Worlds Collide, Criminals Collude

badguysScientists. Are they the smartest guys in the room, or just the New Great Imitators?

In the beginning, there was one guy who was the First Person Ever to have Chronic Fatigue Syndrome. (There’s a guy who trolls the Facebook groups and thinks he is this particular guy, but he’s not, and I’m being hypothetical, anyway.) So, “chronic fatigue” existed, and the “scientists” who were tasked with finding a cause and a cure began a long tradition of obfuscation and playing a semantics game.

Meanwhile, on the opposite side of the country, a vast tropical storm supposedly carried an African bird borreliosis many thousands of miles to deposit it near the USDA facility at Plum Island. This borrelia then apparently acquired a plasmid (OspA/B) that allowed it stick to the inside of a hard-bodied tick. This new borrelia can live in the hard body-tissues of the hard bodied tick, rather than in the gut alone, as it does in a soft-bodied tick. Isn’t that curious?

Even more curious was the assignment of the case to EIS Officer and “rheumatology specialist” Allen Steere. Polly Murray, the Connecticut mother who raised a big enough stink to get the situation investigated, never said it was about arthritis, alone. There were chronic fatigue signs too, but hardly anyone knows that, because once Steere was on the case, they christened the illness “Lyme disease.” Then began a long tradition of obfuscation and playing semantics, just like the hostile takeover of CFS.

Both diseases went through a variety of name changes and case definition updates, independent of each other, driven mainly by government-funded researchers who apparently were directed to obfuscate and semantificate. But why? What is the point of keeping millions of people sick? What would be the harm in diagnosing and treating them?

Based on all the evidence, we can only surmise that 1) Lyme disease was, oops, an accidental release from the Plum Island research facility—the circumstantial scientific evidence says so—and 2) to acknowledge diseases of immunosuppression and their astronomical impact would reveal massive systemic problems with the vaccine industry and its government bedfellows (immunosuppression in the presence of live vaccine viruses).

So, to prevent the embarrassment of “Oops, we let out a deadly, debilitating, life-sucking disease whose biological mechanism would reveal the source of the autism epidemic,” the Lyme “scientists” set out to convince the world that their earlier research should simply be ignored and that everyone should believe their *new* research, instead.

Meanwhile, back at CFS research headquarters, they were busy trying to pretend that Epstein-Barr Virus has absolutely nothing to do with chronic fatigue, and that those suffering were a bunch of lazy lunatics. Both groups continued their own, separate campaigns of non-diagnosis and producing garbage “research” to cover their tracks.

One has to wonder what makes these people such heartless psychopaths as to deny proper healthcare to millions of suffering Americans. Do they think that it’s our patriotic duty, somehow, to suck it up and embrace our illness? Perhaps they do, since the alternative would be to expose the U.S. as simultaneously incompetent in 1) biowarfare research, 2) controlling the power of corporate Pharma, and 3) treating its own citizens in a way that’s consistent with our founding principles. Yeah, these crooks surely see themselves as merely doing their civic duty to save face for ‘Murica.

They carried on for 30 years with the obfuscation and semantics games, claiming that their 20 million or more victims must be creating these symptoms with their magical brains. But now they are cornered.

No, Lyme is not about the fake case definition of “arthritis-only” or autoimmunity, or lots of antibodies—it’s about the opposite mechanism. Likewise, Chronic Fatigue Syndrome/ME (or whatever you want to call it) and fibromyalgia are not about being depressed or attention-seeking, or having an autoimmune disease. They are about this phenomenon (now known as post-sepsis syndrome, per the NIH) that the crooks knew about for 30 YEARS and spent their life’s work to fraudulently claim does not exist. The crooks are cornered now, by real scientists who have caught up.

Real scientists are publishing over and over about how fungal-type antigens like OspA/LYMErix cause fungal antigen tolerance, or immunosuppression. They are prolifically publishing about these fungal-type antigens causing cross-tolerance to other types of antigens, including TLR4 agonists (lipopolysaccharide, or LPS—common to other bacterial phyla) and TLR7/9 agonists (viruses). Real scientists are showing us repeatedly how EBV-mutated B-cells replicate to create more mutated B-cells, but don’t always proliferate (become cancerous). THIS is what ALL these diseases are about.

