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

01 Oct 2017


File List, RICO

1988 Steere says Lyme is like a B cell leukemia

Assoc Blogs-n-Webs:




Fungal Exosomes Inhibit Apoptosis

IDSA: "Vaccines serve the mfgs, not their victims"


BlumenthalAntiTrust Lawsuit

Exosomes, Blebs


CDC Admits Fraud, 2016
Dattwyler, 1988
Golightly, 1988
Dressler, 1994
BarbourFish, 1993
Dearborn, 1994

Pathogenic Fungi

Bush's warcrimes, Oct 2000





Chapter 3 of Cryme Disease-

What did Allen Steere do in Europe to falsify the diagnostic standard for Dearborn ??

There were 2 reports and not one- not just Desssler/Steere, that were involved in falsifying the antibody panel for the current, CDC diagnostic standard.  The most significant one was not included in the CDC's Dearborn booklet - this one:  STEERE_IN_EUROPE.htm

This was how Allen Steere left OspA and B out of the antibody panel to set up the RICO which included Imugen, Yale's L2 Diagnostics and Corixa as formal business "partners":

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

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



Allen Steere is the author of both CDC standards, the 1990 standard and the 1994 Dearborn standard.  For the fake standard - the current CDC Dearborn standard - Allen Steere went to Europe alone in 1992
with bogus high-passage strains and recombinant OspA-B with no lipid attached and therefore little immunogenicity (means, "produces antibodies")  to leave OspA and B out of the standard.  Osp A in the diagnostic test, when the antigen is also the vaccine, invalidates the test.  One never tests for vaccine efficacy with the same antigen as the vaccine.  Steere also falsely claimed that his pool of Dressler/Steere neurologic Lyme patients must have proteins or cells in the CSF, when it was known that at least half of neurologic Lyme victims do not have antibodies in their CSF or is an "aseptic meningitis."  So, all of Dressler/Steere was deliberate scientific fraud.  Steere had previously proposed that we perform sequential Western Blots to diagnose Lyme.

FAIRY-ALERT!!   "The Non-Stalking of Allen Steere - the TRUE story of my interview with David Grann of the NYT Magazine."


NINDS' MS Group Leader, Roland Martin, went back home to Germany after not exactly discovering that autoimmune T cells are the result of Lyme infection:

Studies of Lyme arthritis and chronic neuroborreliosis suggest that spirochete-specific T cells cross-reacting with self-antigens may be at least partly responsible for autoimmune mechanisms possibly leading to chronic disease manifestations (8, 12, 25).

Cross-recognition of self-antigens by B. burgdorferi-specific CD4+ T cells has been implicated in the pathogenesis of chronic manifestations of the disease. Patients with treatment-resistant Lyme arthritis, but not other forms of arthritis, expressing the rheumatoid arthritis-associated MHC allele HLA-DRB1*0401 [STEERE's DEARBORN HAPLOTYPE] generated clonal responses to both the immunodominant borrelial outer surface protein A and the human leukocyte function-associated antigen 1, which was tested as a candidate autoantigen (8). In a patient with chronic NB expressing the MS-associated HLA-DRB1*1501 [MARTIN's "LYME RESULTS IN MS" HAPLOTYPE] allele, we previously showed that a single TCC preferentially recognizes different borrelial peptides but also responds to human autoantigenic mimics (12). Our data clearly indicate that degenerate antigen recognition that includes pathogen-derived and self-epitopes is not restricted to chronic and treatment-resistant manifestations of the disease. Molecular mimicry alone is thus not sufficient to induce chronic Lyme disease, and other genetic, environmental, and infectious factors must be involved. Probably the best risk-conferring candidate is the HLA haplotype, since both of the aforementioned studies were performed with patients who expressed HLA class II alleles associated with autoimmunity in the affected organ compartment. However, studies investigating the association between HLA haplotypes and chronic Lyme disease have up until now been lacking, and a clear association between certain HLA alleles and organ involvement other than the joints, e.g., the brain and/or spinal cord, has not yet been documented.


Apparently, NINDS' Roland Martin did not hear about the other, secret, Mark Klempner's, MS haplotype (HLA-DQB1*0602):

Or maybe he did, and that's the reason he went home to Germany.

I point out that brains are somewhat more significant than knees except to Yale staff, who have suggested (literally) that the brain should be thrown out. 

Comparison between the Western Blots of 1) people who have Steere's haplotypes or a genetic link to having a hypersensitivity or allergy reaction to Borrelial antigens (Lyme arthritis or acrodermatitis) and 2) normal people.  You have to actually look at this graphic, and then the whole cryme will be clear to you.



Ya wanna go to the USDOJ "reading room" (although there not be evidence that the US Attorney's read anything other than Woman's Day, or People, or Soap Opera Digest, due to the influence of eunuch-fication of the DOJ by the likes of the fairy-ass, girly-man-gossip and evil twerp, Karl Rove) and read about what is the nature of a "false claim" against the United States, because that's what "Lyme Disease" is, as will be shown in this chapter.

921 False Claims

[Allen Steere's Strains Shenanigans in Europe to create the bogus Lyme Disease diagnostic standard; Lyme is simply part of the Relapsing Fever Group.  "To know Relapsing Fever is to know medicine."]

Title 18, United States Code, section 287--the false claims statute--provides in part:


    Whoever makes or presents to any person or officer in the civil, military or naval service of the United States, or to any department or agency thereof, any claim upon or against the United States, or any department or agency thereof, knowing such claim to be false, fictitious, or fraudulent, shall be imprisoned not more than five years . . . .

See Project, Tenth Annual Survey of White Collar Crime, 32 Am. Crim. L. Rev. 137, 309-32 (1995)(discussing § 287). There is also a companion conspiracy statute, 18 U.S.C. § 286.


In 1863 Congress enacted a false claims and statements statute "in the wake of a spate of frauds upon the government." United States v. Bramblett, 348 U.S. 503, 504 (1955). As originally enacted the statute penalized presentment "for payment or approval" of false claims upon or against the Government. . ." (Bramblett, 348 U.S. at 504) as well as false statements made "for the purpose of obtaining, or aiding in obtaining, the approval or payment of such claim." On June 25, 1948, the statute was divided into 18 U.S.C. § 287 and 18 U.S.C. § 1001, respectively. 62 Stat. 749.


The Section 287 statute is designed to "protect the government against those who would cheat or mislead it in the administration of its programs" (United States v. White, 27 F.3d 1531, 1535 (11th Cir. 1994)), and it has been employed to combat fraudulent claims filed under numerous Federal programs, including Medicare and Medicaid. White (Medicare claims by a chiropractor); United States v. Hooshmand, 931 F.2d 725, 733 (11th Cir. 1991)(Medicare claims for tests); see also United States v. Abud-Sanchez, 973 F.2d 835, 836 (10th Cir. 1992)(Medicare and Medicaid claims); United States v. Siddiqi, 959 F.2d 1167, 1171-72 (2d Cir. 1992)(physician submitted Medicare claims for a period when he was out of the country); United States v. Nazon, 940 F.2d 255, 258, 261 (7th Cir. 1991)(Medicaid claims for lab work not done); United States v. Beasley, 550 F.2d 261, 263-64 (5th Cir.), cert. denied, 434 U.S. 863 (1977)(claims for costs of clinics never built).


Recent Slam-o-Grams to the Steere cabal:
SUNY's Volkman calls UConn's Feder/Zemel liars over the seronegative Lyme assay

MEDLINE LINK:  Allen Steere using the T-cell assay over which Volkman is furious at Zemel/Feder to determine that nearly half his lab workers had inhaled spirochetes

Steere treats his kind of Lyme disease with long term antibiotics:

Czech Republic: "US Research (Yale and UConn)  on Borreliosis is incomprehensible and stupid" (translation:  We're furious that we've been hoodwinked over CDC bullshit)

UConn's Zemel and Feder deliberately harm Czech children

Jemzek rebuttal to Zemel/Feder: "scientific fraud"  ← US Army tells soldiers to be careful not to inhale desiccated spirochetes, LOL (page 13 of the .pdf):



Chapter 3 of Cryme Disease ;

Chapter 3, The Scientific Fraud Crime Committed by Allen Steere in Europe
to facilitate the bogus definition of "Lyme Disease" as an autoimmune bad knee (whoring for BigPharma), needing no intravenous IV treatment (whoring for Kaiser-Permanente, et al).

Previous Chp 2, McSweegan and Goldwater
Subsequent Chp 4, What happed at the Jan 2001 LYMErix Hearing


CDC "officer" Allen Steere went to Europe to set up the FALSE CLAIM that his method (we call it simply "Dearborn," the two-tiered ELISA/Western Blot schema) to diagnose a "case" of "Lyme Disease" was scientifically valid, and the resultant RICO or monopoly on grants, vaccines, tests, and test kits for vector-borne diseases (an "enterprise" called the ), in cahoots with Kaiser-Permanente.   Kaiser bailed out the financially floundering New York Medical College, and is still there, training MDs who are provided to the New York State Medical Board as "experts" against the realists.

