme causes Lupus Klempner on hidden tape LYMErix causes neuro disease ALDF.com files Jan-Nov 2014 home
IDSA's & CDC Biomarkers Klempner & "Guidelines" False Claims Act referenced NIH:  CLD is active herpes Fish @ Internat.Spy Firm
Plum Stupid, referenced New Cryme Disease Videos .

ME/CFS is active herpes

01/27/2015 06:31:13


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Cryme Disease video playlist

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Norway Site

Bad Ass Cryme Blog


141219_post-sepsis Rituximab (again)

Pandora: ME/CFS related to AutismVaccines

Follow the Lyme/LYMErix Scam in the order it occurred, below:

Older data on the incurability of Relapsing Fever

1986, McSweegan trashes Navy for $$$ for ALDF.com

1988, Dattwyler & about immune-suppressing, seronegative Lyme

1990, CDC: "Diagnose Lyme as if it was Relapsing Fever."   

Allen Steere  "NeuroLyme won't test positive," 1990.

1992, CDC officer Allen Steere falsifies testing in Europe

1992, CDC patents with SmithKline show 2 kinds of Lyme

1993, Barbour and Fish slam Neurologic Lyme victims.

Compare the 2 kinds of Lyme in the RICO complaint

1994, FDA LYMErix Meeting

1994, CDC's Dearborn Booklet .pdf

CDC's invitation to participate in Dearborn .pdf

Dearborn, Who Said What?

Igenex, Harris, Dearborn .pdf

Evidence  Lyme criminals knew LYMErix produced the same "multisystem disease" as "Chronic Lyme"

LYMErix Damage Coverup (short)

1998, CIA Oilmen & Israelis plan to overthrow Saddam for the oil.

ActionLyme/Kathleen Dickson predicts all of Bushie's outcomes in Oct 2000

ActionLyme/Kathleen Dickson predicts Bush will have us worshipping his bombs (Shock and Awe"), in Oct 2000 during the Gore Debates    


With 20-30 million people disabled from Fibro, GWI, Lyme, and CFIDS, not to mention the millions of children brain damaged for life (does anyone know the statistics on cost of lifetime of care for Autistic children?) and a workforce that is no more than 50% fully employed (23% of all USA employed are Govt employees), one wonders what the USDOJ thinks they're doing? 

Don't they have anyone there at the USDOJ concerned about the 25% or more disabled workforce? 
Do they have anyone working at the USDOJ who knows anything about math? 
Numbers and stuff? 
Finance or a nations' reliance on economic - trading - activity


There is something fundamentally wrong with Americans' brains. And I am not even referring to those who are disabled with chronic sepsis-like brain illnesses.

These people are straight up NAZIs.  This is the Gestapo that emerged in the 35 years since that moron Reagan, who knew nothing about GNP or work or productivity or physics,... and the Bushies were even dumber. 


Chris Hedges nails it:

"The innate barbarity that war and violence breed is justified by a saccharine sentimentality about the nation, the flag and a perverted Christianity that blesses its armed crusaders. This sentimentality, as Baldwin wrote, masks a terrifying numbness. It fosters an unchecked narcissism. Facts and historical truths, when they do not fit into the mythic vision of the nation and the tribe, are discarded. Dissent becomes treason. All opponents are godless and subhuman. “American Sniper” caters to a deep sickness rippling through our society. It holds up the dangerous belief that we can recover our equilibrium and our lost glory by embracing an American fascism."



This is what the international patient and scientist community needs to know about the 
Turncoats, and the criminal and incompetent CDC.  You can't believe the CDC on vaccines 
at all, and here are several good reasons why:


"There is no such thing as seronegative Lyme or Lyme Disease cases that do not meet the Dearborn case definition" -- CDC officers Allen Steere and Mark Klempner.

Borrelia do not have LPS and are only bearers of lipoproteins which are fungal and TLR2/1-agonists or triacyl lipopeptides which they deliberately shed (bleb off) as "EXOTOXINS." Why do they insist Borrelia are not shedders of fungal, immunosuppressive exotoxins ?? 


Who is Steve Schutzer and why/how is he a liar?

Number One:   Schutzer and Pat Coyle used to publish about antigen-antigen complexes in the spinal fluid of Lyme victims to prove they were seronegative Lyme. You can verify in PubMed.

Number Two: 
Pat Coyle only specializes in MS now, and goes borneo on ya if you mention Lyme at her MS talks.  She acts like she was threatened.

Number Three: 
Schutzer was the editor of the Lyme Disease, Molecular and Immunologic Approaches Cold Spring Harbor conference in 1992 where in they talk about NeuroLyme seriously, and Paul Duray again mentioned EBV possibly being activated in CNS Lyme:

Number Four: 
Steve Schutzer was put on a round table/panel in one of the LDF Lyme conferences in 2000 or 2001 and it was asked if one or two bands would be good enough to detect Lyme. Donta said like Band 23 and 41 should be fine. Igenex's Nick Harris agreed. I ferget who the 4th person was. Schutzer said "NO, BECAUSE CFIDS PEOPLE OFTEN HAVE A FEW LYME BANDS."


Uncle Sam Dot Mil talks about anti-personnel biological weapon Time Bombs or Trojan Horse bioweapons:

"Methods of using antipersonnel agents undoubtedly wary so that no uniform pattern of employment or operation is evident [make sure it does not produce antibodies, is the short version- KMD]. It is likely that agents will be used in combinations so that disease symptoms will confuse diagnosis and interfere with proper treatment. It is also probable that biological agents would be used in heavy concentrations to insure a high percentage of infection [or just use the OspA vaccine- KMD] in the target area. The use of such concentrations [or the multiple infections it causes, due to the immunosuppression like HIV, Lyme, or LYMErix as acquried immune deficiencies - KMD] could result in the breakdown of individual immunity because the large number of micro-organisms entering the body could overwhelm the natural body defenses [or just infect or inject people with an immune suppressor like OspA from a tick or a syringe, and the reverse will happen: people will acquire multiple infections because their immunity is trashed by OspA- KMD].


And the genetics of anserina-come-burgdorferi:


How could all of them be such F*ck-Ups, Turncoats and LIARS?

They all jumped-ship and turned coats right around the time I blew the whistle
on the whole thing, from Dearborn being a fraud to OspA causing immunosuppression
around 1999-2001:



Think about it.  You're gonna believe these CDC assholes about
ANY vaccines?


No way.



Let's make sure we all know what we are talking about since the CDC and IDSA do not.  Even Yale says they do not know what
OspA is - yet they owned that patent for LYMErix.  And you can't make this shit up, because this is America.

We have to OCCUPY the USDOJ in Washington to force the "government" "lawyers" tell the CDC and IDSA spirochetes are not
bacteria and that OspA was a fungal antigen and never could have been a vaccine.

And that is because this is America where only stupid criminal shit happens.


150123 Sweeg in Russia, ALDF Bioweapons Data-Pharming, Tom Dispatch on Weapons $$$

By Kathleen Dickson on Friday, January 23, 2015 at 4:00am

http://travelmag.co.uk/2003/05/sent-to-siberia/  <<  Sweeg really was in Russia, there he is talking about it, LOL.


 THE ARTICLE by TOM DISPATCH on the WALKING DEAD in Washington  (below) ALSO APPLIES to the 30 million of us disabled from Lyme, GWI, ME/CFS and brain damaged from vaccines (Autism),.. actually that could be a higher number if 12 million is the official number of CFS (4 mil) and Fibro (8 mil) alone.  In addition to this "safety" and "intelligence" concern, the cat is totally out of the bag on bioweapons and bad vaccines, internationally.  


*** Recall that in May 2007 the Russian Duma banned export of human DNA to America, when Sweeg himself was allegedly over there in Russia just a few years earlier allegedly heppin-em destroy their biological weapons.***  (That was the era when his buddy Durland Fish said Sweeg was "hung like a horse," - re Sweeg in Akademgorodok, Russia, since Durland is a pig and grotesque.)  


I can't say for sure if it is related but I had begun faxing the foreign embassies in the summer of 2006 and explained what they (Lyme Crooks) were doing and told them not to let them sample any DNA because they were bioweapons data-pharming (HLAs).  In Sep, 2006, I had 14,000 visitors to ActionLyme that month, alone, from Russia.


That is, ASSOCIATES of the ALDF.com at New York Medical College were sampling HLA data from around the world (that evidence is on ActionLyme), We know that a successful bioweapon would be undetectable so it would be the ABSENCE of "disease" associated HLAs that would make an effective bioweapon, because no antibodies would be produced.  Recall that in PNAC, the neocons were talking about using race-specific bioweapons.  A race specific bioweapon would be a stealth disabler for that group or would produce few HLA-linked hypersensitivity cases that identified the original infection.


Below this link I will link the evidence for what I am talking about above:




"Russian ban on export of biological samples[edit]

In May 2007, Russian newspaper Kommersant reported that the Russian government banned all exports of human biosamples.[13] The report claims that the reason for the ban was a secret FSB report about on-going development of "genetic bioweapons" targeting Russian population by Western institutions. The report mentions the Harvard School of Public Health, American International Health Alliance, United States Department of Justice Environment and Natural Resources Division, Karolinska Institutet and United States Agency for International Development."



HERE is DURLAND FISH using a fake Lyme victim name to say Sweeg is "Hung Like a Horse" in the conversation about Sweeg in Russia, Akademgorodok:



The PNAC document where the Israeli Neocons discuss using "race-specific bioweapons":



These are the Russian-name -sounding associates of the Lyme crooks HLA-data-pharming all over the world (the publish from and with people at NYMC or the Lyme crooks' ALDF,com):


Some of the other Russian Scientists either publishing in Durland Fish's 'Journal", or New York Medical College- Look closely at all of their publications.  They're very interested in genetic backgrounds of peoples of foreign nations:










That all ^^^ means the bioweapons to be developed against these people have to be stealth against their HLAs.  That is, the disease cannot be an HLA-linked disease or else there will be antibodies against the stealth infection, which would render the disease detectable.  Read more about it here.