Just look at the A to Z examples in our Occam’s Razor report, or simply these, as models in parallel:  http://www.ncbi.nlm.nih.gov/pubmed/?term=fung*+and+%22B+lymphocyte+mutation%22

Here is a specific example of a parallel model of OspA-ish antigens causing B cell mutations:

Mainly unmutated V(H) genes rearranged in B cells forming germinal centers in a cutaneous pleomorphic T-cell lymphoma.

http://www.ncbi.nlm.nih.gov/pubmed/?term=10189248

nicole_baumgarth_2011

Check out the exceptional work of Nicole Baumgarth at UC Davis, pretty much covering all the bases:

http://www.ncbi.nlm.nih.gov/pubmed?term=Baumgarth%20N%5BAuthor%5D

http://ccm.ucdavis.edu/our-science/lyme-borreliosis/

BAUMGARTH_IMMUNOSUPPRESSION

I’ll say it again: the Lyme and CFS crooks are cornered. They have been happily getting away with their “patriotic” but faux research for many years, but now, loads of other research point to a common disease mechanism that unites all of us victims of government-approved obfuscation and semantics games.

Naturally, they have reacted by freaking out and joining forces, themselves. Gone are the days of Lyme “researchers” working in a bubble to trash Lyme victims and CFS “researchers” working in their own bubble to trash their victims separately. Now they must work together in one giant bubble to ensure that their lies are compatible. Never before has science been so unscientific. And they accuse us of hysterics.

EXHIBIT A

Gary_Wormser

Gary “The Wormster” Wormser

I direct your attention to Exhibit A, wherein we have Gary Wormser of “Chronic Lyme is Imaginary” fame, and Suzanne Vernon of “Chronic Fatigue Syndrome is Imaginary” fame teaming up to proclaim together that millions of people are simply cray cray.

Anti-neural antibody response in patients with post-treatment Lyme disease symptoms versus those with myalgic encephalomyelitis/chronic fatigue syndrome

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4638178/

 

“Post-treatment Lyme disease symptoms (PTLDS) and myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) have several clinical features in common, including fatigue, musculoskeletal pain, and cognitive difficulties (Gaudino et al., 1997). Immunologic mechanisms have been suspected to play a role in both PTLDS and ME/CFS. However, biomarkers for the two conditions are currently lacking, creating a barrier to better understand them. In a previous study published in BBI, we developed a semi-quantitative immunoblot assay to compare antibody reactivity to neural antigens in a group of PTLDS patients and controls (Chandra et al., 2010).

…Although often detectable (Chandra et al., 2010), it is unclear whether the presence of anti-neural antibodies has a role in the pathogenesis of certain PTLDS manifestations. If these antibodies do play a role, it would appear that the cause of the somewhat similar symptoms in ME/CFS is different.”

SuzanneVernon

Suzanne “Mycoplasma? What Mycoplasma?” Vernon

 

It’s laughably obvious that they are saying, if you follow their fake case definition of Lyme (which includes only the arthritic knee, lots-of-antibodies HLAs—not the post-sepsis syndrome cases), you’re going to see antibodies that naturally don’t exist in post-sepsis CFS cases.

A quick review of what Vernon and Wormser have said in the past:

Suzanne Vernon, of course, is responsible for the fraud of centrifuging the red blood cells out of the blood so she could then publish a report saying that mycoplasma (which adhere to red blood cells) was not present and therefore not responsible for fatigue in chronic fatigue syndrome.

 

Absence of Mycoplasma species DNA in chronic fatigue syndrome: 

http://jmm.microbiologyresearch.org/content/journal/jmm/10.1099/jmm.0.05316-0

“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).”

Mycoplasma adhere to erythrocytes (red blood cells), interfering with membrane potential and therefore the potential for oxygen to cross the erythrocyte membrane (causing fatigue). But here, Vernon has thrown the baby out with the bath water, and now proclaims, “Amazingly, the baby does not exist!”

A brief reminder that Mycoplasma species were originally called “eperythrozoons” for their ability to parasitize erythrocytes. Any scientist studying mycoplasma surely would be aware of this bit of historical nomenclature.