What Allen Steere did in Europe in 1992-3, revealed in this chapter, resulted in the 1994 CDC Dearborn, MI, farce of a conference and the bogus testing which facilitated the intended monopoly.    OspA or the LYMErix "vaccine," is the key to the "controversy."

Compare what Allen Steere did (discussed in this chapter) at the same time, 1992, to what Fikrig and Magnarelli were doing as regards enhancing a flagellin method, in 1992, discussed in CHAPTER 1.


The CDC apparently thinks we can't see that the 1986-Steere roll-out of "10-11 bands that occur over months to years" is not equal to the 1993-Steere or the 1994 Dearborn version: "most of the 10-11 bands occur together in first few months of Lyme infection and we don't know what happens after that, since we're only talking about EARLY LYME diagnosis."


If Lyme is a Relapsing Fever organism, then some aspect of it gave it that name.  That something was the spirochetes' chronic production of new surface antigens, rendering previously made antibodies, useless.  This is the same process by which Alan Barbour "selects" "mutants."  Barbour (or anyone) can grow some spirochetes in a dish with the antibodies specific to the surface antigens he wants to pharm out of the bug.  In a chronically infected mammal, there will always be spirochetes producing new surface antigens that are changing all the time.  Whenever new antigen is produced, new antibodies are produced, and those new antibodies are IgM type.  If Alan Barbour selects mutants, and antibodies do no good, then a vaccine is impossible, especially if it is true as Yale's veterinarian Stephen Bartold (and all the older, pre-Steere literature) says, that these spirochetes are coated in a slime layer which keeps them protected from immunological attack (REF):

"He finds that during the early stages of infection, B. burgdorferi avoids immune detection by decreasing its expression of surface proteins or cloaking its expressed surface proteins under a layer of slime. "It's using some sort of stealth-bomber-type mechanism," he says. Or, using another diversionary tactic called blebbing, the spirochete can pinch off bits of its membrane in order to release its surface proteins. Explains Barbour: "It's like a bacterial Star Wars defense program," in which released surface proteins might intercept incoming host antibodies keeping the spirochetes safe from immunological attack."
1996, The Crooks.


We, the victims of these crimes and incompetence, are aware that the specific Lyme Disease cabal established itself at New York Medical College in 1990, after the publication of the 1989 Reviews of Infectious Diseases (the former journal of the Infectious Diseases Society of America) special supplement on spirochetal disease (Supplement 6).  Allen Steere began publishing obvious research garbage about "Chronic Lyme" disease around that time.  Anyone following these sequence of events in the crime would find it hard to believe that the crime of "Lyme Disease and LYMErix®" was any accident or the result of research stupidity.  It is research fraud. 

The overall driving force behind these crimes was to TAKE all the funding money and OWN and GRAB all the DNA and LIE and TRASH the Lyme victims and DESTROY all the Lyme treaters with a ferocity never seen before or imagined.  The behavior of the Lyme disease criminals knows no unethical limits.  They will and did cross every red line.  The evil here is insidious and large, and very, very deliberate.


DEARBORN and the 1986- and 1993- versions of Allen Steere:  

The current (2006-2007) CDC-sanctioned testing for hard-tick Relapsing Fever had been changed by the perpetrators into the non-existent entity “Lyme Disease” in 1994 at the CDC's Dearborn, MI, meeting with some goofball labs- standards entity which is apparently brainless and powerless.

The CDC's 1994 Dearborn "two-tiered" testing criteria is meant for the diagnosis of “early Lyme,” or within the second month of illness to less than six months into illness. 

"Two tiered" testing means:  First, one has an ELISA test or a general, or slop-o-metric, screening test to detect the concentration of antibodies in the blood to see if the victim has late stage chronic severe arthritis in a knee with the very, very high antibody concentration. (Steere's kind of autoimmune Lyme is a genetically-linked hypersensitivity reaction, like asthma or Type 1 diabetes). 

If one has a positive ELISA result, one may then proceed to Western Blotting, but the problem is that the ELISA screens out all but the extraordinary cases of a loud, red, swollen arthritis in a knee and misses all of the neurologic or regular Lyme cases.

That is, in order to have "Early Lyme," one must first have "Late Lyme Arthritis in a knee," according to Allen Steere and the cabal and is now the CDC's accepted testing protocol.

We don't know of any more highly regulated testing anywhere in the US.  If you, the lab owner, decided to perform actually scientifically valid testing for Lyme, the CDC will come after you and try to shut you down.  You will recall from the Hartford Courant interview with Yale's Durland Fish:

"He proceeds down the list, name by name: "Totally bogus." "He killed one of his patients." "They tried to shut him down." Words like "crackpot," "wacko," "buffoon" and "fraud" pepper his discourse.

The two tiered testing schema was designed to SCREEN OUT all the neurologic cases of Lyme with the first test.  Some insurance companies even state that they won't pay for a Western Blot if the ELISA is negative.  This is scientific fraud with intent to cause harm since Lyme progresses into all sorts of very severe neurological diseases and death.

The Lyme ELISA only detects late Lyme arthritis, with a full-blown swollen knee.  Late Lyme arthritis in a knee is caused by a hypersensitivity or allergy reaction or too many antibodies to OspA.  The too-many-antibodies against OspA allegedly cross reacted with knee tissue, but now Allen Steere's mob say that OspA is a superantigen for certain persons.  That is, people with a certain genetic background will super-bind the OspA antigen into their HLA molecules, causing an almost toxic level of antibodies (chronic stimulation) or the antibodies exist as a free, toxic immune complex (antibody is bound to the free antigen), and suffer the associated immune response (downstream mechanisms after antibody production that is tissue-damaging).  Other researchers counter that if the Steere superantigen model was true, the phenomenon would not be limited to a knee.

Again, if a Lyme victim passes that test, the ELISA, and has a late Lyme arthritis in a knee, they may graduate on to having a Lyme Western Blot test.  As explained in the first few chapters, one does not validate a test by saying, for example, "Only 7 ton elephants may be diagnosed as elephants, and that 200 pound baby elephants may not diagnosed and treated as elephants."  You can still see the baby elephant and know it is an elephant by its specific features, and know it is there (that being the point of "diagnosis" or "identification" of the offending organism). 

And this is where these evil-and-viciousness-related stupid Lyme criminals are really scary-  Lyme is a bioweapon in the "stealth disabler" class, causing immune-suppression-related and/or immune-dysregulation-related outcomes as we will see in the Plum Island and OspA Chapters.  Thankfully we can't sneeze it on each other (but spirochetes can be inhaled as we will see). 


We will see in later chapters that the pathology associated with the presence of spirochetes is hardly limited to the production of cross-reacting antibodies.  In other words, no one cares if they have "too many OspA antibodies," they only care to know if what is making them sick is something treatable with something so simple as antibiotics.

Again, 5 of the of the 10-11 early-Lyme, pre-1987-Steere, antibodies which occur "over months to years" must now  - after 1994 and after the bogus CDC Dearborn MI conference - occur within the first ~6 months of infection in order to be a case of "Lyme Disease," since that's what CDC-type conferences are about. 

That is, where once Lyme was thought to be a Relapsing Fever, characterized by "changing and expanding IgM antibodies that occurred over a fairly long time and represented persisting infection," it suddenly has been changed to: "5 of 10 IgG bands have to all occur at once" for a person to be able to have a diagnosable (treatable) case of "Lyme Disease." 

When the CDC's 1994 Dearborn conference was proposed and announced, some labs thought it was about standardizing the method and not to create a new interpretative platform.  That is, to any real scientist, to "standardize a method" means, 1) Everyone uses the same equipment and concentration of components in the electrophoretic gel, 2) the standard should be the same (use low passage strains of SPECIFIC organisms; Borrelia that express OspA, B, C, Borrelia-specific flagellin and other specific known antigens that produce antibodies in most humans), 3) Everyone should agree that the assay of the proposed analytes is a method that does not co-elute more than one analyte.  The method should be validated in that the concentration of one analyte is not erroneously added to at the same retention time or kilodalton apparent molecular weight by another (masked) analyte.

The following is the publication of the self-alleged results of the CDC's Dearborn, MI, self-alleged conference:


Notice to Readers Recommendations for Test Performance and Interpretation from the Second National Conference on Serologic Diagnosis of Lyme Disease


The Association of State and Territorial Public Health Laboratory Directors, CDC, the Food and Drug Administration, the National Institutes of Health, the Council of State and Territorial Epidemiologists, and the National Committee for Clinical Laboratory Standards cosponsored the Second National Conference on Serologic Diagnosis of Lyme Disease held October 27-29, 1994. Conference recommendations were grouped into four categories: 1) serologic test performance and interpretation, 2) quality-assurance practices, 3) new test evaluation and clearance, and 4) communication of developments in Lyme disease (LD) testing. This report presents recommendations for serologic test performance and interpretation, which included substantial changes in the recommended tests and their interpretation for the serodiagnosis of LD.