HERE IS ONE OF THE FAXES I SENT ALL OVER in the spring and summer of 2006, re Pam3Cys and an 11 million dollar BIODEFENSE CONTRACT given to the crooks and wherein, it is clear they know a TLR2/1 agonist could never be a vaccine since Corixa, Dave Persing and Robert Schoen knew "OspA was too toxic in the native form."

^^^^  Don't lose that data that is scanned in in that report, above, it's worth billions to us ;)



I'd like to thank all the Govt's biodefense labs for being such huge and persistent fans of ActionLyme.  It came up in conversation recently on the Occupy the USDOJ Facebook group (June 2015), what would be their interest here?  Welp, they'd be somewhat more accountable to new diagnostic/analytical machinery and techniques for identifying infectious diseases, obviously.  They can't allow themselves to get away with being your average typical brainless streetwalker bigpharma ho "MD," who takes no responsibility upon him-/herself to find out what eff is going on with 40 years of "controversy," Blumenthal lawsuits, FDA-retracted "vaccines," ... that fairy-ass Allen Steere saying he was "stalked," when no, I spoke with David Grann in person at the Albany rally and told him everything I told - and showed, with 19 pages out of the Dearborn booklet, provided to all 15 FDA Vaccine Committee members- the FDA 4 months earlier when I blew the whistle on Streere's Dearborn testing scam...  So, how could we be "Stalking Steere" in Boston, when we've been trying to have him BUSTED for over 15 years...

It might be in the Govt bioweapons goons' interest to know what actual science and methods are already out there - long now - on how to perform valid and sensitive analyses on these stealth disablers. 

So, the people need to know what the US Bioweapons Govt agencies are interested in.  ("Doctors," shit, you're better off talking to a pharmacist.  They at least are required to have a science background.)

Virological diagnosis of central nervous system infections by use of PCR coupled with mass spectrometry analysis of cerebrospinal fluid samples

No one can stop this.  Yale and the CDC are going to be busted or the USA will not go forward, much less remain technologically viable in the med sci field.  That's it.  Play or Crash, Uncle Sam spook piggies.  Prosecute or eat dust and put the USA and our allies in danger from a lack of sophistication in biotech and bioweapons agents analyses.



And Now it is Time to Consider the Format of the Indictments...

It's amazing that we have had to put up with this bullshit for so many years just because some Yale related scam artists wanted royalties from their fake fungal "vaccine," LYMErix, and to monopolize their future TBDs enterprise in vaccines and test kits.  You can read more of their same old hysterics in the journals, "new" for 2015.  It's the same old bullshit and nonsense because they can't get any grants - the NIH cut them off.  Besides, how many times can you ask for a grant to study a disease that does not exist.

It's quite obvious they're terrified of being prosecuted.  They can't let it go.   If they weren't guilty and terrified, they would cease and desist and move on.  But it should be obvious to any casual observer that these were the same fellas who said we need a vaccine against Lyme since it was such a terrible disease... and now they spend all their time and energy saying it's not a disease.  Suttins up.   It's about the testing fraud, which is a murder charge, especially over the ALS linkLike any other RICO fraudster prosecution, they will all lose all their personal property as well as spend the rest of their lives in jail, and Yale will lose all of Yale, which is worth at least $20 billion.  That's just the value of their Endowment Fund. 

Yale patented an FDA-validated test for Lyme in 1991-1993, but they did not use this FDA-validated test to assess their other patent, LYMErix, because they knew LYMErix was not a vaccine and caused systemic disease.  You can't inject people with fungi.  That's the reason for the Thimerosal in the first place.



New Yorker Needs to Find a Real Scientist to do their Science Writing (Michael Spector, gimmeabreakii)


By Kathleen Dickson on Saturday, January 17, 2015 at 2:31am


To: Michael_Spector@newyorker.com

Cc: themail@newyorker.com, jacob_lewis@newyorker.com, david_remnick@newyorker.com, bowie@mail.ubc.ca, mbpfeiff@poughkeepsiejournal.com, sr393d@nih.gov, AllenM1@mail.nih.gov, francis.collins@nih.gov, ras8@cdc.gov, olib@od.nih.gov, afauci@niaid.nih.gov, joseph.breen@nih.gov, michael.greenwood@yale.edu, richard.horton@lancet.com, astrid.james@lancet.com, spinlyme@yahoogroups.com, m.zecevic@lancet.com, ideditorial@lancet.com, Lawrence.Tabak@nih.gov, pgauwaerter@gmail.com, letters@syracuse.com

Subject: New Yorker needs to get an actual scientist to write about science ("Lyme Disease")

Date: Jan 16, 2015 6:28 AM

Hi, there yall.


Thanks for this commentary, but it's very obvious the writer (Michael Spector) has no clue what the controversy is about. "Controversy" is a weasel word used by the likes of BigTobacco to offset the pursuit into the heart of the criminal matter. In the case of the Lyme disease crimes, it's simple research fraud mainly having to do with an intended vaccines "enterprise" by the fake non-profit, theALDF.com.

      It's a complex issue, but not really. Not to someone with a basic biology science background, and that is my point, here, as regards your magazine. Where do we start? Probably with the "New Great Imitator, Lyme Disease," according to Allen Steere and IDSA, that causes RA and MS and Lupus and ALS (all proven/revealed by the same people who now deny Lyme spirochetes cause any kind of neurologic disease). So why is what was once a Great Imitator (more correctly, “Detonator”), now only strictly an autoimmune arthritis in a knee that needs no treatment? 

      And an even better question, now that psychiatry has been officially debunked and no one can even get a grant if they use scientifically invalid terms like "somatoform," what new kind of derogatory language will be used to demonize and discredit people with neurologic New Great Imitator outcomes?Why are neurologic outcomes from a neurologic disease no longer allowed? 

      It’s not too much about lame-brained ILADS.org and their “long term antibiotics.” They’re discredited scientifically not only for this stance, but because they refuse to even delve into the matter of the research fraud committed by primarily CDC employees (Allen Steere, Barbara Johnson, Mark Klempner, Alan Barbour), over the Dearborn case definition (1994-5), but also how the OspA vaccines caused the same systemic, “multi-system,” (Persing and Schoen), "protean" (Ben Luft) - read, neurologic Great Imitator -, disease as what most of the rest of us call Chronic Lyme.

How does OspA cause chronic neurologic disease if it is only a recombinant antigen? 

       Are there any parallels in the scientific literature about how if you inject fungal antigens into people that could be a bad thing?


It's a simple thing.

      There are no Tuberculosis vaccines for the same reason. They put Thimerosal in vaccines for the same reason. Fungal antigens are sometimes called superantigens or toxins. Maybe the magazine can hire someone who knows this little about science.




"Anecdotal reports of inadequately documented clinical or laboratory associations with B. burgdorferi infection ill serve the medical community and the public.  Convincing and compelling evidence (e.g., like not playing the RNA/DNA PrimerShellGame with human specimens) should be required to support extraordinary associations." http://www.journals.uchicago.edu/doi/pdf/10.1086/313541


Now that it has been proven (1 , 2, 3), re-proven (4, 5) and re-re-proven (6, 7) once again and in recent history, that indeed “Lyme Disease (8, 9)” is a chronic, un-eradicable infection primarily of the central nervous system, formerly, formally serologically known as Relapsing Fever (10, 11, 12), and that long term intravenous antibiotic treatment generally results in relief-but-then-relapse (3, 5), one wonders, “Where do we go from here?”

The first order of business is the clarification of falsified antibody testing for “Lyme Disease.”

In 1992 Allen Steere went to Germany, with, as he claimed,

“The group 1 strain of B. burgdorferi, G39/40, used in this study and in the previous study of US patients was isolated from an Ixodes damini tick in Guilford, Connecticut [21].  The group 2 strain, FRG [Federal Republic of Germany], was isolated from Ixodes ricinus near  Cologne [22].  The group 3 strain, IP3, was isolated from Ixodes persulcatus near Leningrad [23].  All three strains used in this study were high passage isolates, which were classified by Richard Marconi (Rocky Mountain Laboratory, Hamilton, MT) using 16S ribosomal RNA sequence determination as described [11, 24].  The recombinant preparations of OspA and OspB used in this study were purified maltose- binding protein-Osp fusion proteins derived from group 1 strain B31 [25].  The fusion proteins contained the full-length OspA or OspB sequence without the lipid moiety or the signal sequence -"

-- illegal, plasmid-dropping, antigen-and-antibody dropping, “high passage strains” and OspA and B with no lipids attached (not likely to produce antibodies), resulting in the new, 1994, Centers for Disease Control (CDC), “case definition” of “Lyme Disease (8, 9)."

At the Dearborn, MI, Consensus Conference regarding the “standardization” of Western Blotting for “Lyme Disease,” the invited labs assessed Steere’s scientifically fraudulent proposal for a new diagnostic standard for Lyme from 8% to 28% accurate (detected % of known cases).

As part of their Dearborn submission, New York Medical College (NYMC) assessed the Steere proposal in 1993 as:

“Overall, 51 of 59 (86%) convalescent-phase serum specimens were reactive by IB, 35 of which were interpreted as positive: 26 based on IgM criteria, 8 based on both IgG and IgM criteria, and 1 based on IgG criteria,”

or 9 out of 59 patients were positive for Steere’s Dearborn proposal in IgG.  Or, 15% accurate (13).

With this Steere-Goes-To-Germany standard the two OspA vaccines (ImmuLyme and LYMErix) were allegedly assessed for safety and efficacy (
14, 15), which meant 85% of known cases would be thrown out of consideration, which, hypothetically, was the game plan all along.  Later we found out that the Western Blots in OspA vaccinated people were not readable due to multiple reactive species or generalized darkening of the Western Blot strips, rendering any potential bands that would demonstrate illness/Lyme breakthrough in vaccinated persons, undecipherable (16, 17).

That leaves us with the years 1992 to the present, almost 2011 (2015), completely wasted.

In terms of research dollar-years and lives we’re now back at Square One, wondering what is to be done with the testing for “Lyme Disease,” and even more importantly, what do we call a “case” of “Lyme Disease” once the millions of people who were misdiagnosed in the Lyme-OspA scam process have gone on to chronic illness?

