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1988 Steere says Lyme is like a B cell leukemia
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Fungal Exosomes Inhibit Apoptosis
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Exosomes, Blebs
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PDFs
CDC Admits Fraud, 2016
Dattwyler, 1988
Golightly, 1988
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1994
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1994
BarbourFishpdf.pdf
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"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"
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]"
========================
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
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