A two-test approach for active disease and for previous infection using a sensitive enzyme immunoassay (EIA) or immunofluorescent assay (IFA) followed by a Western immunoblot was the algorithm of choice. All specimens positive or equivocal by a sensitive EIA or IFA should be tested by a standardized Western immunoblot. Specimens negative by a sensitive EIA or IFA need not be tested further. When Western immunoblot is used during the first 4 weeks of disease onset (early LD), both immuno- globulin M (IgM) and immunoglobulin G (IgG) procedures should be performed. A positive IgM test result alone is not recommended for use in determining active disease in persons with illness greater than 1 month's duration because the likelihood of a false-positive test result for a current infection is high for these persons. If a patient with suspected early LD has a negative serology, serologic evidence of infection is best obtained by testing of paired acute- and convalescent-phase serum samples. Serum samples from persons with disseminated or late-stage LD almost always have a strong IgG response to Borrelia burgdorferi antigens.

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).

The details of both plenary sessions and the work group deliberations are included in the publication of the proceedings, which is available from the Association of State and Territorial Public Health Laboratory Directors; telephone (202) 822-5227.



Engstrom SM, Shoop E, Johnson RC. Immunoblot interpretation criteria for serodiagnosis of early Lyme disease. J Clin Microbiol 1995;33:419-22.

Dressler F, Whelan JA, Reinhart BN, Steere AC. Western blotting in the serodiagnosis of Lyme disease. J Infect Dis 1993;167:392-400.

The apparent molecular mass of OspC is dependent on the strain of B. burgdorferi being tested. The 24 kDa and 21 kDa proteins referred to are the same.

Disclaimer   All MMWR HTML versions of articles are electronic conversions from ASCII text into HTML. This conversion may have resulted in character translation or format errors in the HTML version. Users should not rely on this HTML document, but are referred to the electronic PDF version and/or the original MMWR paper copy for the official text, figures, and tables. An original paper copy of this issue can be obtained from the Superintendent of Documents, U.S. Government Printing Office (GPO), Washington, DC 20402-9371; telephone: (202) 512-1800. Contact GPO for current prices.

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The CDC apparently thinks we can't see that the 1986-Steere roll-out of "10-11 bands that occur over months to years" is not equal to the 1994 Dearborn version: "most of the 10-11 bands occur together in first few months of Lyme infection and we don't know what happens after that, since we're only talking about EARLY LYME diagnosis."


This is Steere's first, 1986, standard/observation of serology set  full text link

J Clin Invest. 1986 Oct;78(4):934-9. Links

Antigens of Borrelia burgdorferi recognized during Lyme disease. Appearance of a new immunoglobulin M response and expansion of the immunoglobulin G response late in the illness.

Craft JE, Fischer DK, Shimamoto GT, Steere AC.

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.  PMID: 3531237 [PubMed - indexed for MEDLINE]


As an aside, Mark Klempner, CDC "officer," and now a Boston University apprentice provost, alleges that the meaning of: "only 78 out of 1800 (4%) persons" who are "Chronic Lyme" victims, and who all have been treated before with antibiotics - yet still have the CDC bogus positive early Lyme/late Lyme IgG blood testing criteria of Allen Steere  - means that the probability that a person who claims to have Chronic Lyme "is 96% likely to be a kook."  An antibiomaniac.  A Munchauser.  A Lyme paranoiac.  No one knows what kind of victims Klempner captured and abused in his "Chronic Lyme is imaginary but cured by the placebo effect of antibiotics 'study,'" since the Steere early Lyme/Late Lyme criteria for a "positive case of Lyme," has never been studied, much less validated for late, treated, chronic Lyme.  The victims or class of people Mark Klempner claimed to have assessed for antibiotic efficacy, should have been "seronegative," due to the host adaptation of their own particular spirochetes and the immune suppression caused by chronic infection and the chronic blebbing.


Amazing as it is to believe, few people realize that the CDC IgG method to diagnose “Lyme Disease” is only to be used in the first few months after infection, but that also,  "IgG means past infection and not a treatable case," according to Imugen Labs (Norwood, MA). 

That is, the 1994 Dearborn (Dressler/Steere) early Lyme criteria to be used to diagnose early Lyme comes from an imaginary standard that was revealed (to Allen Steere) as a series of antibodies developed against antigens "over months to years," but IgG means old or previous infectious, so most people will not have a treatable case of Lyme no matter what the circumstances.  IgG means past infection.  And no treatment.  IgM means current.  But almost no IgM bands may be identified and reported towards a positive test.  Which means no treatment.



Most MDs don't realize that this bogus testing standard is to not be used for persons who have been sick for more than a year because the spirochetes become “host adapted."  That is, spirochetes that arrive into a person fresh from a tick are expressing different surface antigens than those spirochetes which have been cohabitating with their human victims for years.  Therefore, the long-infected person produces different antibodies than the newly-infected. 

Not only are these later, host-adapted antibodies not predictable, not detectable, and not occurring early in the disease (and thus will yield a negative test result), but due to the immune suppression cause by these shed Osps (CHAPTER 15 RELATED PLUM ISLAND GOODIES) - the Alan Barbour "Star Wars blebbing" - has the effect desensitizing its human victims or tolerizing the immune system to them, with the result that antibodies are not produced.  The antigen presenting molecules or HLA molecules are down-regulated.  If the blebs or the surface antigens can not be presented (presented to B cells, which make antibodies) because the HLA (human leukocyte presenting antigen) molecules have been removed, fewer antibodies will be produced.  This is also important because the blebs were made into "vaccines," one of the patents for which was owned by Alan Barbour (ImmuLyme), who said of them (besides the "rich vein of gold from which to mine virulence determinants" comment),

"One of the lipoproteins, OspA, has already been crystallized and structurally characterized5, and it is undergoing human field trials as a vaccine against Lyme disease, although no one yet knows what it does." - because the adverse events were deliberately not reported to the FDA.

These late, undetectable, antibodies are not detectable or become not detectable because 1) everyone has their own special collection of spirochetes' antibodies (which have become host-adapted and are constantly undergoing antigenic variation), 2) everyone has their own genetically-determined tendency to find certain kinds of antigens irritating (HLA differences), although there are clearly clusters or genetic histories are shared by peoples (see the "race-specific bioweapons" comment in the Israeli's PNAC document), 3) many people, especially the sickest- usually "seronegative (seronegative to the imaginary Steere Dearborn criteria case)" - are likely to be multiply-infected with the other immune suppressing organisms, Babesia and Ehrlichia (ref Dave Persing), and have the neurologic kind of Lyme [since only the knee-kind tests Steere/Dearborn positive; only the knee-kind of Lyme people make sufficient antibodies and "may even be called immune-competent,"  according to Vijay Sikand, MD (East, Lyme, Connecticut, at the 1998 LYMErix FDA meeting)], and 4), there is now an identified mechanism of immune suppression, the tolerization to these spirochetal antigens, turning off the immune system to these types (triacyl Palmitoyl 3 Cys lipopeptides like OspA, the vaccines), rendering some people perhaps permanently seronegative and SERONEGATIVE to or TOLERANT TO or CAN'T FIGHT OFF OTHER INFECTIONS that bear the same type of antigens.

We will see in the Biomarkers chapter that it was known in 1992, that the lymphocytes of chronic Lyme victims look like Epstein-Barr transformed or mutated cells.  That's yet another can of worms which we think is co-related to LYMErix outcomes and cancer.  Again, the pathological outcomes of Lyme have all been subjected to the Negative Data Rule:  Don't look for or fund the research into information you don't want to discover or want revealed.  The most well-known sufferers of the Negative Data Rule are the Gulf War Illness Veterans.  Naturally, the keeper of this fraud is the British psychiatrist Simon Wessely.  Whether or not these Lyme crimes are bioweapons-related or just evil, profiteering frauds tripping over their own dicks may be resolved by looking deeper into Simon Wessely's history.  One thing we will find out about Simon Wessely is that he knows absolute zero about ethics or integrity, but his counterparts in the USA will be subject to the same scrutiny.

Some of the other infections which bear these same type of antigens as LYMErix or the shed Osps are HIV, Foot and Mouth Disease, Tuberculosis, mycobacteria, and mycoplasma.

A huge can of worms. 

Maybe the AMA can tell us about it. 

Maybe not.

. mycoplasma associated with arthritis and immune suppression outcomes.