We know from scientifically valid biomarkers of illness (scientifically valid in the sense that valid methods were used to assess the markers or signs that a person suffered real illness or health irregularities), the true and correct DNA and RNA methods to determine chronic infections status, and especially of the prominent question of “seronegativity” being associated with the greatest apparent suffering.  In 1994 at the meeting of the Food and Drug Administration regarding potential Lyme vaccines, Raymond Dattwyler (SUNY-Stony Brook) noted that “the ones that failed to mount a vigorous immune response tended to do worse, clinically. So, there was an inverse correlation between the degree of serologic response and the outcome.”

In 2005, Mark Klempner (Boston University) and Gary Wormser (NYMC) reported that the arthritis cases and seroposivity tended to be associated with Allen Steere’s alleged haplotypes over which SmithKline was sued in a class action after the Yale-owned LYMErix trial (18): “Patients generally feel well aside from their arthritis symptoms.”

In 1988, Raymond Dattwyler published that he wondered about seronegative “Lyme” and the suppression of NK cells (
19), and he wondered enough to come up with a new assay to determine if exposure to Lyme and a lowered immunological response (20).  His new assay was called “Seronegative Lyme disease. Dissociation of specific T- and B-lymphocyte responses to Borrelia burgdorferi.”  Later, Allen Steere used this same seronegative “Lyme” assay and determined that 4/9 of his lab workers had been exposed to Borrelia (21).

The question was why.

We know from the previous history of Relapsing Fever (before the era of Allen Steere, et al), that antigenic variation was the nature of the relapse, and that spirochetes become host- and tissue- adapted. This meant that persons who had missed the opportunity for early diagnosis and treatment would not have the Dearborn “case definition” of “late, OspA-hypersensitivity, specific HLA-linked, Lyme Arthritis” in “early Lyme,” would be left to his/her peril in finding a competent MD who had been exposed in pre-medicine undergraduate study to a course in genetics.  These organisms are taxonomically classified by differences in flagellin. The best way to detect Lyme with antibody testing is via all-borrelial-specific anti-flagellin antibody detection, because flagellin is not a variable antigen.   The group who perfected and patented the anti-Borrelia- burgdorferi specific flagellin method was Yale’s Erol Fikrig and Richard Flavell in 1991 (22, 23).

Why this test was not used to assess Fikrig and Flavell’s OspA vaccine patent, LYMErix, is anyone’s guess.

Regardless of this State of Nonsense (Connecticut), …

People wonder what to make of the serious illness they suffer as a result of “Lyme” and LYMErix vaccination, which appeared to be similar (
24).  In 1995, David Persing and Yale’s Robert Schoen patented a method wherein they, the winners, would be in receipt of all the government funding and also a national monopoly on the - as they hoped and intended - post-OspA-vaccinated United States:

“Additional uncertainty may arise if the-vaccines are not completely protective; vaccinated patients with multisystem complaints characteristic of later presentations of Lyme disease may be difficult to distinguish from patients with vaccine…. ” (25, 26).  

And they, most of all, would have access to all the potentially patentable goodies in the national blood with this monopoly on testing.

Further investigations into the outcomes of other lipoprotein/fungal vaccines revealed a similar outcome to that observed in the un-reported LYMErix adverse events patients, resulting in the January 2001 FDA hearing on the matter and the class action lawsuits.  Adverse events were only reported to the FDA by the vaccines trials' administrators if they were of the arthritis kind, since “arthritis only” had become the new “case definition” at the 1994 Dearborn ”conference.”  When Dennis Parenti of SmithKline reported that there were only two neurological adverse events to LYMErix at the 2000 Lyme Disease Foundation Conference in Hartford, CT, several physicians and attendees immediately got up and walked out of the conference room, while the rest groaned.

The functional results of OspA vaccination were, we hypothesize, not dissimilar from the results of structurally similar vaccine antigens that are managed by TLR2:

“These results are consistent with a model in which the presence of the 19-kD protein [of Mycobacteria tuberculosis] has a detrimental effect on the efficacy of vaccination with live mycobacteria.” (27)

“Synthetic analogs of lipopeptides from Treponema pallidum also inhibited Ag [antigen] processing.” (

“the immunosuppressive effect is dependent on glycosylated and acylated 19-kDa lipoprotein [of Mycoplasma tuberculosis] present in the phagosome containing the mycobacterium. These results suggest that the diminished protection against challenge with M. tuberculosis seen in mice vaccinated with M. smegmatis expressing the 19-kDa lipoprotein is the result of reduced TNF-alpha and IL-12 production, possibly leading to reduced induction of T-cell activation. (

“Thus, tolerance to LPS and mycobacterial components cannot be attributed solely to a decrease in TLR/MD-2 expression levels, suggesting inhibition of expression or function of other signaling intermediates 2002, Induction of bacterial lipoprotein tolerance is associated with suppression of toll-like receptor 2 expression.”(

"Surprisingly, in 27-kDa-vaccinated mice (protein or DNA vaccines) challenged by M. tuberculosis H37Rv or BCG strains, there was a significant increase in the numbers of CFU in the spleen compared to that for control groups. Furthermore, the protection provided by BCG or other mycobacterial antigens was completely abolished once the 27-kDa antigen was added to the vaccine preparations. This study indicates that the 27-kDa antigen has an adverse effect on the protection afforded by recognized vaccines." (

And, we know that:

[((2003) Borrelia burgdorferi-induced tolerance as a model of persistence via immunosuppression.]
“If left untreated, infection with Borrelia burgdorferi sensu lato may lead to chronic Lyme borreliosis. It is still unknown how this pathogen manages to persist in the host in the presence of competent immune cells. It was recently reported that Borrelia suppresses the host's immune response, thus perhaps preventing the elimination of the pathogen (I. Diterich, L. Härter, D. Hassler, A. Wendel, and T. Hartung, Infect. Immun. 69:687-694, 2001). Here, we further characterize Borrelia-induced immunomodulation in order to develop a model of this anergy. We observed that the different Borrelia preparations that we tested, i.e., live, heat-inactivated, and sonicated Borrelia, could desensitize human blood monocytes, as shown by attenuated cytokine release upon restimulation with any of the different preparations. Next, we investigated whether these Borrelia-specific stimuli render monocytes tolerant, i.e. hyporesponsive, towards another Toll-like receptor 2 (TLR2) agonist, such as lipoteichoic acid from gram-positive bacteria, or towards the TLR4 agonist lipopolysaccharide. Cross-tolerance towards all tested stimuli was induced. Furthermore, using primary bone marrow cells from TLR2- deficient mice and from mice with a nonfunctional TLR4 (strain C3H/ HeJ), we demonstrated that the TLR2 was required for tolerance induction by Borrelia, and using neutralizing antibodies, we identified interleukin-10 as the key mediator involved. Although peripheral blood mononuclear cells tolerized by Borrelia exhibited reduced TLR2 and TLR4 mRNA levels, the expression of the respective proteins on monocytes was not decreased, ruling out the possibility that tolerance to Borrelia is attributed to a reduced TLR2 expression. In summary, we characterized tolerance induced by B. burgdorferi, describing a model of desensitization which might mirror the immunosuppression recently attributed to the persistence of Borrelia in immunocompetent hosts”. (32)

AGAIN:  “Next, we investigated whether these Borrelia-specific stimuli render monocytes tolerant, i.e. hyporesponsive, towards another Toll-like receptor 2 (TLR2) agonist, such as lipoteichoic acid from gram-positive bacteria, or towards the TLR4 agonist lipopolysaccharide. Cross-tolerance towards all tested stimuli was induced.”

Epstein-Barr’s activity regarding TLR2:

(2007) Epstein-Barr virus induces MCP-1 secretion by human monocytes via TLR2.

“Epstein-Barr virus (EBV) is a gammaherpesvirus infecting the majority of the human adult population in the world. TLR2, a member of the Toll-like receptor (TLR) family, has been implicated in the immune responses to different viruses including members of the herpesvirus family, such as human cytomegalovirus, herpes simplex virus type 1, and varicella-zoster virus. In this report, we demonstrate that infectious and UV-inactivated EBV virions lead to the activation of NF-kappaB through TLR2 using HEK293 cells cotransfected with TLR2-expressing vector along with NF-kappaB-Luc reporter plasmid. NF-kappaB activation in HEK293-TLR2 cells (HEK293 cells transfected with TLR2) by EBV was not enhanced by the presence of CD14. The effect of EBV was abrogated by pretreating HEK293-TLR2 cells with blocking anti-TLR2 antibodies or by preincubating viral particles with neutralizing anti-EBV antibodies 72A1. In addition, EBV infection of primary human monocytes induced the release of MCP-1 (monocyte chemotactic protein 1), and the use of small interfering RNA targeting TLR2 significantly reduced such a chemokine response to EBV. Taken together, these results indicate that TLR2 may be an important pattern recognition receptor in the immune response directed against EBV infection.” (

And we know that:

“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.” (34)

which is what we call the auto-vaccination with OspA - the immune-suppressing fungal antigen amd TLR2-agomist known also, structurally, as Pam3Cys (35).

In short, “Lyme Disease” is chronic and seronegative because it is chronic, or chronically shedding variable (Relapsing Fever-esque) outer surface lipoproteins like OspA, or, as Alan Barbour states in his US Patent #6,719,983:

“2.1 Methods of Treatment

”An important aspect of the invention is the recognition that Borrelia VMP-like sequences recombine at the vls site, with the result that antigenic variation is virtually limitless. Multiclonal populations therefore can exist in an infected patient so that immunological defenses are severely tested if not totally overwhelmed. Thus there is now the opportunity to develop more effective combinations of immunogens for protection against Borrelia infections or as preventive inoculations such as in the form of cocktails of multiple antigenic variants based on a base series of combinatorial VMP-like antigens.”

“antigenic variation is virtually limitless. Multiclonal populations therefore can exist in an infected patient so that immunological defenses are severely tested if not totally overwhelmed.”

What are the other functional outcomes of the chronic agonism of TLR2 – the one that manages triacyl lipopeptides like OspA or Pam3Cys that render the immune system overwhelmed, not to mention the persons who late in the disease who do not serologically (antibodies) react to antigen from spirochetes fresh out of a tick due to antigen variation,… not to mention the diminution of antibody production due to chronic TLR2 agonism?

