Blowing the Whistle at the FDA, Jan 2001, exposing Dearborn and how OspA causes immunosuppression rather than, "was a vaccine."
 


8 March 2017


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PDFs
CDC Admits Fraud, 2016
Dattwyler, 1988
Golightly, 1988
Dressler, 1994
BarbourFish, 1993
Dearborn, 1994
BarbourFishpdf.pdf
 

Pathogenic Fungi

Predicting all of GW Bush's warcrimes, Oct 2000

Trainer

 

 

 

"And with the hopes and powers will come dangers out of all proportion to the growth of man's intellect, to the strength of his character and to the efficacy of his institutions. Once more the choice is offered between Blessings and Cursings. Never was the answer that will be given harder to foretell." - Winston Churchill, 1932, Popular Mechanics, which is also no longer respectable since they pulled the post-911-non-physics stunt re the collapse of WTC7, cute.

The rise and fall of civilization - you can see the inverted U, the arc, in your mind, and wonder what was that point where we started to turn downward into the present stupid-o-metric civilization that the USA now delusionally assumes it leads?  Freud and the philosophers of- or the Religion of Me!  It was the confluence of stupidity where the Protestants struggle with the idea of a homeless, un-employed Jesus who helped people anyway, ... and the Darwinism of racist capitalism.  That was it.  "The Enlightenment" wasn't at all enlightening since no one came up with a Universal theory. Just the current social schizophrenia, or unscalable theories about whose job it is to care for ANYONE.   But Evil has no creative abilities.  Thence, failed institutions, permeated with people at all levels who are only in it for themselves... "government" "employee" and union cults like cops and the state-sanctioned kidnappers...  medical "doctors" who were never trained in any basic science.... the CDC caught lying about EVERYTHING...

We can plant a spaceship on a comet, but 30 million people in America alone are disabled with "waste basket" diagnoses, merely because the CDC does not want anyone to know how 1:50 children are brain damaged for life from "vaccines?"

 

4 Dec 2014:

Greetings, again, Hi,...

This report is more for the "journalists" and the "lawyers" who just don't seem to get it, reminiscent of the people with CFIDS-brains (see the 3 Dec report below in the yellow box).

Originally posted in WaPo in Sept, 2014 "Lingering Effects of Lyme Disease"
http://www.thestarphoenix.com/health/lingering+effects+Lyme+disease/10210998/story.html

It should be entitled, the "Lingering Effects of LYMErix, spoken- and written- about by the very same perps, is the reason the CDC vaccine patent-owning pimps and their whorey ALDF/IDSA perps falsified the case definition at Dearborn, Michigan in 1994"

It should be, "What is LYMErix?  Why did it cause a disease identical to late Chronic Lyme Disease?  What are they hiding?"


It's very clear that the CDC/ALDF crooks (leave IDSA out, we've just learned from an insider that IDSA are total morons, much like the State Health Departments) can't admit what chronic Lyme is because they know the vaccine caused it too. So what is the disease? It's post-sepsis syndrome (chronic active herpesviruses and other opportunistics), or like AIDS, caused by shed fungal OspA-like toxins.
 

The CDC also does not want to admit to the mechanisms of disease caused by Lyme and LYMErix because that same fungal-induced immunosuppression data/mechanism reveals the cause of the Autism pandemic.  The criteria for a bioweapon is also identical to post-sepsis syndrome - "overwhelm the immune system."  Everyone is either playing dumb or is dumb.  Never was there such complete perfection in perpetrating the total absence of knowledge or even of questioning.  Key to it was the inability of "doctors" to either read, or be trained in basic sciences like chemistry, taxonomy, biology, ... like asking what is this molecule, OspA?  Why does it suppress antibody production?  Why is it a "vaccine" because it is 100% specific to Lyme, but if you have this 100% specific marker, you can't have that disease?
 


On LYMErix-Disease, 1998, at the FDA, BEN LUFT:

"The point that I wanted to make in regard to the study is that there is very heavy dependence on serologic confirmation. And when we start thinking about the adverse events, *** it was stated originally when we got the overview of the disease that the disease is really quite protean [means not limited to "bad knees- KMD]. And actually the adverse events are very similar to what the disease manifestations are.**** And if you start to, as I think Dr. Hall was eluding to -- if you start to kind of say well how often do you actually become sero positive, you can start to have a different take on when someone has an adverse event of whether it is disease specific or infection specific versus vaccine specific. And I think that that is an important issue that we have to deal with. I can only say from my own..."
http://www.fda.gov/ohrms/dockets/ac/98/transcpt/3422t1.rtf


 

Persing and Schoen's RICO strain and intended monopoly on post-LYMErix blood patent:

"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 failure....

http://patft1.uspto.gov/netacgi/nph-Parser?Sect1=PTO1&Sect2=HITOFF&d=PALL&p=1&u=%2Fnetahtml%2FPTO%2Fsrchnum.htm&r=1&f=G&l=50&s1=6045804.PN.&OS=PN%2F6045804&RS=PN%2F6045804

(?? Wait, what? You can’t tell the difference between late chronic Lyme and LYMErix Disease ???)

 

Dave Persing discussing why you should not use the native or original Osps as vaccines (and Robert Schoen would know this too):

"Accordingly, the methods of the invention provide a powerful and selective approach for modulating the innate immune response pathways in animals without giving rise to the toxicities often associated with the native bacterial components that normally stimulate those pathways."

http://patft.uspto.gov/netacgi/nph-Parser?Sect1=PTO1&Sect2=HITOFF&d=PALL&p=1&u=%2Fnetahtml%2FPTO%2Fsrchnum.htm&r=1&f=G&l=50&s1=6%2C800%2C613.PN.&OS=PN%2F6%2C800%2C613&RS=PN%2F6%2C800%2C613


 

1988, Raymond Dattwyler & immune-suppressing, seronegative Lyme; supernatant (lipid layer) of borrelia mash causes NK cell anergy or a blunted immune response.
Later Dattwyler tells the FDA Vaccine committee that the seronegative patients are the sickest (now we know why, as shown above where Lyme and LYMErix are the Great Detonators of the latent herpesviruses and expanded or cross tolerance to other than TLR2/1-agonist bearing antigens; in short, they’re double-fatigued and neurologically damaged):
http://actionlyme.org/DATTWYLER_NK_SUPPRESSION.htm
http://actionlyme.org/1988DATT_SUPRNATNT_FUNGAL2.gif

 

Transcript of June 1994 FDA Meeting Minutes, Dattwyler
http://actionlyme.org/141113_1994_DATTWYLERMINUTES.jpg

“So, individuals with a poor immune response tend to have worse disease.”


 

1990, Allen Steere reports that "NeuroLyme won't test positive;" uses Dattwyler and Volkman’s Seronegative Lyme T Cell Assay
http://www.actionlyme.org/STEERES_SERONEG_LYME_ASSAY.htm


 

Hence, the RICO complaint filed with the USDOJ in July 2003, explains the crime very simply - so simply even a lawyer can follow it :
http://www.actionlyme.org/USDOJ_COMPLAINT_RICO.htm
 

The crooks changed the disease definition at Dearborn (1994, Michigan, as CDC conference) to suit the about-to-be-falsified vaccines outcomes, as I told the FDA in Jan 2001:
http://www.fda.gov/ohrms/dockets/ac/01/slides/3680s2_11.pdf
 

They threw out all the neurologic cases. You can see how Steere did this in Europe when he came up with the Dearborn proposal:
http://www.actionlyme.org/STEERE_IN_EUROPE.htm

 

Here is a fully referenced report on what the crooks did, especially on how Allen Steere left OspA and B out of the diagnostic standard for his later monopoly on blood, testing, vaccine candidates and HLA-bioweapons datapharming.  You don't give people a bioweapon when too many or the residents or people will have the HLA-linked hypersensitivity response that identifies the initial Trojan Horse infection or antigen.  In the case of Lyme, it was OspA that made these organisms more invasive (OspA hijacks plasminogen allowing greater tissue penetration) and detonators of EBV/similar herpesviruses.  OspA was the Greatest Detonator. 
http://www.actionlyme.org/PLUMSTUPID.htm
 

CDC's lies at Dearborn, and Steere traveling to Europe and Russia, were meant to fool people wprldwide into thinking "Lyme Disease" was a different disease than Relapsing Fever.  They were counting on ignorance of spirochetal diseases.  It was a competency test for all American "doctors," essentially testing their ability to you know, go on the internet or the original MedLine (now PubMed) and read the literature.
 


For non-Americans reading this, you can see that the entire USA has dementia.  "Doctors," "journalists," the "lawyers," at the USDOJ, State "Health Departments," the FDA, ... One should wonder more about that, really, than OspA-Disease.

How is it that no one says anything true, and so few even know true things are available to be said?



 


 

Dec 3, 2014

Greetings, friends. 

Please join this group: http://www.facebook.com/groups/OccupyUSDOJ/ for discussion and explainers; use Google Translate, if necessary. 

Three matters have recently come up, one being our consistent failure to make the connection understood by ME/CFS victims, between ME/CFS and "Chronic Lyme," .... and Chronic Active EBV/Cytomegalovirus, HHV-6 etc, plus fungal antigen tolerance, plus expanding tolerance to other types of TLR agonists, antigens and infections (see the next report in the gray box, below).  ME/CFS and Chronic Lyme are like AIDS or Post-Sepsis Syndrome, technically or scientifically speaking.  They are diseases of immunosuppression, ongoing reactivated herpesviruses, and not classical HLA-linked autoimmunity, at least humorally - that means don't look for antibodies, you have to use DNA testing. 

In the brain, however, the opposite: These diseases seem to be a state of chronic inflammation in the brain (confirmed recently in the NYTimes).  This was discovered by the NIH and they reported that this was a result of exposure to fungal antigens like OspA or TLR2-agonists.  Please see the "7 reports" in the Introduction to Yale's Vaccine Scam for that published data, - particularly the NIH's data -, on how OspA was the thing that caused these chronic active herpes infections and generalized, post-sepsis-like, AIDS-like opportunistics without any antibodies.  You don't need to be exposed to spirochetes, but exposure to antigens like LYMErix, yes.  That was it.

So, I propose we call these diseases Post-LYMErix Syndrome, particularly because it was the NIH's MS-Lyme Group who discovered that it was the fungal antigen and failed "vaccine," OspA, that was responsible for the generalized immunosuppression and chronic activation of the immune system in the brain.


Secondly, there is some issue - once again and always - with how you FDA-Validate an Analytical Method, and why band 41 or the anti-flagellar antibody (made Specific) is the only one you can use to detect Borrelioses ("Lyme Disease" is the HLA-linked thing and those people are not even sick).  Use the PRIMERSHELLGAME report and data to see the FDA's criteria for the validation of an analytical method.  Your method must detect 100% of the cases or be 100% Accurate and the closest marker we have to that is the flagellar antibody, since 95% of people with Lyme have it.  That was why Yale went ahead and validated that method and patented it (US 5,618,533) between 1991-3 or so.
 