Related to the immune suppression/dysregulation outcomes and according to CDC's bioweapons officer Alan Barbour in his US Patent 6,719,983,,719,983

2.1 Methods of Treatment

"An important aspect of the invention is the recognition that Borrelia VMP-like sequences recombine at the vls site, with the result that antigenic variation is virtually limitless. Multiclonal populations therefore can exist in an infected patient so that immunological defenses are
severely tested if not totally overwhelmed."

TRANSLATION:  "The Lyme infected person's immune system could be completely overwhelmed by their chronic infection with multiple 'clones' of spirochetes, all of which continuously undergo antigenic variation (negating the validity of the term "clone") creating seventy five bahzillion different antibodies which overwhelm the immune system.  But everyone who says they're chronically ill, but who don't have Dearborn Lyme, is a hypochondriac and please read my totally unreferenced book entitled, 'Lyme Disease, the Cause, the Cure and the Controversy,' and never mind the fact that I am a CDC clone lying profiteer, since there are no other CDC officer species."

--Homo bovis excrementii; CDC Officer Alan Barbour


Therefore, due to antigenic variation and likely being infected with multiple types of spirochetes (burgdorferi, or barbouri, or wormserii, or popeyei, etc) and over the longer term, becoming immune-suppressed/dysregulated, the only way to see if a chronically infected person is chronically infected using an antibody method, is to capture some spirochetes from said chronically infected person, grow a few, and use that current-human-spirochete-slurry to Western Blot the same infected person and see if they have antibodies against their own spirochetes.  (But they might not, due to the effect of OspA or Pam3Cys-related immune suppression.)

We could only expect such stupid science from the Steere camp.  We know that if they performed such a stupid science experiment, the Steere camp would still try to tell the patient from whom spirochetes were extracted that their antibodies were only IgG antibodies, and that that meant that the patient only has past-Lyme disease or is therefore no longer infected and does not need treatment.

'Since no one ever needs treatment.  'That being the part about Kaiser-Permanente rescuing the financially failing New York Medical College in return for the opportunity to train the New York Office of Medical Conduct's "experts" on "Lyme disease" in preparation for the Bush Senior-Karl Rove-esque harassment of Lyme treaters and establishing the racketeering cabal, the "American Lyme Disease Foundation."

The entire point of the erroneous and criminal final solution dictated to us from Dearborn "conference," is that "We should look for 5 of 10 IgG bands and ignore most of the IgM bands, because the presence of IgM bands is a phenomenon that demonstrates persisting infections, according to the 1986 version of Allen Steere."  If every single iota of medical malarkey from the Steere camp were an H2O molecule, we'd all have wished we built arks and captured pairs of animal species (not ticks).

Examples of explanations of host-adapted spirochetes or the proof that late neurologic Lyme will never test positive to the CDC Dearborn method (and these are repeated in the PRIMERSHELLGAME chapter, since the fraud in testing by antibody is related to the fraud in testing using DNA and RNA methods):

1) Pachner and Brains, 1990  "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. "


"By repeatedly coincubating spirochetes with primary mouse lymphocytes that were immobilized by adherence to immunomagnetic beads, we were able to preferentially enrich cultures for or against bacteria with constitutive affinity for murine B and T cells."

3) Using monoclonal antibodies "to select "mutants" in vitro- Barbour

4) Antibody selection: Fikrig discussing OspA’s uselessness


5) "New antigen milieu" from Fikrig re brains

If Fikrig claims there is new antigen expression over time as the spirochetes host-adapt, and the Yale OspA vaccine was to be given annually due to the fact that the IgG antibody concentration fades (this was probably due to the immune suppression it caused, as revealed in the Plum Island chapter), and if Steere claims that only people with his genetic HLA relation to Lyme arthritis maintain a high IgG antibody concentration for "months to years," why does Fikrig not make a public announcement that the new antigen-antibody milieu negates the Dearborn criteria?


The usual case of a chronic Lyme victim is that they have had chronic fatigue and neurologic/brain signs for several years before finding their way to a specialist who understands that the blood testing schema proposed by the 1993 version of Allen Steere, fraudulently accepted by the Centers for Disease Confabulation and accepted by the American Medical Kool-Aid Drunkards Association, is an elaborate concoction of nonsense intended to set up a monopoly on testing for “Lyme Disease” around the OspA vaccine. 

Keeping in mind that the camp are interested only in the profit in vector borne diseases and not in anyone’s better health outcome, “Lyme Borreliosis” – the serologic definition previously established by Allen Steere and the CDC as a Relapsing Fever organism, the diagnosis of which was to be in the performance of serial Western Blots in order to look for "changing and expanding IgM and IgG antibodies" - was spun into "Lyme Disease."


Time hardly flies when you're chronically sick; imagine you're Christ on the cross with the dislocated shoulder; imagine the agony of never having a good day and all of these YEARS have gone by where none of the people whose job it was to investigate and prosecute these crimes, did so, despite being given the evidence.  And so I say:

Way, way back about a hundred years ago in 1992, Allen Steere went to Europe with an illegal high-passage strain of Borrelia- strain G39/40 from Guilford, Connecticut:

Says Alien Steere, from Europe:  "Supernatants from sonicated lysates of whole spirochetes were prepared as described (20).  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 921).  The group 2 strain, FRG [Federal Republic of Germany], was isolated from Ixodes ricinus near Cologne (21).  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."


So, Steere did not find too many antibodies to the B31-associated recombinant Osps A and B in people in Europe, using G39/40 and FRG, as we will later see.  We think these shenanigans with strains and recombinants were the reason Steere went to Europe to perform this crazy nonsense for two reasons:  European journal articles might not be reprinted full-text online such that American researchers could see what he had done (and they were not, I had to go to the Yale Medical Library to get them), and Frank Dressler was a young, innocent, inexperienced lab rat. 

It makes no sense to have done this, when Steere previously (1986) worked this all out, no matter how you look at it.  There was no reason to go to Europe to come up with a new antibody panel/immune response profile.  There was no reason for Americans to have accepted this from Europe, secondly, because the CDC simultaneously claims they lend European researchers no credibility whatsoever. 

The CDC CLAIMS that whatever happens elsewhere does not exist...  (why then did we end up with Willy Burgdorfer from Switzerland and the German scientist, Roland Martin?)...  except for this crazy nonsense by Steere in Europe.


The OspA is/does:

The electronegative core in between the lipid ends and the water-soluble protein end, is what is hyperstimulative about OspA or the Osps.  Without the lipid end, this would not be such a wild, immunostimulatory lipoprotein.  Remember, to a chemist, and now to you the reader, what a chemical compound is, is what it does.  The crooks discovered, but kept secret, the fact that OspA in it's native form was too stimulatory.  This experience with OspA led to its later modification by David Persing at Corixa, who tried to sell an entirely new class of lipopeptides or glycolipids or similar-looking compounds as vaccine adjuvants. 

The following are graphics of the structure of OspA (by Mass-Spec, since you can't recrystalize a lipid). You can see the highly densely lipidated end (water-insoluble) is combined to the protein end (water-soluble), by a highly electronegative cysteine core (molecules speak to you visually; chemistry is sort of like hieroglyphics or Chinese):


and from a Korean journal:

~OspA stuck on an HIV vaccine: 



Here is Dave Persing (Lyme testing RICO patent owner) Corixa's "We modified OspA for use to sell in our adjuvant business because the real OspA is too awful" advertisement which has since been taken off the web, and Corixa has since been purchased by SmithKline:  EMBASSIES_CORIXA_TLR_13_JULY_06.htm

And here is Dave Persing of Corixa talking about how the native OspA proteins are too awful to be used alone as a vaccine in another patent:,800,613

"While not wishing to be bound by theory, it is believed that the efficacy of the prophylactic and therapeutic applications described above are based at least in part on the involvement of the mono- and disaccharide compounds in the modulation of Toll-like receptor activity. In particular, Toll-like receptors Tlr2, Tlr4, and others, are believed to be specifically activated, competitively inhibited or otherwise affected by the non-toxic LPS derivatives and mimetics disclosed herein. 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."


In this instance they are talking about a polysaccharide in place of the protein, but it's the union and the opposing solubilities that are toxic or immunostimulatory or "too immunostimulatory in the native form."

Note that one of the claims for this modified OspA vaccine as an adjuvant or immune-booster is that this could be used for:
7. A method in accordance with claim 2, wherein said infectious disease is a chronic infection.


I don't know of any "chronic infectious diseases," do you?  (Tully, bioweaponeer on mycoplasmas and immune suppression.)



Returning to the issue of Allen Steere's fraudulent experiments in Europe to invent his new idea of what a "positive" blood test for "Lyme Disease" should be:

"High-passage" is almost exactly like George W. Bush.  Too much inbreeding leads to incompetent strains.