Says Paul Duray of the National Cancer Institute and Ft. Detrick (hint, hint):

"On occasion, these atypical-appearing large lymphocytes have been  misinterpreted in biopsy by several laboratories as cells of a malignant lymphoma or leukemia.  Bb antigens, then, may stimulate growth of immature lymphocytic suibsets in some target organs, as well as in the cerebrospinal fluid (Szyfelbein and Ross 1988).  Usual bacterial infections do not produce such lymphocytic infiltrates in tissue.  These immunoblastoid cells in Bb infections at times resemble those found in Epstein-Barr virus infections.  Does Bb reactivate latent virus infections in tissues?  Do some tick inocula harbor simultaneous infectious agents (ixodid ticks can harbor Rickettsiae, Babesia microti, and Ehrlichia bacteria, in addition to Bb), producing multi-agent infections in some hosts?  Further studies can clarify these issues by mans of tissue-based molecular probe analysis." (36)

The lymphocytes of these chronic “Lyme” victims look like Epstein-Barr transformed cells.

In 2003, Hulinska et al report in

“Interaction of Borrelia burgdorferi sensu lato with Epstein-Barr virus in lymphoblastoid cells: 
“Since the possibility of interruption of latent EBV infection has been suggested by the induction of the lytic virus cycle with chemical substances, other viruses, and by immunosuppression, we hypothesized that the same effect might happen in B. burgdorferi sensu lato infection as happens in Lyme disease patients with positive serology or both agents. We have observed EBV replication in lymphoblastoid cells after superinfection with B. garinii and B. afzelii strains after 1 and 4 h of their interaction. We found that viral and borrelial antigens persisted in the lymphoblasts for 3 and 4 days. Morphological and functional transformation of both agents facilitate their transfer to daughter cells. Association with lymphoblasts and internalization of B. garinii by tube phagocytosis increased replication of viruses more successfully than B. afzelii and chemical inductors. Demonstration of such findings must be interpreted cautiously, but may prove a mixed borrelial and viral cause of severe neurological disease.” (37)

One of the characteristics of chronic neurologic “Lyme” is that it is called an “aseptic meningitis” (38, 39, 40). This is, of course, while the German Multiple Sclerosis expert Roland Martin had been recruited by the National Institute of Health to research the association between “Lyme” and Multiple Sclerosis.(41, 42).  Martin went home once he found out that OspA-induced immunosuppression was the likelier reason “Lyme” was mistaken for Multiple Sclerosis or vice versa.

DISCLAIMER: We Lyme victims did not dream up this nonsense.  We only report it.

Could the co-TLR2 agonists (inducing tolerance and a lack of antibodies) Epstein-Barr and Borreliosis be simply responsible for:  “These immunoblastoid cells in Bb infections at times resemble those found in Epstein-Barr virus infections.  Does Bb reactivate latent virus infections in tissues?  Do some tick inocula harbor simultaneous infectious agents (ixodid ticks can harbor Rickettsiae, Babesia microti, and Ehrlichia bacteria, in addition to Bb), producing multi-agent infections in some hosts?”(36) ?

It is common knowledge that 95% of the adult population in Western cultures has been exposed to Epstein-Barr and its common similar herpes viruses.  Hypothetically, there is a mouse herpesvirus (gamma2herpes) that to our knowledge has not been investigated regarding transmission to other hosts via ticks.  We’re not privileged to know much about what happens on Plum Island.  We only know there is a “Plum Island” strain of mycoplasma, and that Yale’s Durland Fish experimented with trying to get African Swine Fever virus to “take” to local hard-bodied ticks at that Not-Bioweapons/Just-Helpin laboratory (
43,  44).

However, it's something that might have been discovered 10 or 15 years sooner had not certain persons associated with Yale and New York Medical College made an agreement with Kaiser-Permanente (
45) to sell a vaccine against a disease they suddenly decided doesn’t actually cause any illness (and the world is flat, the moon made of green cheese, and all hospitals are going to become brothels because it’s cheaper and therefore cost-effective to deploy self-alleged MDs who never perform any scientifically valid rule-outs before making theoretical diagnostic assumptions based on “projection,” rather than bog down the likes of the actual laboratories with the fancy machinery that serves no purpose other than to take up space and look shiny, just like the misguided folks at Silly NASA…).

“Epstein-Barr virus (EBV) efficiently drives proliferation of human primary B cells in vitro, a process relevant for human diseases such as infectious mononucleosis and posttransplant lymphoproliferative disease. Human B-cell proliferation is also driven by ligands of Toll-like receptors (TLRs), notably viral or bacterial DNA containing unmethylated CpG dinucleotides, which triggers TLR9. Here we quantitatively investigated how TLR stimuli influence EBV-driven B-cell proliferation and expression of effector molecules. CpG DNA synergistically increased EBV-driven proliferation and transformation, T-cell costimulatory molecules, and early production of interleukin-6. CpG DNA alone activated only memory B cells, but CpG DNA enhanced EBV-mediated transformation of both memory and naive B cells. Ligands for TLR2 or TLR7/8 or whole bacteria had a weaker but still superadditive effect on B-cell transformation. Additionally, CpG DNA facilitated the release of transforming virus by established EBV-infected lymphoblastoid cell lines. These results suggest that the proliferation of EBV-infected B cells and their capability to interact with immune effector cells may be directly influenced by components of bacteria or other microbes present at the site of infection.--  
Toll-like receptor agonists synergistically increase proliferation and activation of B cells by epstein-barr virus. (

We know that “Lyme” is associated with the production of Amyotrophic Lateral Sclerosis (in 47% of the ALS cases in Lyme-endemic areas) (47) and Multiple Sclerosis.  And we know that ALS is associated with mycoplasmal infection (tolerance to TLR2 agonists), and, MS, and apparently “Lyme” is associated with Epstein-Barr virus or something like it (36, 48).

We know that 90% of Chronic Fatigue patients found out they had “Lyme Disease” when finally assessed by a reputable laboratory – one not like Quest Diagnostics, which uses strain B31, the non-neurotropic, non-OspC- bearing, non-band-23-producing strain (
49).  We hypothesize that since it is known that mycoplasmal infections in the blood disrupt the osmotic potential in erythrocytes (disrupt the transfer of oxygen), and metabolism (these things need to be fed, after all) (50, 51), and since there has been reported a high association to mycoplasmal infections in Chronic Fatigue and Gulf War Illness victims (52, 53), that the tolerance to TLR2 agonists Lyme/LYMErix results in tolerance to mycoplasma in the blood (Chronic Fatigue) with no relative antibody production (28). 

“Lyme” also produces a Lupus-like syndrome (
54), and recently (and formerly, formally associated with Allen Steere) was linked by the Allen-Steere-Lupus-Lyme group (now known as the biotech spin-off, “L2-Diagnostics”) with Epstein-Barr (55).

We hypothesize that due to the induction of tolerance to TLR2 agonists like fungal or mycoplasmal antigens (Pam3Cys or OspA blebbing or vaccination) interrupting Epstein-Barr latency,

"Chronic infection or colonization by mycoplasma(s) could gradually and significantly alter many biologic properties of mammalian host cells in culture, including induction of malignant transformation. We examined effects of Mycoplasma fermentans infection on the continuing survival and immortality of human peripheral blood mononuclear cells (PBMCs) from healthy blood donors. Without specific supplemental growth factors, human PBMCs normally die rapidly, with few cells other than macrophages/monocytes surviving after 2 weeks in cultures. Only occasional Epstein-Barr virus (EBV)-positive B lymphocytes would continue to proliferate and undergo spontaneous immortalization. Our present study revealed that infection of human PBMCs in culture with the incognitus and PG18 strains of M fermentans, but surprisingly not with some other strains tested in parallel, markedly enhanced the rate of EBV-positive B lymphocytes to undergo immortalization (74% vs 17%).  Compared with spontaneously immortalized PBMCs, the PBMCs immortalized in cultures infected with the mycoplasmas often had prominent karyotype changes with chromosomal loss, gain, or translocations. Furthermore, many of these immortalized B lymphocytes were found to be monoclonal in nature. The in vitro findings would be of relevance to lymphoproliferative disorders that occurred in patients with immune suppression. The mycoplasma-mediated promotional effect in cell immortalization and its potential clinical implications warrant further study. --2004; Blood; Mycoplasma fermentans infection promotes immortalization of human peripheral blood mononuclear cells in culture.  (56)

the induction of chronic Lyme results in the un-latency of Epstein-Barr.  Says one researcher,

Regulation and dysregulation of Epstein-Barr virus latency: implications for the development of autoimmune diseases.

"Epstein-Barr virus (EBV) is a human herpesvirus hiding in a latent form in memory B cells in the majority of the world population. Although, primary EBV infection is asymptomatic or causes a self-limiting disease, infectious mononucleosis, the virus is associated with a wide variety of neoplasms developing in immunosuppressed or immunodeficient individuals, but also in patients with an apparently intact immune system. In memory B cells, tumor cells, and lymphoblastoid cell lines (LCLs, transformed by EBV in vitro) the expression of the viral genes is highly restricted. There is no virus production (lytic viral replication associated with the expression of all viral genes) in tight latency. The expression of latent viral oncogenes and RNAs is under a strict epigenetic control via DNA methylation and histone modifications that results either in a complete silencing of the EBV genome in memory B cells, or in a cell-type dependent usage of latent promoters in tumor cells, germinal center B cells, and LCLs. Both the latent and lytic EBV proteins are potent immunogens and elicit vigorous B- and T-cell responses. In immunosuppressed and immunodeficient patients, or in individuals with a functional defect of EBV-specific T cells, lytic EBV replication is regularly activated and an increased viral load can be detected in the blood. Enhanced lytic replication results in new infection events and EBV-associated transformation events, and seems to be a risk factor both for malignant transformation and the development of autoimmune diseases. One may speculate that an increased load or altered presentation of a limited set of lytic or latent EBV proteins that cross-react with cellular antigens triggers and perpetuates the pathogenic processes that result in multiple sclerosis, systemic lupus erythematosus (SLE), and rheumatoid arthritis. In addition, in SLE patients EBV may cause defects of B-cell tolerance checkpoints because latent membrane protein 1, an EBV-encoded viral oncoprotein can induce BAFF, a B-cell activating factor that rescues self-reactive B cells and induces a lupus-like autoimmune disease in transgenic mice."(57)

Down-regulation of MHC class II expression through inhibition of CIITA transcription by lytic transactivator Zta during Epstein-Barr virus reactivation.