ALSO, I was informed by an insider that IDSociety.org does not know anything about HLA-linked diseases or non-HLA-linked diseases.  That is, they have very little training in Infectious Diseases, just as we suspected.  They, IDSociety.org or IDSA, do not know much about diseases at all.  All they do is push vaccines, which is the same as the CDC.  It's no wonder then, that those 2, the CDC and IDSA, work together since they have so little knowledge of anything, and only do what the vaccine manufacturers tell them.  So that's new.  It's no longer a guess that IDSA is just plain stupid.  It is a fact.

So, come on over and join that OccupyUSDOJ group for more science and explainers.  IDSA does not know what they are talking about and are hopeless.

 

 

141201--    Feedback from diverse sources is telling me I am failing to make the connection between Lyme and ME/CFS again. It's OspA or fungal antigens that are not typically classified as "toxins" perhaps mainly because in the past it was hard to determine the structure of a lipoprotein, but now we go with FUNCTION, which is TLR2-agonist. The chronic exposure to fungal antigens, as is the case with Lyme from the spirochete's chronic shedding of surface antigens like OspA, results in a disease exactly like post-LYMErix Syndrome (immunosuppression resulting in a post-sepsis like syndrome with the chronic active herpes viruses and tolerance spreading to other infections, like AIDS).  At the same time, not everyone with CFIDS has Lyme or spirochetes.

Your post-sepsis syndrome (1, PSS website) could have been initiated by something else. It does not matter in the end, because we are all treated like trash, and the data says we are all dealing with reactivated herpesviruses, compounded by expanded tolerance to other infections like Candida and whatever other bacteria and common viruses. You're all, say "carriers," perhaps of Strep, Candida, various herpes, etc.

But mechanisms, no, we have this down. We know how fungal antigens turn off the immune response (2, Harding & Radolf); gum up the normal immunity works (3, Wormser); how OspA acts like a BCL2 molecule, inhibiting NORMAL apoptosis in an infected cell (4, 101016.htm, numerous) ; we know fungi adhere to mitochondria (5), causing fatigue, we know how EBV hijacks this same cell machinery (6) ; we know how it has been known since ancient times that fungi injected together with viruses activates the viruses (1953) (7) ; that they put Thimerosal in vaccines for this reason - to inhibit fungi – (8); that BigPharma has reported that kids could be getting the viruses (9); the CDC has reported that immunosuppressed kids should not get live attenuated viruses, but fully dead ones (10); and we know the CDC has flat out committed research fraud while trying to claim mycoplasma is not involved in Chronic Fatigue Syndrome by throwing out the very cells to which mycoplasma adhere and hide within, before analyzing for DNA and finding none (11); and we have seen several mechanisms where TLR2-agonist tolerance expands to viruses and bacteria (12 Medvedev, 13 Harding, 14 newer one, 15 wustl.edu, 16, NIH). That the CDC would do that is CRUCIAL to your understanding that they are committing FRAUD on behalf of the Bigs.
 

As an aside, we should note that what is incorrect about this this incorrect report in the NYTimes about the brains of CFIDS people that points to to a right-brain deficit, is that the right side of the brain is where your visual-spatial abilities are, not speech.  Speech is on the left. [To Wit: High Functioning Autistic people (and not Asperger's) process speech in the visual hemisphere, where all the science is also processed, since science is visual.]  So, this condition could be part of their defense mechanism repertoire, where CFIDS people usually become very angry whenever you mention science or facts.  The same is true, we might assume, for the Witches of Lyme, the LDA, and we know it is true for lawyers who are normally very competent liars (when do you ever see a lawyer working on his car or doing his own house construction?):
http://well.blogs.nytimes.com/2014/11/24/brains-of-people-with-chronic-fatigue-syndrome-offer-clues-about-disorder/
Why there is a tendency for right-brain damage, no one knows.  Someone once said that whatever is your natural deficit before Lyme or CFIDS becomes an exaggerated deficit.  In other words, your weak points become weaker. 

However, this does not explain why CFIDS-land does not have any actual, genuine scientists working for them.  The bigger picture, however, points to our society respecting loud-mouth-braggarts and do-nothings, and the American or Western social dogma where everyone's opinion weighs the same, regardless of facts or content - the Will trumps the Truth.  This social dogma is of a diabolical influence or is a diabolical delusion brought to us by psychiatry and the modernist philosophers. The short version is, if you insist on winning in this world, expecting other people to bear the burden of your selfishness, particularly in selling "expertise" you don't have, you won't win in the next.  That's a Guarantee, so, un-advise.
 

1) http://www.sepsisalliance.org/sepsis/post_sepsis_syndrome/
2) http://www.jimmunol.org/cgi/content/full/167/2/910
3) http://www.ncbi.nlm.nih.gov/pubmed/10865170
4) Numerous, search for apoptosis: http://actionlyme.org/101016.htm
5) Numerous, search for mitochondria: http://www.actionlyme.org/101016.htm
6) Numerous, search for mitochondria or Epstein-Barr: http://actionlyme.org/101016.htm
7) http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2136329/?tool=pubmed
8)
http://www.nytimes.com/2012/12/17/health/experts-say-thimerosal-ban-would-imperil-global-health-efforts.html?_r=2&
9) "Finally, there is the risk that the virus may not be fully or completely inactivated or attenuated and thus, the vaccine may actually cause disease."

http://patft.uspto.gov/netacgi/nph-Parser?Sect1=PTO1&Sect2=HITOFF&d=PALL&p=1&u=%2Fnetahtml%2FPTO%2Fsrchnum.htm&r=1&f=G&l=50&s1=7%2C632%2C510.PN.&OS=PN%2F7%2C632%2C510&RS=PN%2F7%2C632%2C510
10) http://www.cdc.gov/mmwr/preview/mmwrhtml/00053391.htm
11) CDC throwing out blood cells to which mycoplasma adhere so as to falsely claim no mycoplasma are associated with ME/CFS : http://jmm.sgmjournals.org/cgi/pmidlookup?view=long&pmid=14532349
12) Medvedev http://www.jimmunol.org/content/170/1/508.long
13) Harding on bacterial-viral co-infection: "This novel mechanism, whereby TLR2 inhibits IFN-I induction by TLR7/9, may shape immune responses to microbes that express ligands for both TLR2 and TLR7/TLR9, or responses to bacteria/virus coinfection."
http://www.ncbi.nlm.nih.gov/pubmed/22227568
14) newer one on same topic as Harding’s above: http://www.nature.com/cmi/journal/v9/n4/full/cmi201211a.html
15) wustl.edu “Latent viruses such as cytomegalovirus are normally held in abeyance by cellular and immune surveillance mechanisms which if impaired, for example by immunosuppressive medications, often result in viral reactivation, replication, and virally-mediated tissue injury [15]–[20]. Sepsis impairs innate and adaptive immunity by multiple mechanisms including apoptosis-induced depletion of immune effector cells and induction of T-cell exhaustion thereby possibly predisposing to viral reactivation and dissemination [21]–[23]. …”
http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0098819
16) THE NIH >> "Surviving Sepsis: Detection and Treatment Advances"
By Carolyn Beans for the National Institutes of Health | August 18, 2014 08:43am ET
http://www.livescience.com/47387-sepsis-diagnosis-treatment-research-nigms.html
"Preventing Secondary Infections
"Some people who survive sepsis can develop secondary infections days or even months later. A research team that included Richard Hotchkiss, Jonathan Green and Gregory Storch of Washington University School of Medicine in St. Louis suspected that this is because sepsis might cause lasting damage to the immune system. To test this hypothesis, the scientists compared viral activation in people with sepsis, other critically ill people and healthy individuals. The researchers looked for viruses like Epstein-Barr and herpes simplex that are often dormant in healthy people but can reactivate in those with suppressed immune systems. [Sepsis Has Long-Term Impact for Older Adults, Study Finds]"


 

41113 The Lyme Vaccine Scam, Facebook "Occupy the USDOJ" Group version
 

You need to study this information in order to file your Adverse Event (AE) to the Dearborn Lyme case definition to the Food and Drug Administration.  Hopefully, when this cryme is prosecuted you can be compensated by the USDOJ in a similar manner to the other Vaccine Injury Compensation cases the USDOJ handles.  THAT is our ultimate goal.

Here is the FDA's AE reporting form re bogus medical testing:
https://www.accessdata.fda.gov/scripts/medwatch/index.cfm?action=consumer.reporting1

You need to study this report (in this yellow box) as well as the Primers Shell Game in order to see why you only ever needed antibody band 41 and the triad of Neurological, Cognitive, and Musculoskeletal signs after ruling out cancer, etc. for a diagnosis of borreliosis.
 

And if you already know about this cryme and are still wondering why the US "government" is so friggin stupid and incompetent, don't.  They just are.  It goes with the territory of government-employee-cults and government-employee union-cults.  Read about cults - they just protect themselves, their retirement funds and investments, and each other, you know, like cops.


First let’s examine the following 7 compelling reports from the “20 Reports that show the Lyme-and-LYMErix-Post-Sepsis Cover-up has to do with Hiding Autism Brain Damage from Vaccines
(http://www.actionlyme.org/POST_LYME_SEPSIS_2014_SUMMER.htm );”
 

These next 7 reports are basically by the NIH, especially the NINDS’s Lyme-And-MS group (Martin and Marques) which confirm and endorse the idea that the Lyme vaccine (OspA, which is a basic Pam3Cys molecule type and a TLR2/1-agonist) gave people the same New Great Imitator and especially Multiple Sclerosis outcomes as “Chronic Lyme” or Late Neurologic Lyme;

These reports are from the NIH, IDSA, the US ARMY, Ft. Detrick, the National Cancer Institute (NCI), and Washington University, St. Louis, MO (wustl.edu) about post-sepsis and the reactivation of the herpesviruses, et al (like AIDS) from exposure to Lyme. [This is how it appears anyway. If it is some other virus like a mouse herpesvirus from a tick bite, we don’t have that data yet. It’s something like that, that obviously no one at the Uncle Sam “government” seems too worried about, therefore, it must be a common thing like from the herpes family. There are easily 20 million of us with a CFIDS, Lyme, or Fibromyalgia etc junk-science diagnosis in America alone (NIH’s own published stats) and no one’s panicking like we got a new, slow Marburg, or contagious scrapie, or a new HIV or whatever going on.]
 

==================== The 7 Reports, 6 of NIH’s plus wustl.edu’s =================


1989 (this is in IDSA's own journal):

NCI and US Army Ft Detrick Pathologist Paul Duray on the CSF cells looking like "Epstein-Barr-like transformed cells" in IDSA's 1989 Reviews Supplement on Spirochetal Diseases:
Rev Infect Dis. 1989 Sep-Oct;11 Suppl 6:S1487-93.
Clinical pathologic correlations of Lyme disease.

"Immature B cells can also be seen in the spinal fluid. These cells can appear quite atypical- not unlike those of transformed or neoplastic lymphocytes." --
http://www.ncbi.nlm.nih.gov/pubmed/2814170 

Full Text: http://www.actionlyme.org/IDSA_CLINIPATH_DURAY.htm

=====

1992:

Duray again in 1992, in Steve Schutzer's review of the 1992 Cold Spring Harbor Conference on Lyme:

"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." -

Paul Duray, NCI, NIH, Ft. Detrick, at the 1992 Cold Spring Harbor Crooks' Conference, published in Steve Schutzer's Lyme Disease: Molecular and Immunologic Approaches. - book.