The National Institutes of Health’s Rocky Mountain Labs recommended not using high passage strains to diagnose “Lyme Disease" because they drop plasmid expression or drop the expression of specific diagnostic antigens (or fewer bands will show up in a Western Blot).  You can't see the antibodies in the blot even if they're in the blood because they're not in the Western Blot antigen mix for the antibodies to bind to and be detected.

Spirochete cultures that have been passed many times in vitro without being pharmed back into ticks and rodents start growing populations which have lost the ability to infect, because they have lost the code for the surface antigens - the speckles or the Osps or the Vmps or the Vsps - which they use to bind surface molecules on the cells of their hosts.  In other words, they clone themselves badly.  They're, like, couch-potato spirochetes.  Wimpy.

With fewer of the surface antigens spirochetes use to invade tissue and penetrate or adhere to cells, these spirochetes can cause less damage.  Spirochetes are parasites and must take something from the host in order to survive.  The surface antigens encoded on the plasmids help the spirochetes find nice delicious cells to invade and steal metabolic goodies.  They do worse things like destroy cells, too, but for all intents and purposes, they would probably not be as harmful were it not for the immune response.  This we know from the histology studies in monkeys (non-human primates, a term that should not be limited to the hairier guys who walk around on their knuckles, as we've learned from exposure to Lyme crooks in addition to spirochetes).  The monkey nerve damage studies will be included in the Biomarkers section, which is associated with the 1989 IDSA REVIEWS section, since the topic of how sick we are as a result of this scam is too extensive to include with this one really incredible topic, What Allen Steere Did in Europe.

If the surface antigens are dropped, we can surmise that they're less invasive.

Logically, one would want to look at what is the makeup of spirochetes, since that would suggest what are its metabolic needs.  However, these Borreliae spirochetes can apparently adapt to any environment, any mammalian environment, any tissue type as we have previously seen from the David Dorward Rocky Mountain Lab tissue-tropism studies.  Forward advancing studies as to what spirochetes actually do to cause us damage has been inhibited by the Lyme criminals who spend all their energy and our tax-supported grant money on telling us we have no disease for which OspA was their vaccine.

NIH Rocky Mountain Labs, including Willy Burgdorfer, say to use low passage strains to Western Blot because high passage strains drop plasmids- yet high passage strains, G39/40 and FRG were used by Steere to concoct the Dearborn standard: 


The CDC’s diagnostic standard in 1990, before Steere went to Europe, was based on Steere’s own original 1986 observations that Lyme was a Relapsing Fever organism and that the antibody profile for Lyme would change over time, producing new (IgM) antibodies when viewed via Western Blotting.  Under the pretense of “standardizing” all the US testing for Lyme in America, in 1994, the CDC sent out invitations to numerous labs across the country, inviting them to “contribute to the proceedings.”  However, apparently the decision had already been made that the CDC would adopt the new Steere method- the one he developed in Europe with bogus strains that dropped plasmids, and thus, likely, the expression of the OspA-B plasmid- a plasmid replaced with the "American protypical B31 strain's OspA and B recombinant antigens," against which EUROPEANS were blotted.  This would have the effect of creating a new bogus profile from among Steere’s victims that resulted in the current bogus CDC IgG criteria for a positive case of “Lyme Disease” that left OspA and B antibodies (band 31 and 34) out of the standard. 


What the labs invited to the farcical CDC 1994 Dearborn, MI, conference determined, in regard to Steere’s new proposal for an IgG standard were:

1)      Gary Wormser at New York Medical College, "Steere’s method detected 9/59 or only 15% of all cases"

Read carefully what Wormser says in this report:

He says he is assessing the accuracy of what was later to be called the Dearborn Method, the Dressler/Steere proposal, in the field, and he found that the IgG method detected only 9/59 of the Wormser cases.

2)      Imugen's Dearborn submission: "Steere’s method detected 14% of the cases"

[CAPTION] You can see from that graphic where I circled the 14% for the January 31, 2001 FDA Vaccine Committee Hearing (CHAPTER 4), that Imugen was assessing the accuracy of the Steere/Dressler IgG proposal, but that Imugen thought that their antigen-antibody complex capture method was more accurate, or detected more cases.


3)      Igenex, "Steere’s IgG detected 8% of the cases" or misses 92% of the cases.


4)      Wisconsin,  "Steere’s method was 15% accurate" or misses 85% of the cases.


5)      The University of Child Abuse -  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 every Steere band."


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"


Lutheran Hospital said it would be better to standardize the method before standardizing the interpretation of results.  Lutheran Hospital clearly believed this nonsense about Steere's "area curves" (the elephant rule, or the Steere idea that happens to be the reverse of Limit of Detection or Limit of Quantitation as a parameter that is supposed to suggest to those creating and validating analytical methods and the companies who try to sell us very sophisticated and SENSITIVE equipment that we want to detect the LOWEST concentration of stuff, always), made Steere's proposal INSENSITIVE, or would be inappropriate for use on humans or would not detect as many cases of Lyme as possible.

Note that the only place in the entire world, at the current time in history, where you hear anything about how we could improve the testing for Lyme, is on ActionLyme.  It's a repeat or a rebroadcast of the crooks' work from the early 1990s.  Think about what that means in terms of the integrity and competence of your MD or any MD you know.  Not a single MD in America felt obliged to look at this data and our complaints and report this crime to the proper authorities.

The above is the very essential graphic for interpreting Steere's Elephant Diagnostics Rule.  He tried to assert that the higher the antibody concentration, the more "valid" the test, falsely claiming that by "narrowing the number of persons who will test positive," that makes his test more SPECIFIC, and claimed that "the higher the concentration of antibodies in the blood makes the test more SENSITIVE," when as we know, SENSITIVITY is a function of LIMIT of DETECTION or the ability of the test to detect very low concentrations of analyte.  

The new Steere fantasy term "receiver operating characteristic" is not a criterion for the validation of an analytical method.  It means the opposite of sensitivity or the goal of detecting increasingly lower quantities of analyte.

Cross apply that to what you know from Chapter One on Chromatography Methods Development and Validation.  No one in their right mind would buy a chromatography detector that detects less than what you can see with your own eyeball.  No one goes hunting for viruses with a magnifying glass.  We know from Chapter One, that by 1991, Yale's Erol Fikrig already made the most common band to ALL CASES OF LYME, band 41, SPECIFIC by pharming sections of the DNA from Bb flagellin into E. coli, producing a protein fragment, and comparing the antibodies from the blood of people infected with known spirochetal or flagellated infections and found that he had captured a fragment of recombinant flagellin that was SPECIFIC to Borrelia burgdorferi, or only detected Lyme-infected patients. 

Yale also claims that their recombinant vaccine, OspA or LYMErix, was SPECIFIC enough to prevent Lyme, so why isn't one specific antibody specific enough to detect Lyme?  Why was OspA left out of the diagnostic standard, if to have that antibody from a vaccine, that was supposedly specific enough to PREVENT "Lyme Disease?"

You can see how silly Dressler/Steere is on its face.  You need 5 out of 10 band in order to be diagnosed with a case of Lyme, but you only needed one antibody, band 31, to be PROTECTED against Lyme, according to these loonies and accepted as a truism by the American Medical Association and all of their related incompetent MDs..

The reality is that each antibody band is as ACCURATE for diagnosis as its assigned percent specificity.  If we had Steere at the helm, detecting Anthrax during the Mossadesque Anthrax-mailing stunt in October, 2001, well, nobody would be too happy.


10)  MarDx Labs – recommended adding bands 31 and 34, but were given Steere-Dressler  positive / arthritis-positive blood samples to qualify their test strips.  MarDx was contracted to provide blot strips for both the ImmuLyme OspA vaccine trails and the LYMErix OspA trials.  The ImmuLyme trial started in March of 1994 before Dearborn had taken place, but the trial administrators claimed they were using the Steere-Dressler proposal for the interpretation of a "positive" result (or vaccine failure).

Later we learned the same perpetrators of the ImmuLyme trial who were using MarDx blot strips admitted that they could not read their Western Blots in OspA-vaccinated people:

Sigal:  "Hmm.  How amazing.  The Western Blots are unreadable in OspA-vaccinated people, even though I reported that ImmuLyme was 92% "safe and effective" two years ago, heh, heh, I hope nobody notices..." = ImmuLyme Trial


11)  CDC Atlanta, at their own conference, talked about mouse antibodies and not human antibodies.  The mouse criteria was 2 out of three from OspC, 16 kD, 17.9 kD.


Says the CDC, "DON'T MISS THE OPPORTUNITY TO PARTICIPATE IN THE PROCEEDINGS after which we intend to blow you all off!!  heh, heh"


So, who was there and who said we would adopt this Steere in Europe method?

From the Dearborn booklet:

CDC officer Alan Barbour, owner of the ImmuLyme patent, a clear conflict of interest
Ray Dattwyler who said we should perform serial Western Blots to assess OspA outcomes.

