Lyme Crymeline of the Worst Human Rights Abuses in History
How much longer are we going to keep running from the truth?When will we rise up to this Medical Holocaust? When is enough enough? How many more lives must be stolen? Childhoods destroyed and robbed? How many more warriors must die? Starve? Go homeless? Commit suicide? Medically kidnapped? The atrocious crimes, genocide and murder committed by CDC officers for profit and greed have been layed out on a silver platter by the whistleblower herself for us all. Lymeland, it's time for us all to rise up, we are in the fight of our life. ILADS and non-profits won't stand up for us, they continue running away from the truth. We're alone in this fight, it's up to us and only us. Below is a breakdown of the Lyme Crymes to humanity generated by TruthCures
1980: The Bayh-Dole Act is passed.
This event set the stage for the gold rush to the patent office--not only in the U.S., but also in Europe, as evidenced by Barbara Johnson's (CDC officer) multiple patents with SmithKline in Europe. We also saw Alan Barbour's 30+ patents, and Yale's patents for both LYMErix (5,747,294) and the only valid test method for diagnosing both bad-knee Lyme and neuroborreliosis (5,618,533).
It became clear at this time that the mission of the Centers for Disease Control and Prevention became laser-focused on "prevention" by way of vaccines.
Here is apaper by MIT student David Levenson on the consequences of the Bayh-Dole Act.
1986: Allen Steere forms the basis for the 1990 case definition.
Here, in 1986, Steere not only says you only need band 41 for diagnosis, but he says treatment fails in half the cases.
This was the source of the first, 1990, CDC surveillance criteria - just do repeat Western Blots to look for new IgM bands, because that meant the bug was still alive after treatment.
"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 spirochetes 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."
1986: Alan Barbour publishes “THE BIOLOGY OF BORRELIA SPECIES”
In this report, Alan Barbour, CDC officer, states:
"The propensity for borrelia to go to the brain of infected mammals suggests that the relationship between these spirochetes and neural tissues is not trivial. Further study of this attraction and the interaction that follows may reveal the basis for the significant nerve and brain involvement in Lyme borreliosis."
All the way back in 1986 it is not trivial that Borrelia have an affinity for brains. It is also not trivial that you cannot kill spirochetes, and that the nature of the disease as a Relapsing Fever germ is in fact, to relapse. This paper also states that it was attempted to treat syphilis with a wimpy high passage strain of Borrelia to cause fever because antibiotics didn’t work.
Barbour later became the patent king of tick-borne diseases.
1986: Allen Steere talking about how Lyme is like post-sepsis with the leukemia-like, EBV-transformed immune cells.
"Not only are plasma cells plentiful in the spleen, lymph nodes and bone marrow, they are also represented by large and somewhat atypical-appearing precursor B cells as well."
"Numerous names have been given to this stage, including pseudolymphoma, lymphoid hyperplasia, follicular hyperplasia, lymphocy- toma cutis, Spiegler-Fendt lymphoid hyperplasia, and lymphadenosis benigna cutis of Baverstedt."
"The immune response involves virtually all of the organs and structures of the reticuloendothelial system including the bone marrow, and clinical pain and discomfort seems to correlate with hyperplasia of lymph nodes and spleen and bone marrow. Diffuse visceral involvement in this acute stage mimics infectious mononucleosis or disseminated viral syndromes. These include conjuctivitis, pharyngitis, pneumonitis with dry cough and mild pleuritic pain, hepato-splenic tenderness, lymph node swelling of the neck and groin, and orchitis. There is lymphoid hyperplasia of the lymph nodes and spleen consisting of prominent germinal centers and numerous perifollicular lymphocytes, with prolifera- tion of plasma cell precursors and mature plasma cells. The plasma cell precursors are large, appear tumor-like, and can resemble Reed-Sternberg cells."
Lyme is like cancer, he says.
1986: Edward McSweegan's fake whistleblower letter to steal tick-borne disease funding from the Navy.
Here Edward McSweegan writes a fake whistleblower letter intending to steal the US Navy's (his employer) funding and give it to all his cronies at the future American Lyme Disease Foundation (ALDF).
He does not know spirochetes undergo antigenic variation or that its surface antigens, formerly called "mucopeptides," were fungal-type antigens and therefore a vaccine can't be made out of them. It's the same for most of the other tick-borne diseases; they are bearers of fungal antigens, which is why they were always known to make nice bioweapons.