=====

2006:

The NIH (NINDS’s MS-Lyme Group) group that discovered that *** OspA *** was the cause of the MS/New Great Imitator outcome of Lyme reporting in the New York Times in the summer of 2013 (Martin and Marques, 2006);
this article says these OspA like antigens constantly shed by Borreliae cause immunosuppression in the humoral immune system, but apparently a chronic inflammatory state in the central nervous system:

"Borrelia burgdorferi Induces TLR1 and TLR2 in human microglia and peripheral blood monocytes but differentially regulates HLA-class II expression."
http://www.ncbi.nlm.nih.gov/pubmed/16783164


and this report means you might not even have anti-flagellar antibodies (flagellin is a TLR5-agonist) after being exposed to shed fungal OspA like antigens (TLR2/1-agonists):

"Borrelia burgdorferi lipoprotein-mediated TLR2 stimulation causes the down-regulation of TLR5 in human monocytes.
http://www.ncbi.nlm.nih.gov/pubmed/16479520
 

2013 - Same NIH MS-Lyme Group as above, Martin and Marques:

"When Lyme Disease Lasts and Lasts" – Jane Brody

"Complicating the picture is the fact that some people with PTLDS symptoms apparently never had Lyme disease in the first place, Dr. Marques said in an interview. There are other infectious organisms — Epstein-Barr virus, for example — that can produce similar symptoms and may be the real culprits."
http://well.blogs.nytimes.com/2013/07/08/when-lyme-disease-lasts-and-lasts/

=====

2014:

Wustl.edu discovers that sepsis is like Lyme, in that the survivors of it are likely to have survived via the immunosuppression (TLR2-agonist tolerance/Endotoxin tolerance), but the result is the reactivation of latent viruses:

"Dormant viruses re-emerge in patients with lingering sepsis, signaling immune suppression"

"Patients with lingering sepsis had markedly higher levels of viruses detectable in the blood, compared with the healthy controls and critically ill patients without sepsis. Among the sepsis patients, for example, the researchers found that 53 percent had Epstein-Barr virus, 24 percent had cytomegalovirus, 14 percent had herpes-simplex virus, and 10 percent had human herpes simplex virus-7.

"These viruses generally don’t lead to significant illness in people who are healthy but can cause problems in patients who are immune-suppressed. "

http://news.wustl.edu/news/Pages/27015.aspx

FULL JOURNAL REPORT, snippet…

Reactivation of Multiple Viruses in Patients with Sepsis

“Sepsis is the host's non-resolving inflammatory response to infection that leads to organ dysfunction [1], [2]. A current controversial hypothesis postulates that if sepsis pursues a protracted course, it progresses from an initial primarily hyper-inflammatory phase to a predominantly immunosuppressive state [3]–[7]. Experimental therapeutic approaches in sepsis have almost exclusively focused on blocking early inflammation or host-pathogen interaction and failed [8]–[10]. Recently, immuno-adjuvant therapies that boost host immunity, e.g., GM-CSF and interferon-γ, have been successful in small clinical trials thereby supporting the concept that reversing immunosuppression in sepsis is a plausible strategy to improve outcome [11], [12]. However, several issues have limited this approach including lack of consensus that immunosuppression is a clinically important phenomenon [5], [6], [13]. Also, difficulty in identifying patients with impaired immunity as well as determining optimal timing for administration pose significant challenges to pursuing this approach [14]. While immuno-adjuvant therapies might improve sepsis survival if administered during the later immunosuppressive phase, these agents might worsen outcome if given during the early hyper-inflammatory phase [4], [14]. Thus, a means to distinguish these two contrasting phases of sepsis is needed not only to verify the hypothesis that sepsis progresses to an immunosuppressive state but also to guide use of potential agents which boost immunity.

“Latent viruses such as cytomegalovirus are normally held in abeyance by cellular and immune surveillance mechanisms which if impaired, for example by immunosuppressive medications, often result in viral reactivation, replication, and virally-mediated tissue injury [15]–[20]. Sepsis impairs innate and adaptive immunity by multiple mechanisms including apoptosis-induced depletion of immune effector cells and induction of T-cell exhaustion thereby possibly predisposing to viral reactivation and dissemination [21]–[23]. …”
http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0098819 

=====

2014, Here the NIH confirms that they agree that post-sepsis, like wustl above describes, matches their own observations of what happens as a result of Chronic Lyme (EBV reactivated; ie, that being generally accepted as the main driver of MS and Lupus):

NEW, by the NIH: "Surviving Sepsis: Detection and Treatment Advances"

By Carolyn Beans for the National Institutes of Health | August 18, 2014 08:43am ET

http://www.livescience.com/47387-sepsis-diagnosis-treatment-research-nigms.html

"Preventing Secondary Infections

"Some people who survive sepsis can develop secondary infections days or even months later. A research team that included Richard Hotchkiss, Jonathan Green and Gregory Storch of Washington University School of Medicine in St. Louis suspected that this is because sepsis might cause lasting damage to the immune system. To test this hypothesis, the scientists compared viral activation in people with sepsis, other critically ill people and healthy individuals. The researchers looked for viruses like Epstein-Barr and herpes simplex that are often dormant in healthy people but can reactivate in those with suppressed immune systems. [Sepsis Has Long-Term Impact for Older Adults, Study Finds]"


======================== End 7 Reports =================

 

So, that data, those 7 reports are hard to argue with, and they also point to someone else potentially hypothesizing on what the treatment is for post-Lyme-post-sepsis, like wustl or the NIH and not me ☺

Importantly, everyone should go to PubMed and look at the data on medical school students and astronauts and see how the stress hormone cortisol is well-known to be activating mono or Epstein-Barr. If you are an astronaut or a medical school student or overworked resident, your chronic fatiguing disease is allowed to be real and not somatoformically produced with your magical brain ☺
 

Let's side step to show that LYMErix or OspA and OspA-like antigens constantly shed by borrelia in an immune-evasion-come-antigenic variation mechanism that can leave the immune system "completely overwhelmed," even if a mammal was infected with just one spirochete (see the Primers Shell Game).  We all have to know what these fungal OspA etc antigens are, that are shed by borreliae such that we know the pathology it causes.  OspA is or Pam3Cys or tripalmitoyl cysteine molecular type (see that this is confirmed by Ray Dattwyler in the "20 Reports that show the link between Lyme Cryme and Autism").  We have to know what these antigens are in order to know what they do (structure predicts function).  So, if you can't determine the structure, you can go by their function or biochemical properties and in this case, Pam3Cys type antigens are managed by TLR2/1 and that means they are fungal.
So what happens when the body is hyperexposed to fungal antigens?  In most cases, immunosuppression as shown by Justin Radolf and Clifford V. Harding, here, in the Plum Island chapter of Cryme Disease.  They cause the HLA molecules to fail to present antigen and thus, no more antibodies are made.  This is called tolerance.  Use PubMed to examine further what people like Medvedev and Harding have to say about what happens to the immune system after chronic exposure to fungal antigens.  Note in parallel, the data on the NO-TB-VACCINES, duh.  The Lyme criminals were too stupid to even try to discover if there had been any successful lipoprotein vaccines in the past. 



http://www3.interscience.wiley.com/cgi-bin/fulltext/120763430/PDFSTART

Use 141114_FUNGAL_FAILED_VACCINES.htm for about 12 reports that show you can't use this molecule type for a vaccine and that the Lyme criminals never gave a shit what it was or if it had been tried before as a vaccine.

 

 


Returning to what happened with LYMErix - the vaccine that gave people the very disease the ALDF-come-IDSA now deny exists and wrote out of the Dearborn serodiagnostic criteria specifically because of that ☺

[Repeat: The definitions of Lyme borreliosis excluded from the Dearborn case definition (falsified by Allen Steere in Europe in 1992) are the very ones caused by OspA vaccination. You just saw how in the above 7 reports, and there is much more data on that available on PubMed about the pathologies caused by chronic exposure to fungal antigens including cancer, and the similar outcomes of worse disease and immunosuppression from other experiments with fungal vaccines of this same TLR2/1 agonist type such as all the failed Tuberculosis vaccines ☺ ]

 

We back up to what was the original case definition serology the CDC published in 1990 such that we know it was falsified at Dearborn, and this data jives with what we know from the 7 reports by the NIH above:

1986, Allen Steere says:
“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.

“Using immunoblots, we identified proteins of Borrelia burgdorferi bound by IgM and IgG antibodies during Lyme disease. In 12 patients with early disease alone, both the IgM and IgG responses were restricted primarily to a 41-kD antigen. This limited response disappeared within several months. In contrast, among six patients with prolonged illness, the IgM response to the 41-kD protein sometimes persisted for months to years, and late in the illness during arthritis, a new IgM response sometimes developed to a 34-kD component of the organism. The IgG response in these patients appeared in a characteristic sequential pattern over months to years to as many as 11 spirochetal antigens. The appearance of a new IgM response and the expansion of the IgG response late in the illness, and the lack of such responses in patients with early disease alone, suggest that B. burgdorferi remains alive throughout the illness.”
http://www.ncbi.nlm.nih.gov/pubmed/3531237


1990, CDC publishes this case definition:
http://www.actionlyme.org/CDC_DOCUMENTS_1990.htm




The 1990 case definition standard (above) was basically based on the 1986 report (above that) by Allen Steere, which was that you have to merely show a person has a Relapsing Fever infection, with the “new IgM and changing bands emerging over time seen in repeat or serial Western Blots.” That meant, according to Allen Steere, “the bug is still alive.” New, IgM type bands meant the bug was still alive and you have not killed it with antibiotics. Steere also wrote in that same report that really all you need is band 41 to diagnose Lyme, just rule out Syphilis. That is important to remember. You only need band 41or the anti-flagellar antibody and the triad of symptoms to diagnose Lyme. The US patent 5,618,533 specific recombinant fragment of Borrelia burgdorferi flagellin of Yale’s is a better test and is an actual FDA-validation according to their criteria (as shown in the Primers Shell Game chapter of Cryme Disease).

I personally – and I am not a doctor – recommend everyone rule out all blood cancers since the symptoms of Chronic Lymphocytic Leukemia for example are identical to Chronic Lyme or MS, not to mention the fact that Lyme and LYMErix both are known to cause cancer as are the mycoplasma to which chronic late neurologic Lyme victims now are tolerized to (fungal).

 

And what is the current, 1994 CDC Dearborn case definition?
http://www.cdc.gov/mmwr/preview/mmwrhtml/00038469.htm

“It was recommended that an IgM immunoblot be considered positive if two of the following three bands are present: 24 kDa (OspC) * , 39 kDa (BmpA), and 41 kDa (Fla) (1).
“It was further recommended that an that IgG immunoblot be considered positive if five of the following 10 bands are present: 18 kDa, 21 kDa (OspC) *, 28 kDa, 30 kDa, 39 kDa (BmpA), 41 kDa (Fla), 45 kDa, 58 kDa (not GroEL), 66 kDa, and 93 kDa (2).”