Arthur Weinstein, member of the Kaiser cabal
Edward McSweegan, who initiated the RICO cabal by trashing the US Navy for his good buddy Durland Fish
CDC officer Allen Steere, formerly at Yale (owner of the LYMErix patent) - clearly to approve his own nonsense, perhaps due to his relationship with Imugen, one of the two main RICO labs, L2 Diagnostics being the other
Russell Johnson, formerly an advisor to the cabal and who knew more about spirochetes than probably anyone, edited the 1976 textbook, Biology of Parasitic Spirochetes, and who claimed in the very first patent for a Lyme vaccine that Lyme was chronic due to persisting infection and he mentioned congenital Lyme deaths in that patent.  In other words, it made no sense at all for Russell Johnson to be hanging out with these crooks.
Raymond Ryan at the University of Child Abuse, who published that strain B31 expresses little or no OspC.


The reason Steere's Dressler/Steere Western Blotting recommendations performed so poorly was because Steere decided that "Lyme disease" would be a genetically-linked autoimmune arthritis in knee.  Because Lyme disease is not a genetically linked autoimmune arthritis in a knee, LYMErix was not a vaccine and came off the market.


The following is an excerpt from the Dressler/Steere report where Steere used high passage strain G39/40 with the recombinant antigen Borrelia burgdorferi strain B31 (no OspC in it, which means the OspC response below was from the FRG and G39/40) bands 31 (OspA) and 34 (OspB) to leave OspA and B out of the diagnostic standard:

[CAPTION] 1993 Dressler, Steere report where OspA and B were left out of the diagnostic standard by using a high passage strain G39/40 (but comparing European blood to the Osps A and B to American strain B31) and is the basis for the current CDC IgG standard criteria to have a diagnosis of "Lyme Disease."   This is part of the submission by Kathleen M. Dickson of southern Connecticut to the FDA Vaccine Committee on January 31. 2001.  It is part of the public record. 

As you can see, the one band that most people had, even in the hands of Allen Steere, was band 41, in both IgM and IgG.  Allen Steere did not care, ever, about patient outcomes, as we will see in an exclusive report on Allen Steere's abuse of the psychiatrist Michael A. Schwartz.  

The Psychoanalysis of Allen Steere, in summary form: "DSM IV : THE EVIL, ABUSIVE BASTARD, ALLEN STEERE, CAUSES LYME RAGE;  as in 'If I see that bastard again I am going to punch him right in the face.'"


The following snippet comes out of the other Steere in Europe report (Antibody in European Lyme Borreliosis), where you can clearly see that each manifestation of the disease has a very different antibody panel. We claim that it is absurd to create a standard that knowingly leaves people out of the detection ranges.  We think it is absurd to even begin to think of creating a test for which only the people with a hypersensitivity response are allowed to be diagnosed as positive.  At Dearborn, almost all of the IgM bands that were accepted for IgG bands were left out of the potential contribution to identifying a case of Lyme.  (Let's face it- Lyme meningitis is the most awful case of Lyme.)  We claim that an ELISA or a titer is not only obsolete, but not appropriate for an immune-suppressing disease, and that you only need one specific antibody and it could be specific band 41.  At this time, by 1992-1993, Steere had already acknowledged that there was an MS form of Lyme, and JJ Halperin has already proven there was a Lou Gehrig's Disease form of Lyme:


From the report submitted by JJ Halperin in September 1989 on what the paired serum (blood) and spinal fluid Western Blots (the faint pencil lines are mine) of people with the Lou Gehrig's Disease version of "Lyme Disease":

[CAPTION] These ALS patients look like they only have bands 41 and maybe 93, and I bet they now would test negative to Steere's Dearborn Lyme, which will be the central homicide charge against Allen Steere and whoever claims the Dearborn method is either valid, accurate or sensitive, to include claims that the "ELISA is sensitive."

"Of 19 unselected patients with the diagnosis of amyotrophic lateral sclerosis (ALS) living in Suffolk County, New York (an area of high Lyme disease prevalence), 9 had serologic evidence of exposure to Borrelia burgdorferi."

So, there is no question that Lyme is deadly, that JJ Halperin knew it was deadly, and that the Steere/Dearborn method would not detect these people until it was too late and they were on their way to dead.



It is possible - check, VERY LIKELY - that by using a bogus "high passage" strain, Steere actually created the low percentage of patients with OspA antibodies intentionally.  Ask yourselves a question:  What in the world would be the reason for using high passage strains, if not to change the proposed antibody panel?

The profile Steere "developed" would not be accurate or scientifically sound no matter how you look at it.  In this Dressler/Steere table (above; given to the FDA Vaccine Committee and is part of public record), antibodies to OspA (band 31 kD) and OspB (34 kilodaltons) suddenly are not as prominent as Steere first observed and reported in 1986 where he said A and B bound prominently to antibodies in Lyme arthritis.

We suspect that that was because they knew they were going to have an OspA vaccine trial, and that blots were unreadable in vaccinated persons unless Western Blotted with a strain of Bb that had no OspA-B plasmid in it,  especially since the Phase I and II trials were underway in 1993.  One would suspect that somewhere along the way in the early, Phase I and II, human trials, someone would have Western Blotted the blood of a vaccinated human and discovered the blot-smudging David Persing and Robert Schoen reported in 1996 and David Persing and Lenny Sigal in 2000. 

We think they knew about the blot smudging earlier than 1996.

There is no other explanation for why Steere went to Europe with bogus high passage strains in the first place, and why in the second place, he would have developed a test that conveniently allowed for the RICO labs (later chapters) to be the only people allowed to Western Blot OspA-vaccinated people (the 1996 patent developed by David Persing of Corixa and Yale's Robert Schoen) - a monopoly on blood and all the patentable goodies in it.  The most obvious question of all is why they thought they should have a vaccine against "Lyme Disease" that Steere and Dressler tried to allege is barely relevant to the infection, OspA, as this truly "bogus article," the Steere/Dressler panel, asserts.  It looks to be due to narrowing the disease definition to just the Steere-alleged Aspirin disease (OspA autoimmunity) because of Steere's and the cabal's association to BigInsurance - Kaiser at New York Medical College (autoimmune knee-diseases do not require intravenous ceftriaxone).  It is also rather routine and rather obvious that one would assess any vaccine outcome by using a different antigen than the vaccine, if the disease is detected by an antibody test.

It wasn't until two years after LYMErix was approved that we learned that none of the Western Blots were readable when using a regular normal spirochete with the OspA-B plasmid in it. 

The 2000  "Whoops we can't read our Western Blots in LYMErix vaccinated people" report was published by the same author- David Persing, owner of the 1996 RICO monopoly patent (the RICO monopoly patent, in 1996, 6,045,804), and he was re-reporting the same "unreadable blots" phenomenon that Persing reported 4 years earlier, in 1996.  Note that in between, in December 1998, the FDA approved LYMErix and it was put on the market the following spring.  These crooks never told the FDA that they had no way to validly assess whether or not LYMErix or ImmuLyme prevented Lyme, but they reported 76 and 92% "safe and effective" vaccines anyway, in the journals in 1998.


Note, and this is extremely important:

Ann Intern Med. 1983 Jul;99(1):76-82.

The early clinical manifestations of Lyme disease.

Steere AC, Bartenhagen NH, Craft JE, Hutchinson GJ, Newman JH, Rahn DW, Sigal LH,
Spieler PN, Stenn KS, Malawista SE.

Lyme disease, caused by a tick-transmitted spirochete, typically begins with a
unique skin lesion, erythema chronicum migrans. Of 314 patients with this skin
lesion, almost half developed multiple annular secondary lesions; some patients
had evanescent red blotches or circles, malar or urticarial rash, conjunctivitis,
periorbital edema, or diffuse erythema. Skin manifestations were often
accompanied by malaise and fatigue, headache, fever and chills, generalized
achiness, and regional lymphadenopathy. In addition, patients sometimes had
evidence of meningeal irritation, mild encephalopathy, migratory musculoskeletal
pain, hepatitis, generalized lymphadenopathy and splenomegaly, sore throat,
nonproductive cough, or testicular swelling.
These signs and symptoms were
typically intermittent and changing during a period of several weeks. The
commonest nonspecific laboratory abnormalities were a high sedimentation rate, an
elevated serum IgM level, or an increased aspartate transaminase level. Early
Lyme disease can be diagnosed by its dermatologic manifestations, rapidly
changing system involvement, and if necessary, by serologic testing.