1988: Raymond Dattwyler associates immunosuppression with borrelial lipoproteins.
"Figure 1 demonstrates that there was a marked and highly significant inhibition ( p < 0.0005) of invivo endogeneous NK activity in two patient populations: (1) patients in the early stages of Lyme disease (ECM stage) and before treatment, and (2) patients exhibiting chronic active stages of the disease."
Natural Killer Cell activity is muted, and Dattwyler also says Borrelial supernatant (where the fatty Osps are) does this too. That means it was known in 1988 that Borrelia and its shed mucopeptides or lipoproteins cause immune system blunting.
1988: Raymond Dattwyler develops a seronegative Lyme assay.
“We studied 17 patients who had presented with acute Lyme disease and received prompt treatment with oral antibiotics, but in whom chronic Lyme disease subsequently developed. Although these patients had clinically active disease, none had diagnostic levels of antibodies to B. burgdorferi on either a standard enzyme-linked immunosorbent assay or immunofluorescence assay. On Western blot analysis, the level of immunoglobulin reactivity against B. burgdorferi in serum from these patients was no greater than that in serum from normal controls.”
Here, knowing Lyme (especially chronic neurologic Lyme) is seronegative, they develop an assay that Steere later uses to assess "Chronic Neurologic Lyme" cases, proving he knows these cases are seronegative.
1989: Duray publishes in IDSA's journal that chronic Lyme is like syphilis and may be permanent.
“Nervous system involvement. Biopsy of the sural nerve in patients withe peripheral neuropathy associated with chronic Lyme disease has demonstrated the presence of lymphocytes and plasma cells in the nerve itself as well as in the perineurial region (figure 10). This is not dissimilar to the pattern of infiltrates seen in stage II. What differentiates this complication from stage II involvement, however, is its apparent permanence.”
“Further complicating the staging of this infection is the fact that serologic tests often do not show any correlation between titer and extent of damage to organ systems.”
1990: The ALDF is formed.
The American Lyme Disease Foundation (ALDF) was formed apparently for the purposes of spinning Lyme disease as merely a nuisance disease that at the same time, was serious enough that we needed a vaccine to prevent it. It is the racketeering organization at the center of the Lyme Cryme.
In an article from New York Medical College, where the ALDF was conceived, Arthur Weinstein explains its founding:
"This year, Dr. Weinstein is working with more than half a million dollars in grants from the NIH, pharmaceutical companies and private foundations on research that includes systemic lupus, rheumatoid arthritis and scleroderma. But the bulk of the funds belong to chronic Lyme disease, which was not his interest when he joined New York Medical College from the University of Connecticut School of Medicine in 1985; lupus was. Still, Dr. Weinstein became intimately involved in the evolution of Lyme here as his experience with the disease went from nothing to plenty, and fast.
"The College has recognized that Lyme disease is a major clinical and research interest on this campus. The main players in the development of the program were Fish, Wormser and Connolly," Dr. Weinstein advises. The entrepreneurial trio are Durland Fish, Ph.D., former director of the College's Lyme Disease Center and now a research scientist at Yale; Gary P. Wormser, M.D., still professor of medicine and pharmacology and chief of the Division of Infectious Diseases at the College; and John J. Connolly, Ed.D., former College president and current chairman of the board of the American Lyme Disease Foundation, Inc., which had its genesis on the Valhalla campus in 1990."
Click here to see a 990 tax form that shows the ALDF receiving grant money from the CDC.
1990: Steere uses the Dattwyler Seronegative Lyme Assay to assess Chronic (Seronegative) Post-Tick Bite Sepsis or Neurological Lyme.
“Of the 27 patients, 24 (89%) had a mild encephalopathy that began 1 month to 14 years after the onset of the disease and was characterized by memory loss, mood changes, or sleep disturbance. Of the 24 patients, 14 had memory impairment on neuropsychological tests, and 18 had increased cerebrospinal fluid protein levels, evidence of intrathecal production of antibody to B. burgdorferi, or both. Nineteen of the 27 patients (70%) had polyneuropathy with radicular pain or distal paresthesias; all but two of these patients also had encephalopathy. In 16 patients electrophysiologic testing showed an axonal polyneuropathy…Among the 27 patients, associated symptoms included fatigue (74 percent), headache (48 percent), arthritis (37 percent), and hearing loss (15 percent).”