"The presentation of peptides to T cells by MHC class II molecules is of critical importance in specific recognition to a pathogen by the immune system. The level of MHC class II directly influences T lymphocyte activation. The aim of this study was to identify the possible mechanisms of the down-regulation of MHC class II expression by Zta during EBV lytic cycle. The data in the present study demonstrated that ectopic expression of Zta can strongly inhibit the constitutive expression of MHC class II and CIITA in Raji cells. The negative effect of Zta on the CIITA promoter activity was also observed. Scrutiny of the DNA sequence of CIITA promoter III revealed the presence of two Zta-response element (ZRE) motifs that have complete homology to ZREs in the DR and left-hand side duplicated sequence promoters of EBV. By chromatin immunoprecipitation assays, the binding of Zta to the ZRE(221) in the CIITA promoter was verified. Site-directed mutagenesis of three conserved nucleotides of the ZRE(221) substantially disrupted Zta-mediated inhibition of the CIITA promoter activity. Oligonucleotide pull-down assay showed that mutation of the ZRE(221) dramatically abolished Zta binding. Analysis of the Zta mutant lacking DNA binding domain revealed that the DNA-binding activity of Zta is required for the trans repression of CIITA. The expression of HLA-DRalpha and CIITA was restored by Zta gene silencing. The data indicate that Zta may act as an inhibitor of the MHC class II pathway, suppressing CIITA transcription and thus interfering with the expression of MHC class II molecules." (58)


It could be that it’s actually OspA-induced Epstein-Barr that is the “New Great Imitator.”

And that the Yale-Plum-Permanentes are the Greatest Great-Imitators.

Of either physicians or scientists.

Still, where do we go from here?

“We don’t know.”  First, we have to deal with the sugarplum fairy-dancing cocoanut-heads, masquerading as “MDs” and “scientists,” doing perpetual, eternal lapses and re-lapses between the green cheese moon and the flat earth on the dot guv dime because they haven’t the plain old regular nuts to admit that they knew all along - and from the beginning, 1992, when Allen Steere went to Europe with his “high passage” plasmid-dropping spirochete strains and “recombinant OspA-B with the no-lipid attached” to come up with a “diagnostic standard” for “Lyme” that ended up with none of the two “primary immunodominant antigens” represented -  that OspA was not a vaccine.

-- -- -- -- --

“To be most effective, advances in regulatory science must be fully integrated into the entire product development process,”  says the new FDA chief, Margaret Hamburg.

The Biomarkers if Illness, developed by the ALDF.com or IDSociety.org

And the End of the Almighty Checklist - a sign of the auto-detonation of the adherents to Psychiatry:

What do the Biomarkers, published by the same gang who now says "Lyme is a consequence of inadequate sexual release," say "Chronic Lyme/LYMErix Disease" is?. 

      Using Dark Field
to study the modified erythrocytes, modified via the tolerance induced from chronic stimulation of TLR2 by spirochetal blebbing of the likes of TLR2 agonist OspA, and subsequent colonization by mycoplasma [recall that many sufferers of “Chronic Fatigue Syndrome” have been found to own a colony of Candida (a fungus)].

Brazil makes fun of US "Lyme" "scientists"  mycoplasma-like and spiroplasma-like organisms in the blood of Lyme-like illness

See Erythrocytes of RBC in Biomarkers page.  Crooks don’t want anyone using Dark Field to look at the blood.  Sweeg went after Lisa Masterson for making this proposal.

2)  The "We Don't Know What You Have" Negative Data Rule re the DNA/RNA testing for all the mycoplasma and activated viral infections that won't be producing antibodies (because some are also TLR2 agonists like Epstein-Barr, and chronic TLR2 agonism results in no-antibodies (Justin Radolf: ,” Inhibition of MHC-II Ag processing by either MTB bacilli or purified MTB 19-kDa lipoprotein was dependent on Toll-like receptor (TLR) 2 and independent of TLR 4. Synthetic analogs of lipopeptides from Treponema pallidum also inhibited Ag processing. Despite the ability of MTB 19-kDa lipoprotein to activate microbicidal and innate immune functions early in infection, TLR 2-dependent inhibition of MHC-II expression and Ag processing by MTB 19-kDa lipoprotein during later phases of macrophage infection may prevent presentation of MTB Ags and decrease recognition by T cells.”
http://www.jimmunol.org/cgi/content/full/167/2/910  )]

This may be the main reason the crooks don’t want us treated with antibiotics- we will create antibiotic resistant Tuberculosis (because we will likely have seronegative TB oand other primarily TKR2 agonising infections like Staph aureus), not to mention, changing the RNA of the likes of mycoplasma as the Chinese did:
J Clin Microbiol. 2010 Sep 22. [Epub ahead of print]
Nested PCR-Linked Capillary Electrophoresis and Single-Strand Conformation Polymorphisms for Detection of Macrolide-Resistant Mycoplasma pneumoniae in Beijing.

 3) QEEG or Fibro-Lenny Sigal’s  (who we’ll now refer to as Lenny Squiggy) findings that persons with chronic Lyme have changes to electroencephalograms.
http://www.ncbi.nlm.nih.gov/pubmed/7554300  “Abnormal QEEG and/or EPs were found in 75% of the active Lyme disease patients and in 54% of the post CNS Lyme disease patients.”

  modified cytokine profile
suggested by Lenny Sqiggy in the Cold Spring Harbor Conference book (1992, Schutzer:) mentioned above, to which Paul Duray attended and re-iterated his “EBV-modified lymphocytes” findings:
page 205: 
Says Sigal: 
“Since cytokines can alter endothelial cell function and increase the entry of inflammatory cells to the organ whose vasculature has been modified, the presence of cytokines in the Lyme synovium may have an important indirect effect on local inflammation [Yednock et al. 1992].  The presences of circulating levels of these cytokines may be the cause of the certain clinical features of Lyme disease; eg., sleep disorder due to elevated levels of IL-1 (Opp and Krueger 1991) may be part f the cause of fibromyalgia seen during and after active Lyme disease (Sigal 1990)

1991, Steve Schutzer.

5) MMP-130 and GFAp in the CSF of Mark Klempner's Neuroborreliosis (which is not "Lyme Disease," BTW, because Lyme Disease became "only the HLA-linked knee-presentation" at Dearborn),

6)      Allen Steere's Nitric Oxide in the CSF of Lyme victims (we now know that the exposure to these reactive oxygen species/byproducts are downregulators of TLR2)

J Infect Dis. 1994 May;169(5):1014-22.
Borrelia burgdorferi and Escherichia coli lipopolysaccharides induce nitric oxide and interleukin-6 production in cultured rat brain cells.
Tatro JB, Romero LI, Beasley D, Steere AC, Reichlin S.
Division of Endocrinology, New England Medical Center Hospitals, Boston, MA 02111.

      CORRECT Borrelia (all species) DNA/RNA primers
and not the OspA gene, because that changes according to Alan Barbour; we can throw out all "studies" in which the OspA gene was the determinant for infection with the "Lyme" spirochete  [~10 citations]

8)      Quinolinic acid and the degradants of monoamines in the CSF of borreliosis victims (JJ Halperin),

9)      brain SPECT and PET imaging (we now know that the metabolism of erythrocytes are hijacked by the mycoplasma in the blood - infections we can't fight off because they have OspA or TLR2 agonizing lipoproteins in them),   NOTE: psychiatry likes to suggest that changes to the brain perfusion seen in chronic Lyme/Fatigue victims is a result of Bipolar, when not ever once was anyone who was diagnosed with Bipolar have shown hyper- or hypo- perfusion as a result of any of the “poles” without other true, real, scientific valid biomarkers of real illness first performed as a rule out.  Secondarily, when studies have been performed in which there are brain structural changes to the likes of 17 year olds who are determined to be psychopathic or sociopathic, have these conditions studied a contribution by trauma.  As a third outstanding parameter, why, we wonder, are lawyers undable to view anything from a scientific standpoint?  Why do they score so low on the visual-spatial scale of cognitive abilities?  Why are lawyers so left-brain dominant and why do they have no understanding of vocabulary as a simple means to draw a picture in the mind of another. 
Most of all, why is this seen in both lawyers and psychiatrists?  Why are the best scientists and engineers known to be visual-spatial or right-brain dominant?  Is this nature or nurture?  The victims of their chronic fraud crime are not entitled to know why self-alleged scholars as these are clearly unable to think.  We are not entitled to see their own cognitive differentials and potentials.

  Allen Steere's
anti-phospholipid antibodies (now known to be caused by activated Epstein-Barr, as reported by Allen Steere's own Lyme/Lupus reporting team member, Joe Craft at Yale), (54)

  the auto-reactive band 41
[specific to borrelia or not; scientists seem to think an antibody against flagellin cross reacts with nerve and other tissues, such as skin and intestine (H. pylori and Campylobacter, producing autoimmune hives, thyroid disease, GERD...)], [Refs, Barbour patent, Lenny Sigal]

Biochim Biophys Acta. 1993 Mar 24;1181(1):97-100.
Molecular mimicry in Lyme disease: monoclonal antibody H9724 to B. burgdorferi flagellin specifically detects chaperonin-HSP60.
Dai Z, Lackland H, Stein S, Li Q, Radziewicz R, Williams S, Sigal LH.
Center for Advanced Biotechnology and Medicine, Piscataway, NJ.

12)  anti-heat shock proteins (a sign of MS), (others besides Sigal)  Bands 60, 74, etc.

13)  anti-gangliosides, Benach, Steere

1989; Total, anti-viral, and anti-myelin IgG subclass reactivity in inflammatory diseases of the central nervous system.