 

That is very different criteria from the first criteria. First you only needed band 41, or test using repeat Western Blots to look for new IgM bands since Lyme is a relapsing fever organism, and the nature of the relapse is antigenic variation (producing new antigen and thus new IgM bands will be produced in a human), … and now all of a sudden you have to have all these bands showing up at once (indicative only of the hypersensitivity, HLA-linked response) and just ignore IgM bands, basically.
 

You can assume that the reason the IDSA/ALDF/CDC/Yale Lyme criminals do not want anyone treated for Lyme is because late in the disease it’s really about fungal antigen tolerance and cross tolerance, as well as reactivated herpesviruses. They don’t want Lyme victims being treated with antibiotics because that might help transfer antibiotic resistance genes between all the OTHER infections we have, like fungal, like Tuberculosis, Chlamydia, Candida, and whatever else … for which we are now carriers, … and you don’t treat the herpesviruses and subsequent B cell mutations with antibiotics.

IDSociety.org likes to say what diseases are not, but they never say what diseases are. It’s pretty strange but we got no Einsteins in that bunch. IDSA be like… an incomplete sentence. They’d be good screenwriters for American soap operas. The rest of MD-America does not even notice that IDSA’s is one funny script, even after these crooks lost their “vaccine,” Senator Richard Blumenthal (a former USDOJ prosecutor) sued them for Anti-Trust, and Edward McSweegan became America’s infamous NIH employee and America’s one and only “Man With No Work.”

 

So, Follow: First, Lyme was a regular old Relapsing Fever organism and a “New Great Imitator!” Later, it at the same time the crooks had a vaccine candidate in early phase trials, become nothing and a non-disease. We were then about to get “a vaccine for a disease that causes no illness.” That is still the current position of Yale, CDC, IDSA, and the ALDF/EUCALB. “Lyme patients are not sick, and OspA was a vaccine.” IDSA still makes that claim today. No one in the AMA or Mass Medical Society or NEJM or any other association or society of “doctors” even blinks at these contradictory notions. To me it looks like a case of Kraepelinian split-brain. We should wonder what other evidence there might be that medical school is a cult that produces schizophrenia.


 

Here is basically of the series of events that occurred in the process of redefining Lyme as a non-disease to pass off a bogus vaccine:

 

1986, Edward McSweegan trashes U.S. Navy for $$$ for his psycho buddies at the ALDF.com cabal in a letter to Senator Barry Goldwater. See the Navy’s furious response. Sweeg thinks there can be a vaccine for Relapsing Fever, confirming the paraphysical theory that arrogance is the seed corn or germinal element in true, genuine stupidity and/or the development of a criminal mind.
http://www.actionlyme.org/GOLDWATER_LETTER.htm


1988, Raymond Dattwyler & immune-suppressing, seronegative Lyme; supernatant (lipid layer) of borrelia mash causes NK cell anergy or a blunted immune response. Later Dattwyler tells the FDA Vaccine committee that the seronegative patients are the sickest (now we know why, as shown above where Lyme and LYMErix are the Great Detonators of the latent herpesviruses and expanded or cross tolerance to other than TLR2/1-agonist bearing antigens; in short, they’re double-fatigued and neurologically damaged):
http://actionlyme.org/DATTWYLER_NK_SUPPRESSION.htm




1990, CDC: "Diagnose Lyme as if it was Relapsing Fever."
http://www.actionlyme.org/CDC_DOCUMENTS_1990.htm


1990, Allen Steere reports that "NeuroLyme won't test positive," uses Dattwyler and Volkman’s Seronegative Lyme T Cell Assay
http://www.actionlyme.org/STEERES_SERONEG_LYME_ASSAY.htm
http://www.actionlyme.org/DATTWYLER_NK_SUPPRESSION.htm

CHRONIC NEUROLOGIC MANIFESTATIONS OF LYME DISEASE (NEJM, Nov 1990)
http://www.nejm.org/doi/pdf/10.1056/NEJM199011223232102
Says Steere:




“If the patient was seronegative according to these methods, the serum was further tested by immunoblotting (25) and peripheral blood mononuclear cells were tested for reactivity with borrelial antigens by proliferative assay.(26)"

And what was reference number 26?


 


Pretty amazing, huh?


1990, ALDF.com founded, self- proclaimed “entrepreneurial quartet” is McSweegan, Fish, Wormser and Connolly. (You will want to look at who are their sponsors and on their board, seriously.)
http://www.actionlyme.org/CONNOLLY_FISH_WEINSTEIN.htm
http://www.actionlyme.org/ALDF_BOARD.htm

 

1992, CDC officer Allen Steere falsifies testing in Europe:
http://www.actionlyme.org/STEERE_IN_EUROPE.htm
The PubMed links to those 2 reports – no full text available, that is why I got them out of the Yale Medical Library in 2002 and scanned them in are:
“Antibody responses to the three genomic groups of Borrelia burgdorferi in European Lyme borreliosis.”
http://www.ncbi.nlm.nih.gov/pubmed/8106763
“Western blotting in the serodiagnosis of Lyme disease.”
http://www.ncbi.nlm.nih.gov/pubmed/8380611

Of those 2 reports of Steere’s shenanigans in Europe, only the second one is made a part of CDC’s Dearborn booklet but the first one is where you can see how he falsified the testing.

Steere in Europe used bogus high passage strains that drop plasmids helping leave OspA and B out of the diagnostic standard  (by using the recombinant protein end only- you need the lipids to be immune stimulatory) for his later monopoly on post-LYMErix-approval North America, with Corixa, Yale’s L2 Diagnostics and Imugen, officially listed on the Securities and Exchange Commission (SEC) as “partners” in sharing licensing of the RICO Monopoly patent with the strain of Borrelia that had dropped an OspA-B plasmid US Patent 6,045,804 (we will come to this later, it is critical to the whole scam and shows the intent of their entire enterprise);



Here is a transcript of what is in the first report on exactly how Steere defrauded Uncle Sam:

“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 -"




Here is what it says in the Persing/Schoen/Steere or Imugen RICO Monopoly patent, that shows the intended monopoly:

“Method for detecting B. burgdorferi infection”

"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 failure."

"The present invention provides a method useful to detect a B. burgdorferi infection in a subject. The method provided by the invention is particularly useful to discriminate B. burgdorferi infection from OspA vaccination, although it is sufficiently sensitive and specific to use in any general Lyme disease screening or diagnostic application. Thus, the method of the invention is particularly appropriate for large scale screening or diagnostic applications where only part of the subject population has been vaccinated or where the vaccination status of the population is unknown. "
http://patft1.uspto.gov/netacgi/nph-Parser?Sect1=PTO1&Sect2=HITOFF&d=PALL&p=1&u=%2Fnetahtml%2FPTO%2Fsrchnum.htm&r=1&f=G&l=50&s1=6045804.PN.&OS=PN/6045804&RS=PN/6045804


The monopoly on post-LYMErix-FDA-approval testing for all vector borne diseases in America and Canada was their stated intention.  Once LYMErix was on the market, you had to use a strain of borrelia that did not have the vaccine antigens in them, because you never test for vaccine efficacy with the very same antigen as the vaccine antigen (you would not know if the person has the actual virus or whatever, or that antibody came from the vaccine). So, their monopoly depended on LYMErix being on the market.  That way, Corixa, L2 Diagnostics and Imugen would be the only labs in the country licensed to use this RICO strain.  They, at the same time would have access to all the human blood to pharm all sorts of DNA data from humans as well as any new and emerging infectious diseases... meaning even more vaccine patents. 

So, they falsified the case definition to leave out neurologic Lyme cases, and they left OspA and B out for a later monopoly on testing and future patents.  And there, you just read that in a patent developed by Schoen and Persing in 1995.
 

1992, CDC staff, Barbara Johnson and Joe Piesman, own patents with SmithKline that show 2 kinds of Lyme, HLA-linked and non-HLA-linked antigens:
http://www.google.com/patents/CA2135800A1?cl=en

“Summary of the Invention
“In one aspect, the invention provides isolated --B. burgdorferi antigens which are regulated and differentiated by growth of the B. burdorferi in a tick vector. Novel antigens of the invention are listed below in Table I.

“Certain of these antigens are characterized as being B. burgdorferi B31 strain specific and major histocompatibility complex (MHC) nonrestricted. Certain other of these antigens are characterized as being MHC-restricted.”

 

So, what the hell is the CDC talking about ”MHC-restricted and MHC non-restricted?” What we know that to mean is for instance, classic autoimmune diseases tend to be MHC-restricted, or the antigens, due to intermolecular forces, bind in the HLA groove too strongly causing a hypersensitivity response. That is the new definition Steere claimed in these 1992 reports and at the CDC’s 1994 Dearborn conference.
The very re-definition of “Lyme Disease” at Dearborn became “HLA-restricted,” “just the arthritis,” “too-many-antibodies-HLA-associated response.” In short, Steere and the CDC claim Lyme Disease is just an HLA-restricted disease. Here in their 5 1992 patents with SmithKline, the CDC mentions the other outcome? The no- or fewer antibody result?


1993, Barbour and Fish slam Neurologic Lyme victims:
The SOCIAL Phenomenon of Lyme Disease or what the hell ever… where they admit Phase I and Phase II trials of OspA vaccines are underway. Therefore, as is shown in the Persing RICO Monopoly patent from 1995 shown and linked above (US 6,045,804), they already knew the OspA vaccines were causing a disease indistinguishable from vaccine failure, or CHRONIC LYME:
http://actionlyme.org/BarbourFishpdf.pdf

 

Compare the 2 kinds of Lyme in the RICO complaint filed with the USDOJ in July 2003– compare the blots. On the left is neurological Lyme (the sickest, according to Ray Dattwyler) and on the right is the HLA-linked outcomes of arthritis and acrodermatitis:
http://www.actionlyme.org/USDOJ_COMPLAINT_RICO.htm


 

So, these assholes left out the left-sided, neurological outcomes in their Dearborn scam. The whole point of the redefinition of Lyme at Dearborn was to narrow it to just the HLA-linked hypersensitivity cases. This is how and why they get away with perjury. When the IDSA/Yale Lyme crooks say “Lyme Disease” that means HLA-linked arthritis AND NO OTHER SYMPTOMS.

 

Here next, in 2005, Klempner and Wormser re-revealed that “Lyme Disease” is just one thing. There are 2 things, and the controversial thing really does not have a name right now, but “Lyme Disease” is JUST a bad knee and no other illness signs. THAT is the definition. It’s a legal one and a criminal one, and based on bullshit and no consensus, but here is what it is again (2005):

“A Case-Control Study to Examine HLA Haplotype Associations in Patients with Posttreatment Chronic Lyme Disease”


 

People with ONLY the HLA-linked arthritis (the falsified Dearborn case definition)…“Patients generally feel well aside from their arthritis symptoms,” Say Wormser and Klempner. Pretty amazing right? That the people with the falsified Dearborn case definition of “only an HLA-linked arthritis in a knee” have only an HLA-linked arthritis in a knee and no other symptoms?
http://jid.oxfordjournals.org/content/192/6/1010.full

I love it when that happens ☺
You falsify the case definition and say “ONLY the HLA-linked hypersensitivity response can be a ‘case’ of ‘Lyme Disease,’" and then 11 years later say, “Oh, how amazing for us to find only the HLA-linked case definition is HLA-linked and is only a bad knee. Maybe someone can promote me to the head of a CDC bioweapons lab in Boston on accountta my astuteness.”