1990: CDC publishes a Lyme case definition that recognizes it as "relapsing fever."
Here the published surveillance case definition is based on Allen Steere's 1986 report, "Antigens of Borrella burgdorferi Recognized during Lyme Disease."
They say, just do repeat Western Blots to look for new IgM bands, because that meant the bug was still alive after treatment.
To be clear, 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.
1991: Yale's Fikrig & Flavell patent the only valid test method for all "versions" of "Lyme disease."
The current (since 1994) testing method for “Lyme disease” does not make sense when you take into account that Borrelia are relapsing fever germs. Borrelia are differentiated by their Flagellin genes (DNA). Since all Relapsing Fever organisms are capable of antigenic variation (they can change their outer surface proteins as a way of evading the host’s immune system) the only scientifically VALID way to test for Borrelia infections would be to test for Flagellar antibodies instead of outer surface proteins, because it’s specific and never changes.
Testing for so many antibodies all at the same time is NOT logical, or valid, by any standard.
This patented test is 94%-95% accurate during all stages of the disease. This is the test that should be used, obviously.
1991: Allen Steere says he is "convinced seronegative Lyme exists."
... and that this non-HLA linked outcome is "perilously close to Fibromyalgia and Chronic Fatigue Syndrome." In this report, Allen Steere states:
"Most of these patients have subtle encephalopathy affecting the central nervous system. They have memory difficulty, depression, or sleep disturbances but no seizures, myoclonus, or changes in the level of consciousness. They also have sensory symptoms, such as pain in the spine, accompanied by radicular pain in the limbs or trunk, and some have distal parethesias with intermittant tingling sensations in the hands and feet...These symptoms are perilously close to those that occur in fibromyalgia, with the chronic fatigue syndrome, or in stress-induced syndromes-conditions that are ever so much more common than tertiary Lyme disease.
"How then does one identify the patient with chronic neurologic abnormalities of Lyme disease?
"The patients in question have characteristic findings on laboratory evaluations as follows:almost all were sero-positive by ELISA (keep in mind, this is PRIOR TO his research fraud in Europe in which he falsified the ELISA and added it as a bogus screening test.), half of them had increased cerebrospinal fluid (CSF) protein, half had evidence of slight amounts of production of intrathecal antibody to the spirochete, and 70% had one or more of both abnormalities.
"In addition, more than 50% had abnormal EMGs indicating polyneuropathy affecting both proximal and distal nerve segments, and MRI brain scans showing areas of increased T2 signal intensity. In other words, many of our patients had memory impairments on their psychological assessments, had abnormal CSF anaysis, frequently accompanies by EMG evidence of an axonal neuropathy."
1993: Steere does a 180, publishing THE OVERDIAGNOSIS OF LYME DISEASE.
Suddenly, that kind of Lyme Allen Steere talked about before (chronic, neurologic, and seronegative), where once he warned were "perilously close to CFIDS and Fibro," now actually were CFIDs and Fibro and therefore a psychiatric illness. In this report, Allen Steere states:
"We thought that 452 (57%) of the 788 patients had another illness rather than Lymedisease. They had had symptoms for a mean duration of 3 years (range, 1 month to 22 years) at the time of our evaluation. More than half of these patients had chronic illnesses with prominent subjective symptoms, such as chronic fatigue syndrome or fibromyalgia.
"The sex ratio among these patients was 2 to 1 in favor of women, but the age distribution was similar to that in patients with past or current Lyme disease. Although psychiatric disorders such as anxiety, depression, or somatization clearly played a role in the illness of some of these patients, we did not attempt to make psychiatric diagnoses.
"Most of the 452 patients had had multiple serological tests for Lyme disease done in multiple laboratories. Of the 452 patients, 203 (45%) had previously had at least on e positive result in another laboratory, often in a borderline-positive range. In our laboratory, none of these patients was seropositive."
Allen Steere has done a complete 180. Where he once acknowledged the multi-system, protean, chronic disease that is similar to lymphoma, he is now calling it a hysterical hypochondriacal women's disease.
1993: Steere commits research fraud in Europe.