Total IgG subclass levels, anti-viral, anti-myelin basic protein (anti-MBP), and anti-ganglioside 1 (anti-GM1) IgG subclass levels were measured in 6 patients with herpes simplex virus encephalitis (HSVE), 16 with borreliosis, 8 with other bacterial infections, 12 with multiple sclerosis (MS), 13 with subacute sclerosing panencephalitis (SSPE), 5 with glioblastoma and 12 controls. Total IgG1 levels were elevated in cerebrospinal fluid (CSF) from all patient groups (but not in the controls), IgG2 in bacterial infections, IgG3 in HSVE and borreliosis and IgG4 in some SSPE patients. The anti-viral (anti-measles, varicella zoster virus and rubella) IgG antibodies in MS were restricted to IgG1, anti-measles IgG to IgG1 and sometimes IgG4 in SSPE, anti-borrelia IgG to IgG1, IgG2 and IgG3. In contrast to anti-viral antibodies, anti-MBP and GM1 antibodies belonged to IgG1, IgG3 or IgG4 in MS. The nature of the immunological activation appears to be reflected in the subclass patterns elicited in the central nervous system. Different IgG subclass patterns in infectious diseases and MS suggest a difference between antigen-specific and non-specific B-cell activation.

14)  GFAp or glial fribrillary acidic protein in the CSF - signs of gliosis mentioned by Yale's Robert Schoen when he mentioned reasons why we need a Lyme vaccine, http://www.annals.org/content/132/8/661.full.pdf+html (gliosis would be a sign of multiple CNS degenerative diseases),

"Other peripheral neuropathies and Lyme meningitis are also seen at this stage.  In late-stage disease, the central nervous system may be involved.  A new diagnostic test measuring glial fibrillary acidic protein in cerebrospinal fluid may prove to be a useful tool for measuring such involvement (20)." -- Yale's Robert Schoen talking about how serious Lyme is, and that we need a vaccine for this disease that goes away and has no illness signs and is psychiatric and the result of not-enough-sex or self-poisoning.

15)  Gadolinium-Contrast MRI - performed in monkeys with Lyme but never Lyme-MS Victims which show Lyme is an active meningitis, and now performed by the Japanese when deciphering the cause of meningitis in a patient who was mistakenly diagnosed with MS when they had Large B-cell Lymphoma of the CNS:
Primary central nervous system large B-cell lymphoma with prolific, mixed T-cell and macrophage infiltrates, mimicking multiple sclerosis.

16)  EMG  Allen Steere:

I think we should fund an EMG study where we try to find out whether or not Lyme victims suffer “hysteria” or the electrification of our hysters.  I think this most of all would be a fun study:  Could we find out via EMG that not-enough-sex really causes Lyme-ALS, or Lyme-MS or Lyme-Lupus, or Lyme-stroke, or bad knees, or Guillain-Barre?  Who wants to volunteer for that study?  And what about men with Low-T?  Can that study be performed?  Can we women watch? 
We’ll rate their manliness while this EMG study of their genitals to determine if not-enough sex is “The Reason for Low T or the Inability of Psychiatrists and Lawyers to Think like Scientists or Engineers” is performed with our own Checklist

17) T cell proliferation:
Steere references Dattwyler’s report here:

None of these biomarkers were applied by Mark Klempner from 1997 to 2001 when he determined that “there is no such thing as Chronic Lyme,” despite being the author of two of the main signs that it is.  The first was Klempner’s MMP-130 only found in the spinal fluid of chronic Lyme victims and his other two studies from 1992 where he determined and published the reasons he believed ceftriaxone failed to eradicate all spirochetes [REF]


Now, back to Reason:  What we do know about such emotionalisms over science is that aggression comes from cowardice or the fear of being less-than another person.  We call it jealousy, we call is envy and we call it pride, hubris and arrogance.  Or we fear not being believed that we suffer a terrible illness – one not detectable by antibodies, such as those fungal like stealth infections as Relapsing Fever or Relapsing Fever plus the synthetic antigen Pam3Cys. 

Common sense tells us that you can’t see Multiple Sclerosis or Lupus, but sometimes medical schools attract and even accept people who have studied only the likes of English literature or psychology or philosophy in undergraduate study.  These are the toughest nuts to crack.  You can’t teach an old dog new tricks. 

"You hypocrites, rightly did Isaiah prophesy of you:

Or, they purport self-flattering, unscientific concepts as medical doctrine because it is too frightening to see and accept the reality that they’re truly addicted (repetitious cognitive loops or mental frameworks) in a medical sense to some philosophical (psychiatric) Kool Aid, dreamed up by some pervert and drug addict (Freud).

The biggest of the guns in our arsenal – besides all of the published applications of the science that says Pam3Cys or OspA or LYMErix or the HIV antigens gp120 and 41 – are TLR2 agonists and result in the downregulation of the immune response and the inhibition B cell apoptosis… is the RNA/DNA Shell Game, we know to be criminal in anyone’s mind.

1) J Infect Dis. 1992 Aug;166(2):440-4.
Fibroblasts protect the Lyme disease spirochete, Borrelia burgdorferi, from ceftriaxone in vitro.
Georgilis K, Peacocke M, Klempner MS.
Department of Medicine, New England Medical Center, Boston, Massachusetts.

2) Ann Intern Med. 1994 Oct 15;121(8):560-7.
The long-term clinical outcomes of Lyme disease. A population-based retrospective cohort study.
Shadick NA, Phillips CB, Logigian EL, Steere AC, Kaplan RF, Berardi VP, Duray PH, Larson MG, Wright EA, Ginsburg KS, Katz JN, Liang MH.
Department of Rheumatology-Immunology, Brigham & Women's Hospital, Boston, MA 02115.

3) Neurology. 2003 Jun 24;60(12):1923-30.
Study and treatment of post Lyme disease (STOP-LD): a randomized double masked clinical trial.
Krupp LB, Hyman LG, Grimson R, Coyle PK, Melville P, Ahnn S, Dattwyler R, Chandler B.
Department of Neurology, Stony Brook University Medical Center, Stony Brook, NY 11794-8121, USA.

4) Microbes Infect. 2006 Nov-Dec;8(14-15):2832-40. Epub 2006 Sep 22.
Invasion of human neuronal and glial cells by an infectious strain of Borrelia burgdorferi.
Livengood JA, Gilmore RD Jr.
Centers for Disease Control and Prevention, Division of Vector-borne Infectious Diseases, 3150 Rampart Road, CSU Foothills Campus, Fort Collins, CO 80522, USA.

5) Neurology. 2008 Mar 25;70(13):992-1003. Epub 2007 Oct 10.
A randomized, placebo-controlled trial of repeated IV antibiotic therapy for Lyme encephalopathy.
Fallon BA, Keilp JG, Corbera KM, Petkova E, Britton CB, Dwyer E, Slavov I, Cheng J, Dobkin J, Nelson DR, Sackeim HA.
Columbia University, 1051 Riverside Drive, Unit 69, New York, NY 10032, USA. b...@columbia.edu
Microbiology. 2000 Jan;146 ( Pt 1):119-27.

6) Antimicrob Agents Chemother. 2010 Feb;54(2):643-51. Epub 2009 Dec 7. 
Ineffectiveness of tigecycline against persistent Borrelia burgdorferi.
Barthold SW, Hodzic E, Imai DM, Feng S, Yang X, Luft BJ.
Center for Comparative Medicine, School of Medicine, University of California at Davis, One Shields Avenue, Davis, CA 95616, USA.  swbarth...@ucdavis.edu

7) Serum-starvation-induced changes in protein synthesis and morphology of Borrelia burgdorferi.
Alban PS, Johnson PW, Nelson DR.
Department of Biochemistry, Microbiology, and Molecular Genetics, University of Rhode Island, Kingston 02881, USA.

8) J Infect Dis. 1994 Feb;169(2):313-8.
Antibody responses to the three genomic groups of Borrelia burgdorferi in European Lyme borreliosis.
Dressler F, Ackermann R, Steere AC.
Division of Rheumatology/Immunology, New England Medical Center, Tufts
University School of Medicine, Boston, Massachusetts 02111.

9) J Infect Dis. 1993 Feb;167(2):392-400.
Western blotting in the serodiagnosis of Lyme disease.
Dressler F, Whalen JA, Reinhardt BN, Steere AC.
Division of Rheumatology/Immunology, Tufts University School of Medicine, New England Medical Center, Boston, Massachusetts 02111.

10) J Clin Invest. 1986 Oct;78(4):934-9.
Antigens of Borrelia burgdorferi recognized during Lyme disease.
Appearance of a new immunoglobulin M response and expansion of the immunoglobulin G response late in the illness.
Craft JE, Fischer DK, Shimamoto GT, Steere AC.

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Oh, this is rich, LMAO...

In an era of "personalized medicine" and with Obama's "Brain Initiative" to replace the officially DEBUNKED psychiatry, it's past time for this kind of bullshit to be considered TABOO.  Actually, it should be PROSECUTED for medical FRAUD:


"Doctors" don't know dick about medical science.

You know this is true since Thomas Insel had to declare psychiatry "INVALID" (none of them did, LOL, duh),

We Lyme activists got LYMErix off the market by starting a campaign to get all the systemic adverse events reported to the FDA (no doctors did),

No "doctor" testified at the FDA 14 years ago explaining and demonstrating that none of the participates of the Dearborn conference agreed with Steere's proposal.  We got stuck with this RESEARCH FRAUD anyway and it hasn't been prosecuted yet,

No "doctor" revealed to the FDA that LYMErix caused immunosuppression rather than "was a vaccine."

No "doctor" sued IDSA over their research fraud "guidelines," A SENATOR DID.

No "doctor" confronts the FDA over not assuring the Lyme testing meets their own criteria for a VALIDATION - A SENATOR DID...

No "doctor" even gives a shit what OspA is.  They don't even ASK, LOL.


They still don't ask.  Yet, there are no other fungal vaccines.  Duh.  They have a pretty high opinion of themselves for knowing nothing other than "Rx --> PAY ME, NEXT!!!"