 

1994, June FDA LYMErix Meeting (note that June precedes October, so the FDA never approved of the Dearborn method, not to mention it was research fraud and not a consensus):
http://www.actionlyme.org/1994_FDA_MEETING_LYMERIX.htm

Transcript of June 1994 FDA Meeting Minutes:

“So, individuals with a poor immune response tend to have worse disease.”

 

We know why now ☺ Borrelial fungal antigens cause immunosuppression and… a classic “post-sepsis” like result with chronic active EBV, et al.

 

The CDC recently made a big ta-do over the Blumenthal et al letter to the Office of Policy and Management, where the Senators are forcing the FDA to do their jobs and assure that the testing for Lyme is validated according to their own FDA rules (See the Primers Shell Game for more on that). The CDC is trying to say the Dearborn method was FDA validated.

False. The FDA had nothing to do with the Dearborn stunt.



1994, CDC's invitation to participate in Dearborn .pdf   Labs were invited, they said the Steere proposal sucked, CDC blew off these labs recommendations:
http://www.actionlyme.org/DEARBORNINVITATION.pdf

 

1994, October CDC's Dearborn Booklet .pdf
http://www.actionlyme.org/DEARBORN_PDF.pdf

 

Dearborn, Who Said What?
http://www.actionlyme.org/DEARBORN_WHO_SAID_WHAT.htm

1) Gary Wormser at New York Medical College reports that Steere’s Dearborn proposal method detected 9/59 of IgG cases (which, most very sick people being detected too late are obviously not going to have this Early Lyme profile, especially considering Steere’s Late Lyme Arthritis Dearborn falsified definition was intended to be for early Lyme, regardless of his lab shenanigans with the strains and the phony recombinant OspA and B in Europe):
Serodiagnosis in Early Lyme Disease


 

So, Wormser says only 9 of the 59 meet Steere’s Late Lyme Arthritis case definition. That’s 15% accurate.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC266355/pdf/jcm00024-0026.pdf


2) Igenex- Steere’s IgG detected 8% of the cases

3) Imugen – Steere’s method detected 14% of the cases:

4) Wisconsin - Steere’s method was 15% accurate

5) UCONN- Larry Zemel was referring to Lyme as comparable to juvenile rheumatoid arthritis. Recommended adding band 50 for children’s blots.

6) Roche—28% were positive for 5 of 10 Steere IgG bands.

7) Wadsworth – had some different scoring system. Did not report on accuracy of Steere

8) Ontario Ministry of Health

9) Lutheran Hospital— 22 % were accurate by Steere’s IgG

10) MarDx Labs – recommended adding bands 31 and 34, but were given CDC positive arthritis positive blood to falsely qualify their test strips. Theirs were used in both vaccine trials. MarDx was later sold to an Irish company, Trinity Biotech, Dublin, so presumably all they know about the crime was taken out of the country.

11) CDC Atlanta – talked about mice, not humans. The mouse criteria was 2 out of three from OspC, 16 kD, 17.9 kD, for the mice. Wonderful. Everyone is concerned about Western Blotting the poor little mice. Such a tragedy that they have to run around sick. We read about this tragedy at least once a week in the New York Times. People say each other all the time, “Oh, what wonderful weather we’re having, too bad the mice are too sick with Lyme Disease to enjoy it. “ You see those little collection tins at all the supermarket check-outs: “Please Donate One Dollar for the Poor Mice with Lyme Disease!”


 

So, we got this standard anyway, even though none of the invited participants agreed - not by a long shot.  See the Primers Shell Game reports here or at this link:
http://www.actionlyme.org/PRIMERSHELLGAME.htm
for an explanation of how VALID testing is performed according to the FDA rules and how Yale knows all about how to validate a method, validated one (Bb specific flagellar antigen) and patented it (US 5,618,533).  So that's all obvious criminal fraud.


Who was involved with approving the bogus Dearborn method at Dearborn when all the invited labs said it sucked??  Why, none other than the CDC vaccine patent  owners and all the scammers you see here:
http://www.actionlyme.org/Dearborn_Who_Approved.htm





Alan Barbour, Edward McSweegan, Allen Steere. Arthur Weinstein, "The CDC Lyme Disease Group" (Barbara Johnson)

Kind of amazing. The same people involved in the OspA vaccines scam were involved in falsifying the testing.

==================



Igenex, Harris’ view of the Dearborn event .pdf published in the Lyme Disease Foundation’s journal:
http://www.actionlyme.org/HARRIS_IGENEX_DEARBORN.pdf


 

1998 FDA Meeting where Luft says LYMErix produces a multi-system disease just like chronic Lyme:
http://www.fda.gov/ohrms/dockets/ac/98/transcpt/3422t1.rtf

BEN LUFT: "The point that I wanted to make in regard to the study is that there is very heavy dependence on serologic confirmation. And when we start thinking about the adverse events, *** it was stated originally when we got the overview of the disease that the disease is really quite protean [means not limited to "bad knees”- KMD]. And actually the adverse events are very similar to what the disease manifestations are.**** And if you start to, as I think Dr. Hall was eluding to -- if you start to kind of say well how often do you actually become sero positive, you can start to have a different take on when someone has an adverse event of whether it is disease specific or infection specific versus vaccine specific. And I think that that is an important issue that we have to deal with. I can only say from my own ..."


 

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

1) Ben Luft said it at the 1998 FDA meeting (above), 2) Dave Persing said it in his RICO patent (above), 3) Fish and Barbour started trashing us with their “Social Aspects” bullshit in 1993 (above) paving the way, claiming we’re all nuts and hysterics for when the vaccine produced the same result so they’d have a ready made derogatory slander/libel answer and propaganda,…

... 4) Dave Persing and his company Corixa wanted to sell vaccine adjuvants but they had to drop OspA as a candidate adjuvant because, he said… in another patent (applied for May, 2001 while LYMErix was still on the market, harming people and he never said anything to the FDA about it)…
“Prophylactic and therapeutic treatment of infectious and other diseases with mono- and disaccharide-based compounds”
"Accordingly, the methods of the invention provide a powerful and selective approach for modulating the innate immune response pathways in animals without giving rise to the toxicities often associated with the native bacterial components that normally stimulate those pathways."

http://patft.uspto.gov/netacgi/nph-Parser?Sect1=PTO1&Sect2=HITOFF&d=PALL&p=1&u=/netahtml/PTO/srchnum.htm&r=1&f=G&l=50&s1=6,800,613.PN.&OS=PN/6,800,613&RS=PN/6,800,613

5) In 1998 Robert Schoen (involved in developing the RICO monopoly patent - US 6,045,804 - with Dave Persing, 1995) wrote this, once again, paving the way for when the vaccine came on the market and caused the same systemic, seronegative disease damage…

says in 1998 not to test LYMErix victims and minimizes their symptoms knowing chronic Lyme is identical to what Schoen says is "nonspecific" because the exact reverse statement is in the Corixa-RICO patent "multisystem complaints characteristic of late Lyme",  This is that textbook:
http://www.amazon.com/Lyme-Disease-Key-Diseases-Series/dp/0943126584/ref=sr_1_fkmr0_2?ie=UTF8&qid=1341914626&sr=8-2-fkmr0&keywords=lyme+disease+rhan+and+evans





http://www.actionlyme.org/SCHOEN_INSTRUCTING_DOCS_TO_BLOW_OFF_LYMERIX_INJUREES.htm



========

Next, how these crooks lied about their vaccine results, and what happened after LYMErix was approved and on the market.

 

The 1998 Vaccines Reports (ImmuLyme and LYMErix):

LYMErix results (76% "safe and effective"):
http://content.nejm.org/cgi/content/abstract/339/4/209

ImmuLyme results (92% "safe and effective"):
http://content.nejm.org/cgi/content/abstract/339/4/216 

From the LYMErix trial, "categories of outcomes:"
http://content.nejm.org/cgi/content-nw/full/339/4/209/T1


 

Here the crooks claim "we can't read our OspA vaccine results" reports, which means the lied in their OspA vaccine safety and efficacy reports, since they both claimed to be using the Dearborn method and MarDx's Western Blot test strips:

1) SCHOEN and PERSING, with JOHN ANDERSON,1996 - the RICO report:
http://jcm.asm.org/cgi/reprint/35/1/233?view=long&pmid=8968914

2) SCHOEN AND PERSING IN THEIR 1996 RICO METHOD PATENT:
The Dave Persing, Mayo Clinic FRAUD Patent-6,045,804 
3) PERSING WITH SIGAL EXPLAINING THAT THE WESTERN BLOTS WERE UNREADABLE, 2000:
http://www.journals.uchicago.edu/doi/pdf/10.1086/313920

4) Yale's ROBERT SCHOEN in the 1998 Munchausen's Book, instructing MDs to blow off LYMErix systemically injured people ("but send the post-vaccination blood to the Yale L2 Diagnostics RICO lab if you must bother to be a physician").

This ▲ is obviously a FALSE CLAIM or a QUI TAM or FRAUD on the GOVERNMENT since they're declaring to the FDA, in the LYMErix case, saying they had a vaccine.
http://www.usdoj.gov/usao/eousa/foia_reading_room/usam/title9/crm00921.htm


 

I'll just plagiarize myself here and just use the text from the reports below on "Lyme Facts" and "Borreliosis Basics":

So in the Fall of 1998, the LYMErix vaccine was approved, anyway, by the FDA (the FDA panel being loaded with people like Allen Steere, Robert Schoen, and Vijay Sikand – the very people who ran the OspA trials) and came on to the market in late 1998 despite numerous “provisos.” More than 1,000 systemic adverse events were reported through the VAERS from September 1999 to November 2000, whereupon the FDA granted a public hearing, January 31, 2001:

http://www.fda.gov/ohrms/dockets/ac/01/slides/3680s2.htm

Whereupon I blew the whistle on Dearborn and how LYMErix actually caused immunosuppression (the FDA did not scan in the last 19 pages of this booklet, which were 19 pages out of the Dearborn booklet, proving no one agreed with Steere's proposal for an antibody panel for a "case definition":
http://www.fda.gov/ohrms/dockets/ac/01/slides/3680s2_11.pdf

 
Several months later, in the fall of 2001, Karen Forschner of the Hartford, CT based Lyme Disease Foundation (Lyme.org) delivered to the FDA – in person -, a patent owned by Bridgitte Huber at Tufts where it was declared that OspA was technically a “toxin,” right in the abstract (US Patent 6,689,384). The FDA then gave SmithKline and Yale (the assignee of the LYMErix patent), an ultimatum: “Either you remove LYMErix voluntarily or we will order it off the market.” SmithKline chose to avoid the embarrassment and pulled their own non-vaccine.