The effect of Eperythrozoon suis infection on the osmotic fragility of erythrocytes

http://www.ncbi.nlm.nih.gov/pubmed/1471973

“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.”

“Osmotic fragility,” “cell membrane injury” —basic effects of mycoplasma that Vernon sought to eliminate from our collective scientific knowledge. Nice, lady.

Moving on to Wormy…

Gary Wormser, being one of the original Lyme crooks, has a long history of lying about looking for antibodies in Lyme victims when he knows very well that OspA knocks out the immune system, causing no-antibodies.

In this report about dogs getting LYMErixed, Wormser shows the proposed mechanism of disease/vaccine is to cause tolerance to OspA in animals (no arthritis). However no vaccine ever prevented spirochetes, humans do not have dog or mice TLR2s, and this same antigen causes a slow septic shock response in humans.:

Modulation of lymphocyte proliferative responses by a canine Lyme disease vaccine of recombinant outer surface protein A (OspA).

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

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

Immunosuppression in humans or tolerance in dogs, it is the same dynamic. OspA turns off the immune response. It does not cause antibodies, which is the normal idea behind “vaccines.”

We can only imagine the glorious feats of creative scientific malfeasance these two—Wormser and Vernon—will continue to accomplish together, on the taxpayers’ dime. Keep blowing your hot air into that bubble, Gary and Suzy.

EXHIBIT B

Exhibit B: Stanford’s Jose Montoya, lauded as one of the heavies of ME/CFS research, joins forces with Steere, Dattwyler & Aucott to dismantle the Dearborn two-tier method of diagnosing “Early Lyme.”

Development of a multi-antigen panel for improved detection of Borrelia burgdorferi infection in early Lyme disease

http://jcm.asm.org/content/early/2015/10/01/JCM.02111-15.abstract

“The current standard for laboratory diagnosis of Lyme disease in the United States is serologic detection of antibodies against Borrelia burgdorferi (Bb). The Centers for Disease Control and Prevention recommends a two-tiered testing algorithm, however this scheme has limited sensitivity in detecting early Lyme disease. Thus, there is a need to improve diagnostics for Lyme disease at the early stage when antibiotic treatment is highly efficacious.

…The improved sensitivity and comparable specificity of our 10-antigen panel compared to two-tiered testing in detecting early Bb infection indicates that multiplex analysis, featuring the next generation of markers, could advance diagnostic technology to better aid clinicians in diagnosing and treating early Lyme disease.”

What they are saying is that the two-tier test method that they, themselves, came up with, is now not valid. Never mind the fact that their data suggest that this specific method is no better: it is a clear admission that their own two-tier method sucks.

[There are far too many instances of the Lyme crooks contradicting themselves to lay them all out here. Please see the charge sheets for myriad examples of self-debunking, self-incriminating Lyme “expert” behavior.]

Furthermore, what the heck does Montoya suddenly have to do with Lyme disease diagnostics, when all his previous research has revolved around CFS?

It was only a year ago (February 2015) that Montoya proved CFS/ME was a right-brain dementia, or damage. And the Lyme crooks are the authors of all the biomarkers in CNS Lyme brain damage—see the charge sheets. (This was the reason Ely Lilly had to pay a 1.7 billion dollar fine for marketing Zyprexa to old people.) Amazing—both sides admit that brain damage is a factor.

Montoya on right brain dementia in CFS:

Right arcuate fasciculus abnormality in chronic fatigue syndrome.

http://www.ncbi.nlm.nih.gov/pubmed/25353054

“Purpose: To identify whether patients with chronic fatigue syndrome (CFS) have differences in gross brain structure, microscopic structure, or brain perfusion that may explain their symptoms.

…Conclusion: Bilateral white matter atrophy is present in CFS. No differences in perfusion were noted. Right hemispheric increased FA may reflect degeneration of crossing fibers or strengthening of short-range fibers. Right anterior arcuate FA may serve as a biomarker for CFS.”