They don't care what a disease is.  All they care about is this simple, linear "A-->B" formula.  Someone walks in, they get an Rx, they pay, they leave.  That's all "doctors" think about.  Pharmacists have better scientific training than "MDs."  "Doctors" as dumb as any other non-Lyme patient.  ONLY Lyme victims know what is going on in the sci-med world.  We've been left to our own devices.  We figured it all out.  No "doctors" were involved in any of it.

"Doctors" live in a like a Wonderland or Oz or a Medical Matrix.  They can't be trusted because they have no WILL to know, and that is no more than a character flaw.  I'd like to write a new DSM based on these kinds of character flaws.  Maybe that'll be the real "Lyme Whistleblower" book everyone needs to read.


The reason the CDC is lying about Lyme, ME/CFS and Autism, is because these devastating outcomes are all caused by the same mechanisms.  Search for a description of "Post-Sepsis Syndrome" online and you will find it is the same as CFIDS/Chronic Lyme.  So, imagine that kind of brain inflammation seen in sepsis, but in babies undergoing neurogenesis and neurodevelopment...  You can't really expect a good result in babies, when the encephalitis damage is so severe in Chronic Fatigue Syndrome/Post-Sepsis.

Now, importantly, POST-SEPSIS or post septic cytokine storm seen in Lyme, CFIDS, and Autism babies... comes with humoral immunosuppression and not classic "HLA-linked autoimmune inflammation."  So that's the information you need to parse out CDC's bullshit.  These waste-basket diseases are NOT classical inflammation or "autoimmunity" with the self-reacting T cells and the auto-reacting antibodies.




SHAPIRO: Somehow, for that form of the disease, antibiotics are
effective. They do fine. But then there's some other form of the
disease which is, you can't put your hand around it. *** They don't have
objective findings of inflammation, which is the way bacteria cause

So, it's clear that if you don't have the HLA-linked hypersensitivity response, you are
not allowed to have a disease.  That was the Dearborn scam...




Letter to Pandora, explaining how they have been hoodwinked by the CDC:

"CFIDS/FM is/are not “neuro-endocrine-immune diseases.”  They/it are really actually chronic active herpesviruses, immunosuppression with opportunistics, much like AIDS (no T cell killer virus, just T cell anergy).

"First, have a look (in the references, here) at the recent description of “post-sepsis syndrome” (PSS) and the statements/reports by Washington University St. Louis, MO. (wustl.edu) and the NIH confirming that model on what  this disease is, how it comes about, (1-8), the older immunosuppression data on fungi like mycoplasma and mycobacteria- formerly called epERYTHROzoons - clue (9, 1953), past fungal vaccines failures and what those failure-outcomes looked like (10-14), and of course the Autism pandemic, which parallels all these mechanistically (15-21, 51).

"I would like you to note that in this report, I put a lot of the explanations in the references section.  Since CFIDS people have cognitive issues (53), particularly right brain issues or visual-spatial processing deficits, I have to make the overall picture as brief as possible in the body of this report."


This is the year the Lyme cryminals are going to get BUSTED or we are ALL going to know why (usda.gov, Plum Island, & BigVaccines).  We're going to Occupy the USDOJ (Washington, DC) in May-July, 2015 and all abused groups are welcome.  The primary reason for the abuses of Lyme and similar (Gulf War Illness, Chronic Fatigue, Fibromyalgia) victims is that the CDC does not want anyone to know how the childhood vaccinations are causing Autism,... because those mechanisms are the same in Lyme, GWI, Fibromyalgia, ME/CFS.  The children are getting the viruses instead of the protection due to immunosuppression.   And the childrens' immune systems are being ruined by all the hypervaccination, explaining the epidemics of allergies, asthma, ADD, and leukemia in American children, too.

So, everyone is welcome to show up at the Occupy and stay as long as you like.  Come and in Solidarity, demand Justice.  Remember, "America" used to be short for "WE'RE NOT PUTTING UP WITH THIS BULLSHIT!!!"  >>>  https://www.facebook.com/groups/OccupyUSDOJ


Understanding the Govt's Hired Psychopaths:

I just had another thought on this matter of how assholes germinate and grow into psychopaths (psychiatrists, the CDC, and similar vicious tards). That is, as long as we're talking about the replacement for scientifically invalid psychiatry:

Does everyone remember that Susan O'Connell beeotch who used to work for Porton Down and the UK NHS?  How she was the gatekeeper for Lyme/TBDs in the UK,... and worked with the USA Lyme crooks, McSweegan and Durland?

And how she leaked to Lady Mar (who basically goofed her out of it), that "Porton Down was no longer working on Borrelia as a bioweapon" and that they had "given it over to industry?"

It wasn't really given over to industry.  Edward McSweegan, the arrogant moron (showing the dynamic between arrogance and stupidity), cheated the US Navy out of their TBD's funding with his fake Senator Goldwater "Whistleblower" Letter in 1986. Those are the morons who thunk up a vaccine for relapsing fever, the very thing that defies the concept of vaccines (the ALDF.com):

So, what is wrong with Sweeg's brain? Why is he a crazy, vicious moron, like his buddy Durland? How did Sweeg become a psychopath?

He reveals it here:

"As a graduate student twenty years ago, I had a departmental recruiting poster tacked up on the wall next to my desk. It read, in part, "If you are curious, patient, and *** awfully damned intelligent," consider a Ph.D. in microbiology." In 1984 a degree in microbiology seemed like a good idea."

He had convinced himself he was UNIQUE!!! SPECIAL!!! BRILLIANT!!! It's always the same thing. Self-idolatry - believing there is something UNIQUE!! or SPECIAL!! about yourself. It is the same reason Lucifer fell and the source of all the trouble in the world. Same vanity. Same Influence of Spirit to believe you're above the rest.

But evil has no creative abilities. That is probably why it took the HEAD OF THE NIMH to finally declare psychiatry to be scientifically invalid. Notice this did not come from psych.org. None of them thunk up whether or not psychiatry was valid. They, all of psychiatry, did not have THE INSIGHT (keyword).

And speaking of the CDC/Porton Down and beeotches named Susan, let's keep in mind that Susan Vernon (CDC officer) who threw out the cells to which mycoplasma adhere or live inside of, when trying to show that mycoplasma are not involved in Chronic Fatigue Syndrome:

22) CDC’s Lies: “Absence of Mycoplasma species DNA in chronic fatigue syndrome”, throwing out the blood cells in order to find no mycoplasma:

“Blood was collected in sodium citrate Vacutainer tubes (Beckton Dickinson) and shipped by overnight courier to the Centers for Disease Control (CDC), where plasma was collected by separation on lymphocyte separation medium (LSM; ICN Biomedicals). Plasma (1 ml) was concentrated to approximately 250 μl in a Centricon centrifugal filter unit YM-100 (Millipore). Cell-free plasma DNA was extracted by using a QIAamp DNA Mini kit (Qiagen) according to the manufacturer's instructions and quantified by using a DyNA Quant 200 fluorometer (Amersham Biosciences).”

They're all like that.  Where do they get off being psychopaths?  There's your answer.  They have some false idea that they're superior creatures, just like the NAZIs.  But it's transparent and imbecilic.

Psychiatry claims Somatoform diseases are where the alleged victims have scientifically valid signs of illness or detectably pathophysiologies in the absence of real disease - which is the very definition of magic or paranormal, - yet they otherwise ignore all the evidence of paranormal (or paraphysical, as I call it, which refers to intelligences without physical bodies) events.

You have to think long, hard and deep about that.  What does it mean when you have selective cognition, yet claim to be, and charge to be, and claim to be an expert in legal cases, and in the magnitude of lives they ruin who are genuinely sick with real disease like, as you have seen, CFS, ME, Lyme, Fibro, etc., worldwide.

One more recommendation:  Read Hostage to the Devil by Malachi Martin and watch the subtle way Martin trashes these idiots,... and what the demons reveal about psychiatrists ;)

Rings true, because it is.


NEW BAD-ASS Lyme Cryme Website:

... "When it comes to the Lyme criminals – those associated with Yale, LYMErix, and the Dearborn stunt (involving CDC officers), our silence is what keeps them alive in this war between the sick and the unsick. Their strategies are obvious, and involve the three rewards most valued by psychopaths – money, power and fame – in addition to their desire to stay out of prison. Case in point: the University of Kansas doctor credited with “discovering” the Bourbon virus. His patient died, yet he is rewarded with the fame of discovering a new, deadly virus that possibly isn’t deadly at all, but an innocent bystander in the fungal-viral-bacterial septic soup that the CDC can’t acknowledge for fear of losing all credibility, once and for all. (Plus that prison thing.) He’ll likely patent the organism, then get research funds (our tax dollars at work) to invent a vaccine, which will generate more fame and fortune (in the form of royalties) not only for him, but his employer, the State of Kansas....

Lyme Crymes Video Playlist (like a Powerpoint presentation on YouTube, stop at each frame and go at your own pace)

VID1 FLAGELLIN ONLY IS VALID for diagnosis of Lyme or any borreliosis

There has been an FDA-Validated method to detect Borreliosis and even Lyme borreliosis since 1991.  Yale patented it under US 5,618,533.  It detects early, late, neurologic, and all cases of Lyme.  Because these crooks pulled the Dearborn stunt later, their vicious antics you currently see, and abuses against Lyme victims is intended to prevent homicide charges over the Dearborn case definition.  



This is just the beginning of the data on persistence and viability of the spheroplast form.  I will add more on this later.   See more at http://www.actionlyme.org/BRAIN_PERMANENT.htm  and   http://www.actionlyme.org/RICOCHRON.htm



This video, 3, shows the Lyme Cryminals knew LYMErix caused the same "multisystem disease" as we know of as Chronic Lyme. They changed the definition of the disease at Dearborn because they knew LYMErix vaccination caused the same disease. They were prepared for that outcome since they published a book in 1998 anticipating those outcomes and especially as regards children who potentially became ill from this vaccine. They intended to accuse the parents of Munchausen's by Proxy.  