We’re still stuck with this bogus Dearborn case definition, despite numerous attempts at lawsuits against IDSA, SmithKline, and filing complaints to the U. S. Department of Justice. It is still very dangerous for the public to be unaware that the average person, or 85% of us – who are the “seronegative patients are the sickest ,“ according to Raymond Dattwyler at the 1994 FDA meeting on Lyme and LYMErix (which preceded Dearborn) - have no chance of testing positive to this criminal CDC’-Dearborn standard, because the actual disease is one of immunosuppression, or is an Acquired Immune Deficiency,… or is similar to AIDS with all the opportunistic infections that the Lyme and LYMErix victims cannot control.

It was said at the time LYMErix was still on the market that this vaccine, via its claimed mechanism of disinfecting ticks with human antibodies (yes, if you can believe it), that LYMErix would turn humans into walking cannisters of tick disinfectant, when in fact, LYMErix turned people into walking “cesspools of disease.” The same is true for Chronic Lyme. Chronic Lyme victims’ immune systems are “overwhelmed”- a term used by CDC officer Alan Barbour, when describing what antigenic variation in spirochetes does to humans (US Patent 6,719,983). This is a term you want to remember in case you hear it again: “overwhelmed” immune system means: “turned off.” “Turned off” is the complete opposite of an “inflammatory” or “autoimmune disease.”

 

That's all for now, folks.... KMD

 

The Primers Shell Game, a version for the Facebook "Occupy the DOJ" group, a chapter of CRYME DISEASE and a lesson from the new “Khan Academy” of Lyme Cryme and HLA-Negative Diseases (includes all abused groups; CFIDS, ME, FM, Autism, medical rights, Fergusonites, parents rights, psych rights, etc); 141031, KMD.


The primary chapter of Cryme Disease is Chapter One, about Scientifically Valid Testing for Lyme (which is not arbitrary but follows FDA rules), which includes this same information, below, that you need to understand about the genetic relatedness of these kinds of spirochetes.  Chapter 7 (BRAIN_PERMANENT.htm), where the crooks almost always use the OspA gene instead of the flagellin gene or a species-specific spacer gene to find "NO LYME," so you have to compare the following data to that, that is, if you want more examples than the following...

Flagellin is the species distinguisher.

All Borreliae are relapsing fever organisms, and the nature of the relapse is antigenic variation. Therefore you cannot use any DNA from plasmids – which is where the variable surface antigens are ordered manufactured and remanufactured – to assess for spirochetes. No one sane does this. No researchers outside the United States EVER uses plasmid DNA to assess for spirochetes. They only use species-specific spacer genes like 5, 16 and 23 S RNA or flagellin. That’s it.


 

Let’s start at the beginning because the moron “LLMDs” out there are killing me, really. I feel like I am in Beatrice’s World. (“That’s not how this works.”)

 

Now, let's side-step for a minute and talk about the FDA and what their rules are for the "Validation of an Analytical Method."  As you can see there is Accuracy (should detect 100% of the instances when the analyte in question is present), Specificity (only detects one thing), Linearity, Ruggedness, Precision (refers to instrumentation), Limit of Detection (this would be something like, "How low in concentration of the analyte in question can your method detect?"). 

This is from the new announcement July 31, 2014 regarding the FDA now about to ENFORCE their validation rules:
http://www.fda.gov/downloads/MedicalDevices/ProductsandMedicalProcedures/InVitroDiagnostics/ucm407409.pdf


 

 

 

Do you see the FDA wrote their words here?  I underlined them.

 

 




"Sensitivity" MEANS "Limit of Detection." The closest thing to that in the real VALIDITY requirements is Limit of Detection. 

FDA Rules on the VALIDATION of an Analytical Method
Specificity
(only detects one thing)
Accuracy (Should detect 100% of the instances where the analyte is present, and the concentration should be close to 100% of that known to be spiked in, and never should detect "none" as is the case with Lyme Western Blotting and the Lyme ELISA, especially)
Limit of Detection (means "What is the lowest concentration of the analyte in question does your method detect?")
Precision  (system has integrity in performance)
Ruggedness  (anyone can run the test with their own equipment and get the same results)
Linearity (concentration range of analyte for which the test is valid in and out of matrix or "inert ingredients")
 

But first, your test should detect all the cases in question, - or be 100% ACCURATE - and that means, in the case of Lyme, the only analyte that can be tested for is flagellin or anti-flagellar antibodies.  Anti-flagellar antibodies can be found in probably 95% of Lyme cases.  So, Yale went ahead and made that Specific (US patent 5,618,533) in 1991, here, next:


Says Yale:  "Molecular characterization of the humoral response to the 41-kilodalton flagellar antigen of Borrelia burgdorferi, the Lyme Disease spirochete."

"The earliest humoral response in patients infected with Borrelia burgdorferi, the agent of Lyme disease, is directed against the spirochete's 41-kDa flagellar antigen. In order to map the epitopes recognized on this antigen, 11 overlapping fragments spanning the flagellin gene were cloned by polymerase chain reaction and inserted into an Escherichia coli expression vector which directed their expression as fusion proteins containing glutathione S-transferase at the N terminus and a flagellin fragment at the C terminus. Affinity-purified fusion proteins were assayed for reactivity on Western blots (immunoblots) with sera from patients with late-stage Lyme disease. The same immunodominant domain was bound by sera from 17 of 18 patients. This domain (comprising amino acids 197 to 241) does not share significant homology with other bacterial flagellins and therefore may be useful in serological testing for Lyme disease."
http://www.ncbi.nlm.nih.gov/pubmed/1894359
 

Okay, so Yale says there, above, that their method (US patent 5, 618, 533) detects, early, late, neurological, and every other possible kind of Lyme outcome and that it detects 94.4% of the cases, which means it is the closest possible method we could possibly have to detect Lyme ("should be 100% of the cases," says the FDA, verbatim), and this method was made SPECIFIC, which means it does not detect any other flagellins.


When the FDA says "sensitivity," they really mean "LIMIT OF DETECTION" and refers to the METHOD and not the "CASES."  Accuracy addresses cases.  Yale took care of all that in 1991 and went ahead and patented it (but did not use this method to qualify LYMErix, their other patent, which is the essence of this False Claims Act case).


Okay, so in summary >> The only way to detect a spirochetal disease is to use recombinant specific flagellins from most of the specific borreliae - just like Yale did, above, only with the other borrelia - that we know to be at least in the United States.  THAT is what is "VALID," and the FDA and NIH agree with me.


 

Okay, so: DO NOT EVER listen to IDSA, the Lymedisease.org (LDA) or ILADS.org.  IDSA are criminals and the LDA/ILADS are retarded and have no real scientists in their camps.

ILADS and the LDA do not know what they are talking about and consistently come up with stupid, retarded announcements, giving everyone with Lyme-brainscramble and everyone who is an MD but has no science background... even more brainscramble.  It just is not fair. 

If you don't know what you are talking about, kindly do not talk.


 


Single Spirochete Infection and resultant MULTIPLE VARIANTS:

1951: Relapse Phenomena in Rats with a Single Spirochete
http://jb.asm.org/cgi/reprint/62/2/215?view=long&pmid=14861181

Oscar Felsenfeld and CDC officer Alan Barbour talking about/referencing this Single Spirochete Phenomena:
http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=link&linkname=pubmed_pubmed_citedin&uid=14861181

 

Oral Spirochetes infecting Alzheimer’s brains and traveling along inside nerves (this is not the only report that says this, you’ll find it in syphilis report too) (from BRAIN_PERMANENT.htm);  An independent study on spirochetes in the brain from dentists and they say:

Molecular and immunological evidence of oral Treponema in the human brain and their association with Alzheimer's disease.
Riviere GR, Riviere KH, Smith KS.
Department of Pediatric Dentistry, School of Dentistry, Oregon Health and Sciences University, Portland, OR 97201-3097, USA.
“The purpose of this investigation was to use molecular and immunological techniques to determine whether oral Treponema infected the human brain. Pieces of frontal lobe cortex from 34 subjects were analyzed with species-specific PCR and monoclonal antibodies. PCR detected Treponema in 14/16 Alzheimer's disease (AD) and 4/18 non-AD donors (P < 0.001), and AD specimens had more Treponema species than controls (P < 0.001). PCR also detected Treponema in trigeminal ganglia from three AD and two control donors. Cortex from 15/16 AD subjects and 6/18 controls contained Treponema pectinovorum and/or Treponema socranskii species-specific antigens (P < 0.01). T. pectinovorum and/or T. socranskii antigens were also found in trigeminal ganglia and pons from four embalmed cadavers, and 2/4 cadavers also had Treponema in the hippocampus. These findings suggest that oral Treponema may infect the brain via branches of the trigeminal nerve.”
http://www.ncbi.nlm.nih.gov/pubmed/11929559

 

Now, you will see why this "single-spirochete-becomes-multiple-strains" business is important later in this chapter, below, as regards Alan Barbour and Bioweapons, and how spirochetes creating multiple variants and all the individual spirochetes doing their own thing, varying their surface antigens on their own comes into play as far as ruining a person's immune system.  And a ruined immune system is the DAMAGE and is the ILLNESS and is the specific goal of a bioweapon:

           

"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, so assess the HLAs in the population you intend to abuse like the defecting Russian scientists at NYMC have been doing, 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 acquired 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 fungal OspA- KMD].


 

 

Do you see the disease now? ▲▲▲  ??    It's fungal (shed borrelial antigens are TLR2/1-agonists or fungal).  It is about ovewhelming the immune system; it is about not producing identifiable antibodies; your bioweapons should be like a Trojan Horse, setting off other latent infections; your immune system now sucks (overwhelmed means turned off); you don't have "biofilms" at least of borrelia; Lyme was the "perfect stealth disabler;"... and then all of the CDC's ridiculous lies...  From the CDC's lies alone, you could call this an accidental release of a bioweapon.   But we have other circumstantial scientific evidence, as you will see...





Moron LLMDs Alert on “Biofilms”:

Use “Borrelia Staining” or “Borrelia Silver Staining” as search terms in PubMed and discover that Borrelia in vivo do not cluster at all, much less under a “Biofilm.”

Here is one. Look closely now, for the “clustered spirochetes hiding under a biofilm” (there is no such thing):
Demonstration of Spirochaetes in Patients with Lyme disease with a Modified Silver Stain
http://jmm.sgmjournals.org/content/23/3/261.long
 

Here is another one by Paul Duray (same guy who revealed that congenital Lyme brain damage kills babies and the same guy who revealed to us that Lyme and LYMErix diseases cause a leukemia like illness and that the cells in the CSF of Lyme patients "look like Epstein-Barr transformed (mutated, pre-cancerous) cells:
http://www.ncbi.nlm.nih.gov/pubmed/?term=Duray+and+borrelia+and+stain


PAUL DURAY >>> "Morphology of Borrelia burgdorferi: structural patterns of cultured borreliae in relation to staining methods.