IMG_1681

Whitney Dafoe, victim of Stanford

 

So, what is this partnership really about? Conceivably, Montoya has a stake in ensuring that CFS victims are not diagnosed with Lyme. Which is really a travesty when you consider that his colleague Ron Davis’s son, Whitney Dafoe, is fighting for his very life in an unprecedented show of B-cell AIDS patriotism. If Montoya truly knows what this disease is about, then he gets a special medal for psychopathic cruelty.

http://sanfrancisco.cbslocal.com/2015/11/11/palo-alto-family-battles-with-sons-mysterious-medical-illness/

We guess it does not matter if anyone’s famous son gets diagnosed with “Lyme disease,” since it is an incurable AIDS-like disease (acquired immune deficiency). It’s leukemia-like, and is also called post-sepsis by the NIH. The Great Imitator, it turns out, was really latent, reactivated Epstein-Barr.

Is this the beginning of a new era in semantics?

Lyme, Post-treatment Lyme disease syndrome, New Great Imitator, New New Great Imitator, CFIDS, ME, SEID, Fibromyalgia, Hypochondria, Lyme Anxiety, Munchausen’s-by-Proxy…what will be next?

Will they stoop so low as to start calling leukemia something it is not, to distract from the fact that leukemia is one terrible end result of the reactivation of Epstein-Barr, and mutations to B cells?

In the end, a lot of people would have wanted to know about this mechanism, especially the parents of dead Leukemia children. We could have known 20 years ago, when Mayo Clinic’s Dave Persing published with Yale’s Robert Schoen that LYMErix causes the same multisystem disease we know of as Chronic Lyme and that they could not differentiate OspA vaccine failure from injection by tick.

We suppose these “scientists” of Lyme and ME/CFS consider themselves “the smartest guys in the room,” not unlike the greed-crazed, psychopathic corporate criminals of the Enron scandal. https://en.wikipedia.org/wiki/Enron:_The_Smartest_Guys_in_the_Room

They created a financial bubble that grew bigger and bigger, until it burst in a spectacular display of projectile corporate fraud vomit.

Similarly, our favorite science crooks now appear to be playing their semantics games under one collective bubble, expanding with their lies, driven by their fear. Scared of the autism moms, the Lyme zombies with our green signs marching on Washington, the CFS cripples who can’t leave their homes, the brain-damaged veterans with their guns. Are all of us sick people really that scary? Really?

“We are the good guys; we are on the side of angels.” -Ken Lay, Enron CEO

 



Categories: Immunosuppression Diseases, Lyme Disease

Tags: , , , , , , , , , , , , , , , , , , , , , , ,

8 replies

  1. Thanks for taking the time to answer the #May12.org community (CFS/ME) as to what is the problem with Suzanne Vernon and mycoplasma causing fatigue. Apparently Phoenix Rising has never read anything about Lyme, such as to learn that for the past 25 years, the Lyme crooks claimed Lyme caused Chronic Fatigue Syndrome and Fibromyalgia (same thing),… while all the while we were fighting that claim because CFS/ME was considered to be a mental illness and that the fatigue, the bad guys claimed, was not real.
    What a mix-up!! Turns out the CFS/ME community themselves were denying the fatigue for political reasons and wanted a new definition saying they could not exercise. If only they had some real scientists on their side.

    Liked by 1 person

  2. Toll-like Receptor Polymorphisms Are Associated with Increased Neurosyphilis Risk
    “Clinicians in the early 20th century posited that race influenced susceptibility to neurosyphilis, citing a decreased risk in African Americans compared to Caucasians (7). Subsequent work suggested a genetic basis for such differences, with an increased risk of syphilitic dementia, but not other forms of neurosyphilis, in patients with certain HLA types (8) that differed in African Americans compared to Caucasians (9). While more recent reports suggest that there may be genetic contributions to syphilis susceptibility (10-13), to the best of our knowledge there have been no recent investigations of genetic susceptibility to neurosyphilis.”
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4414322/

    Liked by 1 person

    • Jus Sayin, JJ Halperin and McSweegan insist we’re only imaginating the brain damage. Klempner too. Yet, here we see the reason there have been recent investigations of genetic susceptibility to neuro-spirochetosis. The experiment appears to have been an IQ test for all people with “MD” after their names. Their experiment was a success. “Doctors” only need an IQ of around 100. Cheers!

      Liked by 1 person

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