PMID: 6859726 [PubMed - indexed for MEDLINE]

Steere first said Lyme Borreliosis was a systemic disease and acknowledged neurologic outcomes.  Then he said in 1986, when developing his first set of formal antibody observations, that first, band 41 (flagellin) showed up, then next, when focusing on the arthritis cases,

You can see from this early Steere report that Steere did not initially believe a person needed to have 5 of 10 bands early in the disease, but that he did acknowledge that his preferred type of patients (arthritis patients, people who need aspirin and not antibiotics for central nervous system infections), continued to have a hypersensitivity response.  AND he said, a person would have antibodies earliest in the disease against band 41, that these patients would be seronegative to the ELISA cutoff, and that he could tell the difference between Lyme and people with syphilis or Relapsing Fever (not that it really matters).

Clearly his perceptions changed drastically.  Anyone with Lyme Borreliosis knows the crooks discount completely the band 41 or anti-flagellar antibody.

In 1990, the CDC accepted Steere's first, 1986, interpretive criteria, based on this very report.  Labs were to perform serial or sequential Western Blots to look for new IgM antibodies, because that meant the organism was still alive and not killed by antibiotics:


[CAPTION] As you can see with your own eyeballs, the first, CDC, published, diagnostic standard for Lyme Disease was to perform serial Western blots to look for any CHANGE in the antibody profile, especially new IgM type, regardless of treatment status. New IgM meant the bug was still alive, regardless of treatment (or vaccination) status.


Nowadays (2006-7), Steere says he sees antibodies against OspA as frequently as he sees antibodies against OspC.   That’s sort of amazing since these bad guys say the prototypical strain for “Lyme Disease” - Steere's Knees-Only Disease - is B31, which expresses little or no OspC or the brain invasion antigen.  These criminals call Lyme victims insane, when none of us are so demented that we would could have come up with such a bizarre story as Steere's saga with "Lyme Disease," and expect people to believe it. 

The bottom line is that in America, no one is allowed to have neurologic Lyme disease since that requires expensive antibiotic treatment, therefore, strain B31- the one with low or no OspC in it - is "the American prototypical strain." 

B31 is for "No brains allowed."

Connecticut Attorney General Richard Blumenthal at the time of this writing (Nov 2007) would like to know what is these Lyme crooks' association to BigInsurance and BigPharma, although he and the United States Department of Justice, District of Connecticut, US Attorney Kevin O'Connor were in the fall of 2003 already provided with the Kaiser-Permanente-New York Medical College - SmithKline-CDC,  Incorporated, hard evidence.  B31 is also for "US Attorney, District of Corrupticut" and that will be discussed in one of the other pornography chapters.  (The first pornography chapter is CHAPTER 2, McSweegan and Fish's pornography.)  I do not have the benefit of that RICO data now still in the US Attorney's office collecting dust in New Haven to cite the Kaiser-Permanente / references but I know what's there.)

Lots of phallic symbolism for everyone, here.  Not because it sells, but because it has been rammed down our throats as an excuse for science and healthcare.


For the 1994 CDC Dearborn Farce, Outer Surface protein A, once thought to be the cause of Lyme Disease (autoimmune arthritis in a knee), was left out of the diagnostic standard.  That was because it was going to be a vaccine, and in most cases of vaccination, the vaccine antigen itself is not used to diagnose vaccine failure for logical reasons.

Here, in 1994, the vaccine was going to design the disease, the disease was going to be arthritis only, and as a result of this Dearborn conference and Steere in Europe, there came a test for the newly defined disease that leaves out the vaccine antigen to facilitate the Yale (vaccine and post-vaccine test) RICO enterprise. 

What's different here is that there came a "controversy," (Think Big Tobacco or fraud or crime) over what "Lyme Disease" was, ever since the publication of the Infectious Disease Reviews Supplement 6 on Lyme and Spirochetal Diseases,  in 1989.  The 1989, Sup 6 ID Reviews (CHAPTER 8) had pretty much established that Lyme was a chronic parasitic spirochetal infection, like all the rest of the chronic parasitic spirochetal infections.

Kaiser-Permanente pounced on the unsuspecting priests at the Catholic Medical School, New York Medical College, in Valhalla, New York, less than a year later, in 1990.



All Lyme victims should memorize three things:

1) "Lyme Disease" was redefined by Allen Steere at the Dearborn Conference to an autoimmune arthritis in a knee where antibodies against OspA result in an autoimmune arthritis in a knee because OspA was intended to be the "vaccine."

2) No one is allowed to have "Lyme Disease," unless they have an autoimmune arthritis in a knee - an arthritis that is so obvious that it doesn't even need a blood test (red, raised, hot, painful).  It is usually restricted to one joint. This disease does not need antibiotic treatment, even though Allen Steere and Arthur Weinstein treat this autoimmune arthritis with long term antibiotics, including ceftriaxone which is for brain diseases, but that violates the "IDSA guidelines," which are themselves in violation of the American Psychiatric Association's guidelines on the treatment of diseases that need ceftriaxone. 


  Click to enlarge and then click again to enlarge further.   

"Medications for psychiatric disorders can be both the cause of delirium and exacerbate or contribute to delirium from other causes."-  The American Psychiatric Association.

The above means Ely Lilly certainly knew they were committing a crime (malpractice) by recommending Zyprexa for dementia patients (or CNS depressants for the CNS depressed as demonstrated by scientifically valid relapsing and remitting brain SPECT scans in response to the IV drug ceftriaxone), since the American Psychiatric Association's own guidelines say central nervous system depressants make the delirium or dementia worse.

Lyme is an organic delirium as shown by diminished perfusion or blood flow to the brain in brain SPECT scan imaging and Brian Fallon's Relapsing Fever, Relapsing brain disease 4.7 million dollar research study


3) No one is allowed to have antibodies against OspA ("Lyme Disease") and have a diagnosis of "Lyme Disease."  LYMErix is allegedly specific enough to prevent Lyme, but not specific enough to detect Lyme, even though it is 100% specific to Lyme. 

4) Bb strain B31 is the "prototypical American strain," but it expresses no OspC- the brain invasion antigen.  There are no brains in America, and brains are "a complicating variable," anyway, which should be throw out, according to Yale's Steven Malawista.  All psychiatrists at Yale agree that the brain can and should be thrown out, as we will see in later chapters.

Conclusion: "Lyme disease" is an autoimmune arthritis in a knee caused by the antibodies that no one is allowed to have.  It is not caused by OspA, B, or C, which are the "primary immunodominant antigens (produce the most antibodies)."  It does not go into the brain or the knee or anywhere else, since there is no OspC in the prototypical strain and there is no A or B in the diagnostic standard.  Since this is America and Allen Steere is not locked up and Yale is not shut down.  Yet.


To further prove that "Lyme Disease" is a non-disease, Mark Klempner said at the 2001 Diseases of Summer Conference in Rhode Island that CDC does not recognize any other kind of Lyme except this imaginary kind of Lyme.  One of the biggest problems in the Lyme crime world is that is basing their "guidelines" on the very seriously invalid and just plain stupid Klempner Chronic Lyme Treatment report released in July 2001- which is based on the Steere/Dearborn notion of what "Lyme Disease" is.  We now know Steere's Dearborn Lyme was a hoax.  But as regards Mark Klempner, for starters, Klempner pretty much says, "Only the Imaginary Criteria of Allen Steere Invented in Europe with high passage strain G39/40 may be called (diagnosed and therefore treated) 'Lyme Disease'- which is not a real disease, but the placebo response to antibiotics.'"


The following is an excerpt of the Question and Answer session that followed the Klempner Non-Diseases of Summer Conference at South Country Hospital, Rhode Island, July 2001:

[Never mind exact which city in Rhode Island, since it doesn't matter.  South County is formally Washington County, but what's the difference if we talking about a state so small it practically doesn't even need telephones and the MDs are so stupid they already watched this conference and applaud the same nonsense year in and year out.  It's always the same conference:  "There are no diseases and Fibromyalgia is for women, but women are for men's penises so everyone's fine here in Rhode Island thanks and have a nice day."]

Questioner8:  I just have one more question for Dr. Klempner. Um, being that there are inadequacies, inaccuracies in the testing methods, seropositivity, etc, and the surveillance criteria that you used were just that, surveillance. And the CDC recognizes that there are so many more people that have Lyme disease who do not meet the CDC criteria.  What’s your feeling on what percentage of patients who have Lyme disease because they have not met the criteria for diagnosis?

Klempner:  I, um, I think there are a number of inaccuracies in what you just said.  The CDC does not recognize that there are patients who have, um, that are seropositive that don’t meet seropositive criteria.  What they say, is that these are the criteria.  I think what, the question, if I could reinterpret the question a little bit, is are there patients who are out there who had Lyme disease who continue to have symptoms and um, wouldn’t fall into these categories.  And the question is, how do you define patients who have had Lyme disease?  You’ve gotta, you’ve gotta start with  some agreed upon cohort, so what are the agreed upon criteria? And what we were trying to do, since we know this was a controversial topic to start with a group of patients who no one would doubt  had had Lyme disease.  And that was really the point of the study.  Are there other patients who fall into equivocal groups that one could say, it’s difficult to document that they had Lyme disease?  Sure, but remember we were about to do a study that was very risky.  Um, meaning giving people parenteral antibiotics, doing lumbar punctures, doing huge numbers of studies on these people.  It was very important to start patients that everybody agreed had had acute Lyme disease.  Are there lots of other people out there who say they have Lyme disease where the documentation is lacking?  You know that better than I do.  Of course, there are lots of people out there who says they have lots of things that you can’t document.