This video shows you how OspA causes the immunosuppression state of Chronic Sepsis or chronic active herpesviruses as result of being exposed to fungal antigens. These are a series of references by Dattwyler, Harding, Medvedev, etc and re tolerance to other antigens such as viral (TR7/9) and bacterial lipopolysaccharide (TLR4-agonist). Your disease is polymicrobial, ongoing sepsis, much like AIDS.

VID5 Dearborn Falsified Lyme Case Definition

Now that you have seen the first 4 videos and especially the 4th one on how Lyme causes systemic disease, like a chronic sepsis, with the ongoing schmorgasbord of reactivated herpesviruses, tolerance to other infections (bacterial), and that this is an AIDS-like disease... you want to know which criminals are behind this scam and how they pulled it off.


No one knows what Dearborn means, Steere does not know what he is talking about, SmithKline makes fun of him, Klempner's "re-treatment" "study" was anything but, yet is the basis of the IDSA "Guidelines on the Diagnosis and Treatment of Lyme Disease," all of IDSA's aggression - including the "Guidelines" - towards VERY sick people is about avoiding a prosecution over the Dearborn case definition stunt.
Be sure to review the PrimerShellGame to dispel the rumor that "biofilms" are the reason spirochetes are antibiotic resistant.  Spirochetes are individual operators.  They do not cluster in vivo in mammals.



It's hard to think of what to say about this. In 1991, Steere admitted Lyme caused everything, from RA to MS to Fibromyalgia. Later of course he claimed Lyme only caused arthritis. IDSA still claims Lyme only causes a hypersensitivity response in a knee with no other symptoms. Nevertheless, the topic seems to be how the CDC is so good at hiring and creating psychopaths.


VID8 DNA RNA Shell Game

The DNA/RNA gene shell game. This is a short version of this aspect of the crime. The Lyme crooks use the wrong DNA to not find Lyme, say OspA could never be a vaccine due to antigenic variation, and use this nonsense gene to NOT FIND LYME when convenient. But they use the RIGHT DNA when they want to patent something. This information will be very useful to the prosecution since it is so obvious and blatant, and the Klempner non-retreatment report is fraudulently restricting diagnosis and care,... as you will see.

Importantly, we have no MDs in America with any basic science training or you would not be hearing/seeing this from me. (It's a bit much for the patients to have to do all the research, but that's America, Land of the Boneheads.)


Coming soon,  Biomarkers, the RICO Patents, etc.




1) Lyme and LYMErix (fungal, and not bacteria but their own phylum) result in Lupus and MS (both known to be caused by EBV/Similar herpes). 

THOSE ^^^ 2 (MS and Lupus) are "AUTO-IMMUNE" with the lots and lots of antibodies against, in large part, the SECONDARY infections, EBV/similars.  But not everyone has the HLAs for "autoimmune" diseases.


2) The new SEPSIS reports by wustl and the NIH (fungal antigens shut off the immune response ENTIRELY as shown in the numerous reports I have written this last 2 months). *** It is FUNGI or TL2/1 agonists that do this, mainly *** as shown in the videos










And I have found more such reports in PubMed, you can too.



CDC’s Lies: “Absence of Mycoplasma species DNA in chronic fatigue syndrome”, throwing out the blood cells in order to find no mycoplasma:

“Blood was collected in sodium citrate Vacutainer tubes (Beckton Dickinson) and shipped by overnight courier to the Centers for Disease Control (CDC), where plasma was collected by separation on lymphocyte separation medium (LSM; ICN Biomedicals). Plasma (1 ml) was concentrated to approximately 250 μl in a Centricon centrifugal filter unit YM-100 (Millipore). Cell-free plasma DNA was extracted by using a QIAamp DNA Mini kit (Qiagen) according to the manufacturer's instructions and quantified by using a DyNA Quant 200 fluorometer (Amersham Biosciences).”


Bitch centrifuged out all the cells to which mycoplasma adhere or live inside of, then looked for mycoplasma in a test tube full of nothing.  Cute.  That's the CDC and Susan (Suzanne) Vernon for ya.


6) CDC: Measles, Mumps, and Rubella -- Vaccine Use and Strategies for Elimination of Measles, Rubella, and Congenital Rubella Syndrome and Control of Mumps: Recommendations of the Advisory Committee on Immunization Practices (ACIP)

"Updated information on adverse events and contraindications, particularly for persons with severe HIV infection, persons with a egg allergy or gelatin allergy, persons with a history of thrombocytopenia, and persons receiving steroid therapy [are immunosuppressed - KMD]." 



7) CDC: Human Exposure to Brucella abortus Strain RB51 -- Kansas, 1997


In the above, an immunosuppressed pregnant cow was given a Brucella (LYMErix-like) "live, attenuated" vaccine and the baby cow ended up with the disease, which then was transferred to the humans handling the cow and her dead baby. This parallels what is happening to children who are vaccinated while immunosuppressed, or who receive mycoplasmally (LYMErix-like) contaminated vaccines.


8) Fungi Activate Viruses, Rockefeller, 1953 [Go back to the 1950s to see Rockefeller Bioweapons Inc experimenting with mycoplasma antigens like OspA - Enhancing Mouse Leukemia Virus, just like fungally-contaminated vaccines do, which was the reason they put Thimerosal in vaccines, to prevent fungi from doing this (Clue: HIV and "Lyme" bearing the same immunosuppressing triacyl lipopeptide fungal antigen, OspA]:



"In Swiss mice, animals with high natural resistance to hepatitis virus, the pathogenicity of this agent was markedly enhanced by combined infection with eperythrozoa. Eperythrozoa were maintained throughout 18 successive passages in normal Princeton and Swiss weanlings with intact spleens. The combined infection of Princeton mice with eperythrozoa and the virus component of Gledhill, Dick, and Andrewes, which is nearly inactive when injected alone, resulted in acute hepatitis with fatal outcome."


9)  The effect of exogenous corticosterone on West Nile virus infection in Northern Cardinals (Cardinalis cardinalis)

“Corticosterone was administered at levels that individuals enduring chronic stressors (i.e ., long-term inclement weather, food shortage, anthropogenic pollution) might experience in the wild. Corticosterone greatly impacted mortality: half of the corticosterone-implanted cardinals died between five - 11 days post-inoculation whereas only one of nine sham-implanted (control) birds died.

”No differences were found in viral titer between corticosterone- and sham-implanted birds. However, cardinals that survived infections had significantly higher average body temperatures during peak infection than individuals that died.

”In sum, this study indicates that elevated corticosterone could affect the survival of WNV-infected wild birds, suggesting that populations may be disproportionately at-risk to disease in stressful environments.”


When this happens in Medical school students and astronauts - the activation of EBV by CORTISOL and not some mysterious brain energy weapon called somatoformia - they call it something real: EBV.


10)  NYTimes reveals Thimerosal is put in vaccines to prevent FUNGI since it is well known that FUNGI activate viruses.

 NYTimes; Doctors admit Thimerosal is put in vaccines to prevent fungi:

Vaccine Rule Is Said to Hurt Health Efforts (Dec, 2012)

They say:

"But a proposal that the ban include thimerosal, which has been used since the 1930s to prevent bacterial and fungal contamination in multidose vials of vaccines, has drawn strong criticism from pediatricians.

"They say that the ethyl-mercury compound is critical for vaccine use in the developing world, where multidose vials are a mainstay.

"'Banning it would require switching to single-dose vials for vaccines, which would cost far more and require new networks of cold storage facilities and additional capacity for waste disposal, the authors of the articles said.'"


^^ They are revealing why so few doctors' own kids get vaccines-acquired brain damage. Their kids probably get the first shot out of the vial.


11) OspA acts like BCL2, inhibiting apoptosis reactivating EBV/Similars:

Targeting proteins computationally

"Apoptosis is regulated by both pro- and anti-apoptotic members of the B cell lymphoma-2 (Bcl-2) family of proteins. Epstein Barr virus (EBV), the causative agent of Burkitt’s lymphoma, encodes a pro-survival mimic of these Bcl-2 proteins called BHRF1 that inhibits cellular apoptosis during infection and is thought to contribute to lymphomagenesis."



BTW ^^ they're fans of ActionLyme, Fred Hutch Cancer :)


You would think that in the 20th and 21st centuries we in the English speaking world would have some sort of a collective idea on how to prevent all but a couple' percent of our populations from falling through the cracks into poverty, near-starvation, homelessness, chronic illness, drug addiction, getting nothing but assholes-and-morons for politicians, our childish "foreign policy," having to suffer the cognitive-deficits-in-journalism, etc.  But when you consider who are the characters who have self-assigned themselves the Authority, or are the planners, or are the people who originally thunk up the idea that post-WWII, America was going to rule the Earth (Rockefellers, Israelis, Banksters, the Petro-fellas), you would think they would have come up with some sort of a moral theme or motif or humanness concept that ties together the plight of Earth itself, with harmonious cooperation between needs and resources.  But that never enters the Capitalists' minds.  No.  They were convinced by some diabolical influence that humans are mere animals, competing as animals to be the fittest. 

Now consider the word "fit." When you think of "fit," does some bankster or lawyer or salesman come to mind? When someone like Mr. Kahn of Kahn Academy comes along and blows the entire Education industry out of the water - from out of nowhere - what does that say about the Establishment?  What are we doing wrong?  Who comes up with the idea that a formal education on education makes you a teacher?  They consumed this education on education but by what criteria are the planning and the protocols weighted?  Why do we have the entire CDC, NIH, AMA, FDA, DHHS, and all of medical mainstream America not aware of the fact that there is no Tuberculosis vaccine for the same reason there is no Lyme vaccine, ... and is the same reason we put Thimerosal in vaccines (fungi = bad)?  How dare the NIH and CDC (not to mention Yale) tell me they don't know what the Lyme vaccine was?

Where does anyone get off saying they should be paid for being an expert, when they admit they do not know the basic things about human illness and disease ("doctor," or HMO CEO)?

The world now dominated by the USA has no cohesive plan or idea.  No reputable intent.  The United States Government are a bunch of animals who think their job is to control the other animals. Fear is their essential theme and motif. 

The world is ruled by a bunch of cowards

And that's funny to me because COWARD was the thing I was always taught was the LAST thing you'd ever want to be.