"
The microscopic recognition of Borrelia burgdorferi in biologic fluids and tissues is difficult and challenging because of low numbers of organisms occurring as single isolated spirochetes, the apparent lack of colony formation in tissues, and differing lengths and structural morphologies."

http://www.ncbi.nlm.nih.gov/pubmed/1716264

 

Additionally, biofilms are covered in TLR2/1 agonists so the body does not even see them at all any more, if they are there, in this post-sepsis disease called Chronic Lyme, with the multiple reactivated herpes viruses, etc and the expansion of tolerance to other toll-like-receptor-managed antigen types.
 

Okay, so REVIEW:  Biofilms are NOT responsible for the persistent symptoms in Chronic Lyme Disease.  Spirochetes, while permanent - no one sane argues that they're not, since they always were known to be incurable infections, even with arsenic - (RICOCHRON.htm).  So, what is responsible?


Go to POST_LYME_SEPSIS_2014_SUMMER.htm and see the following, among others, FROM THE NIH!!!!
 

10) This is the NIH (NINDS’s MS-Lyme Group) group that discovered that *** OspA *** was the cause of the MS/New Great Imitator outcome of Lyme reporting in the New York Times in the summer of 2013 (Martin and Marques, 2006):

When Lyme Disease Lasts and Lasts – Jane Brody
"Complicating the picture is the fact that some people with PTLDS symptoms apparently never had Lyme disease in the first place, Dr. Marques said in an interview. There are other infectious organisms — Epstein-Barr virus, for example — that can produce similar symptoms and may be the real culprits."
http://well.blogs.nytimes.com/2013/07/08/when-lyme-disease-lasts-and-lasts/ 


Here are the NIH's 2 reports that say OspA (TLR2-agonist) is the cause of the MS/CFIDS/EBV-reactivated kind of Lyme (that also causes humoral immunosuppression),... and that as a result of exposure to OspA-like antigens (shed constantly in a process called blebbing, as revealed by CDC officer Alan "Stealth Bomber" Barbour), you might not even have anti-flagellar antibodies (TLR5-agonists):

Borrelia burgdorferi Induces TLR1 and TLR2 in human microglia and peripheral blood monocytes but differentially regulates HLA-class II expression.
http://www.ncbi.nlm.nih.gov/pubmed/16783164 

and

Borrelia burgdorferi lipoprotein-mediated TLR2 stimulation causes the down-regulation of TLR5 in human monocytes.
http://www.ncbi.nlm.nih.gov/pubmed/16479520 


12) NCI and US Army Ft Detrick Pathologist Paul Duray on the CSF cells looking like "Epstein-Barr-like transformed cells" in IDSA's 1989 Reviews Supplement on Spirochetal Diseases:

Rev Infect Dis. 1989 Sep-Oct;11 Suppl 6:S1487-93.
Clinical pathologic correlations of Lyme disease.
"Immature B cells can also be seen in the spinal fluid. These cells can appear quite atypical- not unlike those of transformed or neoplastic lymphocytes." --
http://www.ncbi.nlm.nih.gov/pubmed/2814170 
Full Text:  http://www.actionlyme.org/IDSA_CLINIPATH_DURAY.htm 
 


NEW, by the NIH:  "Surviving Sepsis: Detection and Treatment Advances"


========================

13) Duray again in 1992, in Steve Schutzer's review of the 1992 Cold Spring Harbor Conference on Lyme:

"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." -

Paul Duray, NCI, NIH, Ft. Detrick, at the 1992 Cold Spring Harbor Crooks' Conference, published in Steve Schutzer's Lyme Disease: Molecular and Immunologic Approaches. - book.


 



Yikes, I hope that is the end of THAT topic. God Save Us from stupid people who only will malpractice-treat rich people with long term antibiotics for post-sepsis immunosuppression, the reactivation of latent herpesviruses, and TL2/1 agonist (and expanded cross tolerance) tolerance, with their own little, “It must be babs, it must be bart, it must be today’s-flavor-of-whack-a-do coinfection number 467… and get a third mortgage, since the money from your second mortgage ran out, thanks, I love my new yacht….” abuse that you get from ILADS.org


===


BACK TO THE DNA SHELL GAME.....  DO NOT SKIP THESE 2 PARAGRAPHS:

So, when talking about the DNA and RNA shell game played by the crooks - where the crooks use the wrong DNA to find “NO-LYME HERE!” and the correct DNA when they want to run to the patent office to claim a new species…- we have to go back to Chapter One of Cryme Disease (CRYMEDISEASE_CHP1.htm is the extension) which is about Taxonomy
The very first thing you need to know about Lyme is that it is technically called Relapsing Fever.
Here is why:
http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?id=138 <<< Click on the larger texted heading, "Borrelia" in the above link. You will see that the taxonomic categorization of these organisms is based on differences in their flagellin, because that is the genetic species distinguisher - and not OspA or any of the plasmid DNA. [All Borrelia are arthropod-borne. That is why they are called borrelia. That is why they're distinct from other spirochetes. And if they are parasites, they cause disease in some way.]

One must understand how these spirochetes are related,… and the phylogeny,… and in the end “they’re all just Borreliae and you really can’t even talk about species ,” Oscar Felsenfeld… But if you must, use the flagellar genes, since those is the species distinguishers, taxonomically.



On second thought... I have decided to add the links and the graphics to Phylogeny Basics so you don’t have to bother going to the Taxonomy database.

Here we see as the key report from the NIH's NLM's Taxonomy (Fukunaga, et al) database showing Burgdorferi is closest to anserina, an African bird borreliosis. They just happen to do this kind of African-Diseases-With-North-American-Vectors-kind of "Research" on Plum Island (verifiably):
http://ijs.sgmjournals.org/content/46/4/898.long
 

 


Here we see the NIH Rocky Mountain Bioweapons Lab using anserina as an out-group, when in fact, it is the origin of the Plum Island burgdorferi group - African bird borreliosis - experimentally introduced to the microscopic bioweapony Ixodes, hard bodied tick: 
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC228430/pdf/332427.pdf

 




More on Evolution and Expansion of the anserina-come-burgdorferi-Plum-Island phenomenon:

SUNY-SB on Lyme/Plum Island as the original outbreak area:
Evolution of a focus of Lyme disease
http://www.ncbi.nlm.nih.gov/pubmed/3577493


UPenn on Lyme being evolutionarily unlikely:
UNCOORDINATED PHYLOGEOGRAPHY OF BORRELIA BURGDORFERI AND ITS TICK VECTOR, IXODES SCAPULARIS:
http://www.ncbi.nlm.nih.gov/pubmed/20394659

Despite the intimate association of B. burgdorferi and I. scapularis, the population structure, evolutionary history, and historical biogeography of the pathogen are all contrary to its arthropod vector.”


Durland Fish and his experiments with African diseases and vectors on Plum Island:
African Swine Fever Virus Infection in the Argasid Host, Ornithodoros porcinus porcinus

“ASFV isolates.

Chiredzi/83/1 (Ch1) was isolated from Ornithodoros spp. ticks collected near Chiredzi, Zimbabwe (26), and was obtained from the Plum Island Animal Disease Center reference collection. Pretoriuskop/96/4/1 (Pr4) and Crocodile/96/1 (Cr1) were isolated from O. porcinus porcinus ticks collected from warthog burrows in Kruger National Park, Republic of South Africa, in September 1996. Nooitverwacht/96/6 (No6) was isolated from O. porcinus porcinus ticks collected from a warthog burrow in the Northern Province, Republic of South Africa, in September 1996.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC109458/



CDC Lying about the viability of the cyst or spheroplast form of spirochetes,... and CDC lying about mycoplasma not being involved in Chronic Fatigue Syndrome: 
 

CDC: "How to Dessicate and Weaponize your Borrelia :) "
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC277387/pdf/jbacter00438-0287.pdf
 

CDC Throwing out the red blood cells (throwing out whole cells of any kind, including immune cells or white cells where the mycoplasma actually lived and used to be called epERYTHROzoa for that very reason:

"Absence of Mycoplasma species DNA in chronic fatigue syndrome"
"Plasma, the liquid portion of peripheral blood that is devoid of cells, is known to contain remnants of numerous physiological and disease processes. We used plasma DNA to detect and characterize bacterial 16S rDNA sequences in a group of individuals with CFS and a group of non-fatigued controls (Vernon et al., 2002). Whilst a variety of bacterial sequences were detected in both fatigued and non-fatigued groups, no Mycoplasma sp. 16S rDNA sequences were found."
http://jmm.sgmjournals.org/cgi/pmidlookup?view=long&pmid=14532349 

 

So, that's all obviously a lot of research fraud performed by CDC staff already, and next, in the DNA Shell game you will see it is almost entirely CDC officers committing this fraud.
 

========== Now on to where the crooks play the shell game with the DNA and RNA ========

 

ALAN BARBOUR playing the DNA/RNA shell game...

You will want to look at The Patents chapter of Cryme Disease (http://www.actionlyme.org/CENTRAL_LYME_RICO_PATENTS.htm ) to see that CDC officer and former head of the NIH’s Rocky Mountain Bioweapons Lab (where there are tons of Relapsing Fever but no “Lyme”) Alan Barbour reported that basically “antigenic variation in one spirochete, times all the spirochetes you have leaves the immune system ‘overwhelmed’ with “an infinite number of new antigens,” which is a bioweapons technique well described by the US Army when speaking to Congress and can be seen on the Bioweapons pages of ActionLyme.org (http://www.actionlyme.org/120702.htm and http://www.actionlyme.org/BIOWEAPONS_ATTRIBUTES.htm )


ALAN BARBOUR states clearly that OspA undergoes true antigenic variation and that you cannot use this as a vaccine, and certainly not for DNA diagnostics as Klempner did in his “BREAKING NEWS!!!” Bogus re-treatment "study" that is now the data used by IDSA for their "Guidelines" from the summer of 2001.

"Antibody-resistant mutants of Borrelia burgdorferi: in vitro selection and characterization."

Says Barbour above: “Second, previous studies had shown antigenic differences in outer membrane proteins, OspA and OspB, between strains (21-26) and also true antigenic variation of these proteins within a strain (25, 27-30).”
http://www.actionlyme.org/BARBOUR_MUTANTS_1992.htm
That’s PubMed ID http://www.ncbi.nlm.nih.gov/pubmed/1339462

Mutants” is code language. They’re all mutants. Antigenic Variation is the nature of the relapse in Relapsing Fever, so to call them mutants is silly and redundant, and not the least bit correct as you will see in Barbour’s patents and in the older data re the Single Spirochete outcome.