Questioner8: But, but according to what I’ve read is that not everyone is going to, number one, see an EM rash, um, so when you’re are using entry criteria, diagnostic criteria, that you need to have an EM rash, and physician diagnosed…


Klempner: If you’re seronegative

Questioner8: Right, okay, but there are seronegative people that don’t have the initial EM rash, And  if they do, they may not see it, being on the back…

Klempner:  So, then how do you know what they have, that is anybody who walks in the door who says, “I don’t feel well”, with this set of symptoms.  Um, that is not a group of people that I would be comfortable putting an intravenous catheter in, an LP on, doing all this very complex study.  I needed to be assured that those patients had had Lyme disease.  You’re describing a group of patients who cluster by virtue of symptoms.  No different from the symptom complex that was given here [previous (Fibromyalgia) talk].   This is a very different symptom complex, very different patient population. Very well documented Lyme disease.  And I just wanted to be sure.  Um, that’s where I started my talk, at that point.  That is, there are a lot of people all over this world that claim to have lots of different things.  But for doing studies, I think it’s very important that we cluster patients by objective findings, strict criteria.


KRÜCH's HYPOTHESIS:  Whilst performing studies with invalid tests where the outcome is predetermined, one should start out with the assumption that the only kind of [fill in the blank disease] is the imaginary Steere kind.  The same thing happens with the "vaccines" for [fill in the blank]. 

Follow:  No one had the imaginary Steere kind of Lyme, therefore no Lyme emerged in vaccinated people, therefore the "vaccines" were "safe" and "effective."  (It is a very good thing that Lyme criminals do not attempt to assist NASA and the world should be grateful.)

Now, cross apply the Krüch's Hypothesis.  In 1996, there was a RARE DISEASES conference put on by the NIH wherein we learned there were tons of Ehlichia out there and that Ehrlichiosis and Borreliosis in combination could make a person very, very sick.  Since it is now more than 10 years later, and there are no tests out there which detect all the Ehrlichias, we can assume they are having trouble with their fake vaccines.

Laboratory studies indicate the presence of different human pathogens in Ixodes scapularis populations and that persons living in tick-infected areas are sometimes exposed to multiple tick-borne agents. Ehrlichial or Babesia organisms may occur concurrently with B. burgdorferi in humans and may complicate Lyme borreliosis infections. Therefore, clinical diagnoses of tick-related illnesses should include laboratory testing for ehrlichiosis, babesiosis, and Lyme borreliosis.-- Lou Magnarelli. 

Naturally, looking for co-pathogens is not standard operating procedure, nor are all MDs aware that they should be because, well, there's nobody yet in the background with a vaccine, ready to profit.  You don't expect KAISER labs to be running any scientifically valid tests on anyone for anything, do you?  Since when, since 1990, when managed care formally took over American Medicine (, have we heard a word from the AMA about the's DNA and RNA primers shell game, for instance?  The AMA is having a clueless cluck contest and the reward is the top position at the NIH.



There are three essential reports that the medical crime sleuth absolutely must obtain:  the 1986 original Steere standard development (adopted by the CDC in 1990, but then replaced with the Steere/Dearborn method), the 1993 Dressler/Steere or the Dearborn IgG method, and the 1992 Steere in Europe, Antibodies in Europe report.

 1) Steere's "Antigens in Europe" which of course, were not, but were "high passage" strain G39/40 plus recombinant OspA and B from the prototypical American strain, B31:


 : J Infect Dis. 1994 Feb;169(2):313-8.Links

Antibody responses to the three genomic groups of Borrelia burgdorferi in European Lyme borreliosis.

Dressler F, Ackermann R, Steere AC.

Division of Rheumatology/Immunology, New England Medical Center, Tufts University School of Medicine, Boston, Massachusetts 02111.

The antibody responses to the three genomic groups of Borrelia burgdorferi (B. burgdorferi sensu stricto, Borrelia garinii, and Borrelia afzelii) were determined in 97 German patients with various manifestations of Lyme borreliosis. The geometric mean antibody titers in each patient group, determined by ELISA, were similar with each antigen preparation. By Western blotting, however, patients with meningopolyneuritis tended to respond to more spirochetal polypeptides of B. garinii, the group 2 strain, whereas those with arthritis recognized more antigens of B. afzelii, the group 3 strain (P < .03), as did those with acrodermatitis. Only 1 patient each with erythema migrans, arthritis, or acrodermatitis had weak reactivity with outer surface protein A (OspA), and none responded to OspB. It is concluded that differences among the three groups of B. burgdorferi may result in variations in the antibody response in European Lyme borreliosis.  PMID: 8106763 [PubMed - indexed for MEDLINE]


 2) Only available free, full-text, online, here on ActionLyme, and in the FDA's archives from the Jan 31, 2001 LYMErix Hearings:

: J Infect Dis. 1993 Feb;167(2):392-400.Links

Comment in:

J Infect Dis. 1993 Oct;168(4):1073.

Western blotting in the serodiagnosis of Lyme disease.

Dressler F, Whalen JA, Reinhardt BN, Steere AC.

Division of Rheumatology/Immunology, Tufts University School of Medicine, New England Medical Center, Boston, Massachusetts 02111.

There are currently no accepted criteria for positive Western blots in Lyme disease. In a retrospective analysis of 225 case and control subjects, the best discriminatory ability of test criteria was obtained by requiring at least 2 of the 8 most common IgM bands in early disease (18, 21, 28, 37, 41, 45, 58, and 93 kDa) and by requiring at least 5 of the 10 most frequent IgG bands after the first weeks of infection (18, 21, 28, 30, 39, 41, 45, 58, 66, and 93 kDa). When these definitions were tested in a prospective study of all 237 patients seen in a diagnostic Lyme disease clinic during a 1-year period and in 74 patients with erythema migrans or summer flu-like illnesses, the IgM blot in early disease had a sensitivity of 32% and a specificity of 100%; the IgG blot after the first weeks of infection had a sensitivity of 83% and a specificity of 95%. Among patients with indeterminate IgG responses by ELISA, 6 of 9 patients with active Lyme disease had positive blots compared with 2 of 34 patients with other illnesses (P < .001). Thus, Western blotting can be used to increase the specificity of serologic testing in Lyme disease. PMID: 8380611 [PubMed - indexed for MEDLINE]


3) Steere's First Observations, 1986:  free full text link

: J Clin Invest. 1986 Oct;78(4):934-9. Links

Antigens of Borrelia burgdorferi recognized during Lyme disease. Appearance of a new immunoglobulin M response and expansion of the immunoglobulin G response late in the illness.

Craft JE, Fischer DK, Shimamoto GT, Steere AC.

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.

PMID: 3531237 [PubMed - indexed for MEDLINE]

- - - -


Yet one more final incident worth mentioning was the June, 1994 FDA Vaccine Meeting (a few months before Dearborn) where State University of New York, Stony Brook's (SUNY-SB) Raymond Dattwyler recommended performing serial or sequential Western Blots to look for Lyme infection after vaccination.  Since Dattwyler proposed using the CDC's 1990 or 1986 Steere method, we can surmise that Dattwyler at that time, was not aware of the problem of reading Western Blots in LYMErix vaccinated people:

Dattwyler also said:


Which means that Lyme is not a knee-disease, but a very scary permanent central nervous system infection- which the crooks all knew in 1989, with the publication of the IDSociety's REVIEWS OF INFECTIOUS DISEASES October Supplement 6 on Lyme and Spirochetal Diseases in addition to their own 20-plus treatment failure reports.  Nowadays, nearly 20 years later, IDSA says there is no such thing as chronic central nervous system disease, despite their own published reports about the persistence and especially, persistence in the brain past antibiotic treatment (CHAPTER 11, PERSISTENCE in the BRAIN).

Following the scientific fraud in the antibody testing, the Lyme criminals proceeded to perform a shell game with the DNA and RNA primers. CHAPTER 5, PRIMERSHELLGAME

The next chapter deals specifically with what the FDA LYMErix Vaccine Committee was told and informed of otherwise with the hard evidence:  that Steere's Dearborn method was a hoax and the REAL outcome of LYMErix.

CHAPTER 4, WHAT HAPPENED at DEARBORN (the whole 30 pages)  on the FDA's website