Here is what Barbour says in one of his patents about antigenic variation and "overwhelming the immune system":
 

"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."

http://patft1.uspto.gov/netacgi/nph-Parser?Sect1=PTO1&Sect2=HITOFF&d=PALL&p=1&u=%2Fnetahtml%2FPTO%2Fsrchnum.htm&r=1&f=G&l=50&s1=6,719,983.PN.&OS=PN/6,719,983&RS=PN/6,719,983


So you can’t use OspA for a vaccine, for post-treatment DNA diagnostics, or for Lyme case detection in antibodies. The only thing you can do or say about OspA is remember it means little except that it helped the normally non-borreliae-bearing Ixodes (hard bodied) ticks acquire a ligand (OspA-B plasmid) with which to attach to and invade the hard bodies of hard bodied (Ixodes) ticks. So, Lyme spirochetes were adapted probably on Plum Island to local vectors. Genetically, the Lyme spirochete is closest to anserina, an African bird borreliosis. All the more better to spread it around, to use a bird strain  (see http://www.actionlyme.org/PIIB.htm and http://www.actionlyme.org/TRAINER_2012SUMMER.htm )


BARBOUR'S 1995 PATENT FOR SPECIFIC 16S RNA and Flagellin that GARY WORMSER DID NOT USE, WHILE
BARBOUR SAYS THIS IS IN LONE STAR TICKS IN MISSOURI (that study is below in this chapter):

http://patft.uspto.gov/netacgi/nph-Parser?Sect1=PTO1&Sect2=HITOFF&d=PALL&p=1&u=%2Fnetahtml%2FPTO%2Fsrchnum.htm&r=1&f=G&l=50&s1=5%2C932%2C220.PN.&OS=PN%2F5%2C932%2C220&RS=PN%2F5%2C932%2C220


 

MARK KLEMPNER, playing the DNA/RNA shell game...

You have previously seen that the OspA gene undergoes antigenic variation (Alan Barbour, owner of the ImmuLyme vaccine OspA patent, above), is not found in all Borreliae and you can't use this DNA for anything, especially not vaccines or detection.

We move on to the Klempner "Study" which resulted in the “Guidelines” and where he references which DNA he used to assess "NO LYME IN LYME VICTIMS" (he doesn’t actually and the peer reviewers never noticed he did not list his primers):

http://www.nejm.org/doi/full/10.1056/NEJM200107123450202#t=articleMethods


 

So, what was that mysterious REFERENCE 21 above ^^ DNA that Klempner failed to report and the so called peer-reviewers did not notice?

http://jid.oxfordjournals.org/content/174/3/623.full.pdf

WHICH SAYS:

 


 

So, the crooks – including Klempner in his bogus non-retreatment report that is now the basis of the IDSA “Guidelines” - say if the OspA gene is not there, there is no Lyme, right? Despite the fact that Lyme is a Relapsing Fever borrelia and OspA undergoes antigenic variation and not likely to be in the same form or produced by the exact same genetic code as one produced inside a tick, late in the disease in humans.


 

DURLAND FISH

And here is Durland Fish using the correct primers to look for new species of Borreliae to patent in 2001:

A relapsing fever group spirochete transmitted by Ixodes scapularis... - PubMed – NCBI

Vector Borne Zoonotic Dis. 2001 Spring;1(1):21-34. Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S. NCBI.NLM.NIH.GOV|BY SCOLES GA , ET AL.

"A 1,347-bp portion of 16S rDNA was amplified from a pool of infected nymphs, sequenced, and compared with the homologous fragment from 26 other species of Borrelia. The analysis showed 4.6% pairwise difference from B. burgdorferi, with the closest relative being Borrelia miyamotoi (99.3% similarity) reported from Ixodes persulcatus in Japan. Phylogenetic analysis showed the unknown Borrelia to cluster with relapsing fever group spirochetes rather than with Lyme disease spirochetes. A 764-bp fragment of the flagellin gene was also compared with the homologous fragment from 24 other Borrelia species. The flagellin sequence of B. burgdorferi was 19.5% different from the unknown Borrelia and showed 98.6% similarity with B. miyamotoi."

http://www.ncbi.nlm.nih.gov/pubmed/12653133



 

Yet, here we see a year later, Durland Fish using the WRONG DNA (OspA gene again), to assess treated mice, to determine if there is any Borrelia, coming to the conclusion that there is pretty much no Borrelia:

http://jid.oxfordjournals.org/content/186/10/1430.long

Detection of Attenuated, Noninfectious Spirochetes in Borrelia...

"PCR of DNA.DNA was isolated from individual ethanol-fixed nymphs or pooled larvae by means of the Isoquick DNA isolation kit (ORCA Research) and was resuspended in 20 μL of double-distilled H2O. Primers used for amplification were as follows: *** ospA *** (GenBank accession no. M57248, product amplicon coordinates 80–781): forward, 5′-AAAACAGCGTTTCAGTAGATTTGCCTGGTG-3′, and reverse, 5′-CAACTGCTGACCCCTCTAATTTGGTGCC-3′; BBE21.1 (GenBank accession no. AE000785, product amplicon coordinates 14663–14921): forward, 5′-AGAATTATGTCGGTGGCGTTGT-3′, and reverse, 5′-ATTAAAGCCGCCTTTTCCTTGGT-3′; and p37-47 (GenBank accession no. AE000794, product amplicon coordinates 1309–1457): forward, 5′-TTCTGATGGCACTGAGCAAACCA-3′, and reverse, 5′-AACCCTTTACACTTTCTTCGATTGCGCT-3′. The primer set for p37–47 has 100% homology to sequences in both B. burgdorferi strains B31 and N40, and the gene has been localized to lp28-1 in both strains [26, 27]. The primer set for BBE21.1 amplifies a unique region in lp25 of B. burgdorferi strain B31 downstream of BBE21 (amplicon coordinates 13403–14530) [28]. BBE21 is located on a similar-size plasmid within B. burgdorferi strain N40 [29]. We have been able to amplify by PCR the region corresponding to GenBank accession number AE000785, product amplicon coordinates 14195–14921, indicating that BBE21 and BBE21.1 reside on the same plasmid in N40 (authors' unpublished data)"


^^^  Those are plasmids, those "lp... " things.  Plasmids are from where the variable surface protein antigens vary themselves.  So, that is a classical Durland Fish type "bogus article."



GARY WORMSER playing the DNA/RNA shell game....

Next we are going to look at Gary Wormser who is in 1992 using the correct primers:
Diagnosis of early Lyme disease by polymerase chain reaction amplification and culture of skin biopsies from erythema migrans lesions.

http://www.ncbi.nlm.nih.gov/pubmed/1452688
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC270592/pdf/jcm00036-0064.pdf

 

Here Gary Wormser in 1999 when using the CORRECT PRIMERS (16S) finds most people are infected with more than one species of Borrelia and that you can't really use Barbour-Kelly-Stoener culture media (the only one anyone sells in the USA):

Genetic diversity of Borrelia burgdorferi in lyme disease patients ... - PubMed – NCBI
J Clin Microbiol. 1999 Mar;37(3):565-9. Comparative Study; Research Support, U.S. Gov't, P.H.S.
NCBI.NLM.NIH.GOV|BY LIVERIS D , ET AL.
http://www.ncbi.nlm.nih.gov/pubmed/9986813


And yet here we have Gary Wormser not finding Lonestari in Missouri because *** he is using the wrong primers*** [he is not using Barbour's lonestari patent primers (1995), and his results conflict with Telford's, below, in 2001 report showing Missouri Relapsing Fever is closest to theileri a cow relapsing fever, and Wormser is using a general 16S primer not specific to Borreliae species at all]; Wormser is also using an OspA gene primer which Barbour determined in 1995 was not in his new theileri-like (cow relapsing fever) patented Borrelia:


2005: Microbiologic evaluation of patients from Missouri with erythema migrans.
http://www.ncbi.nlm.nih.gov/pubmed/15668867
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2773674/

“PCR amplifications were performed in a 50-μL reaction mixture containing 10 mmol/L Tris-HCl (pH 8.3); 1.5 mmol/L MgCl2; 50 mmol/L KCl, 0.1% (w/v) gelatin; 100 μmol/L each of dATP, dGTP, dCTP, and TTP; 1.25 units Taq polymerase; and 20 pmol of each primer. Detection of borrelial DNA in patient specimens and ticks was accomplished by the nested PCR amplification of flaB using primers FlaLL, FlaLS, FlaRL, and FlaRS as described by Barbour et al [11]. PCR of 16S rDNA was performed with broad-range eubacterial primers 8FPL and 1492RPL [26], which yields a product of ∼1.5 kbp. In cases in which no detectable product was obtained, second-round heminested PCR was performed with 8FPL and a reverse primer (519R: 5′-TTACCGCGGCTGCTGGC-3′) targeted at residues 535–518 (numbering corresponds to residues in the 16S RNA sequence of Escherichia coli) in 16S rDNA; this resulted in a fragment of ∼500 bp. Some specimens were also tested by PCR targeted at ospA (forward primer, 5′-CTGCAGCTTGGAATTCAGGCACTTC-3′; reverse primer, 5′-GTTTTGTAATTTCAACTGCTGACCCCTC-3′) and/or recA [27].”


WORMSER did not use the correct^^^ Borrelia-specific flagellin, or Borrelia-specific spacer genes as shown below by Telford and Barbour in his lonestari-like patent, and he did not use genus specific 16S RNA genes ("broad-range eubacteria"?), and he used a reverse primers for E coli ?? LOL.



SAM TELFORD's 2001 REPORT SAYING “Southern Lyme” is CLOSEST TO THEILERI OR BOVINE RELAPSING FEVER:
http://www.ncbi.nlm.nih.gov/pubmed/11158095

 


You can see that the ^^^ crooks have already sequenced the 4 similar strains of flagellar and genus specific 16S RNA spacer genes that are derived from a cow or bovine relapsing fever.

 

TO THIS DATE – from 1995 to 2015 - still, NO ONE IS USING BARBOUR'S RECOMBINANT LONESTARI FLAGELLIN OR 16S RNA GENE or any other of these gallblammed proper DNAs or RNAs TO DETECT HUMAN ILLNESS, NATURALLY.

 

They all know the only way to detect Lyme/Relapsing Fever is with specific recombinant flagellins from all the Borreliae, similar to Yale’s Lyme specific flagellin patented method, US 5,618,533.

 

ROBERT SCHOEN - 1995

J Immunol. 1995 Dec 15;155(12):5700-4.

An ospA frame shift, identified from DNA in Lyme arthritis synovial fluid, results in an outer surface protein A that does not bind protective antibodies.
Fikrig E1, Liu B, Fu LL, Das S, Smallwood JI, Flavell RA, Persing DH, Schoen RT, Barthold SW, Malawista SE.
http://www.ncbi.nlm.nih.gov/pubmed/7499856

 

Oh, you mean Lyme is a Relapsing Fever organism, so you can’t use the OspA gene for human treatment outcomes assessment, Huh Mr. Schoen, or to detect “Lyme” in EM rashes?


Here, next Yale's Robert Schoen (who says Lyme is not a real disease and needs no treatment) using 23S RNA primers to assure his RICO monopoly strain (and later patent with Dave Persing) is related to burgdorferi,...

Borrelia burgdorferi enzyme-linked immunosorbent assay for discrimination of OspA vaccination from spirochete infection.
http://www.ncbi.nlm.nih.gov/pubmed/8968914
http://jcm.asm.org/content/35/1/233.full.pdf


and also reveals there is "Lyme" in the Southern and Western states in 1996.
 


ANDREW PACHNER:


Another report of this type is "Borrelia burgdorferi infection of the brain: Characterization of the organism and immune sera in the mouse model"

"The plasmid content of N40Br was different from that of the infecting strain implying either a highly selective process during infection or DNA rearrangement in the organism in vivo. "


 

141122_COMMENTS_NIHRULECHANGE.htm