In the report "Antibody Responses to the Three Genomic Groups of Borrelia burgdorferi in European Lyme Borreliosis," Allen Steere falsified the testing in Europe.
He used bogus high passage strains, leaving OspA and B out. This means that the bugs have been cultured through many generations and in so doing, they have dropped the plasmid that is encoded with OspA and B.
Steere also added the ELISA as a screening test, averaging the concentration signal between the very low Neuro-Lyme responders and the very high autoimmune knee and acrodermatitis responders. As a result, the new, Dearborn, 2-tiered cutoff for an ELISA, will exclude all neurologic cases and of course, most of the IgM responders--which, to Steere, meant persisting infection in 1986.
1993: Barbour & Fish reveal that OspA vaccine trials are underway and start trashing Lyme victims.
Here we learn that the Phase I and Phase II trials of the OspA vaccines are underway, while Alan Barbour (owner of the ImuLyme OspA patent) and Durland Fish (founding member of the ALDF.com) proceed to trash victims of Chronic Lyme/Sepsis, saying it is a disease of hysteria or catastrophizing...because they know by now that OspA is making people sick, especially after 2 injections.
"However, if a skin lesion is absent, a situation that may occur in 10% or more of infections [4,5], nothing in the clinical presentation can clearly distinguish early Lyme disease from other acute, febrile summer illnesses of temperate latitudes. Later manifestations of Lyme disease, such as arthritis or carditis, can be attributed to other disorders. Neurologic symptoms, especially those involving changes in cognitive functions, are especially difficult to interpret [69- 71]. Moreover, factors such as the premorbid personality and a tendency to somatization may determine the length of convalescence and the response to postinfection fatigue and joint aches [71,72]. Even if the original diagnosis of Lyme disease is undisputed, lingering or recurrent symptoms, many of which are also characteristic of chronic fatigue syndrome or fibromyalgia, may not be attributable to persistent infection."
"Decisions on diagnostic criteria, treatment strategies, research-funding allocation, and insurance reimbursement are being made. Policy-makers are under pressure from some health professionals and lay persons who believe that the spectrum of B. burgdorferi disease is broader than the limits accepted by most peer-reviewed medical journals. The conditions in this larger set include degenerative, inflammatory, and neuropsychiatric conditions not previously thought to be ameliorated by antibiotics . Alternative views of diagnostic criteria and treatment strategies have been presented primarily at regional meetings sponsored by patient advocacy groups and in newsletters devoted to Lyme disease. More recently, the influence of these points of view on the last international scientific meeting on Lyme disease was such that several additional abstracts, which had originally been rejected, were permitted presentation ."
1994: FDA vaccine meeting. Dattwyler recommends using serial Western blots. This is apparently ignored.
In this transcript of the 1994 FDA LYMErix meeting, Raymond Dattwyler repeatedly argued against the intended proposal for an arthritic-knee-only case definition for Lyme disease.
Note that this took place in June 1994, which was before Dearborn, so the serodiagnosis business was still up in the air.
1994: The CDC's "Dearborn" conference, which wasn't about "standardization," but falsification.
What happened was, the labs were invited to "participate in the proceedings!" but then the Lyme criminals blew off all the other labs' recommendations, which, on average, said that the Steere proposal was only 15% accurate--Gary Wormser included. This shows that the FALSE intent was to have a consensus conference, but these criminals never intended to listen to any other participants' proposals.
In the Dearborn Conference Booklet, you will see who said what, that the "Steere in Europe" report is missing, and that there was no consensus or agreement. Towards the end of the booklet see what all the contributing labs said about Steere's and the CDC's proposal for a new diagnostic standard. Everyone said it sucked except MarDx who had been given arthritis positive blood to "qualify" their Western Blot test strips, but even they said OspA and B should not be left out of the case definition.
1995: CDC's falsified case definition is officially published.
1995 "DEARBORN" "Case Definition"published by the CDC in the MMWR (also seehere, just in case the link becomes broken), even though all the labs at Dearborn said 'no way.' OspA (band 31) and B (band 34) are left out, as are most IgM bands.
You will see by looking at the October 1994 Dearborn booklet what all the labs said about the proposal for the 2-tiered testing and Steere’s 5 out of 10 band WB criteria, and then as much as we have in detail about the June 1994 FDA meeting on LYMErix, that there was no consensus that Lyme was just a bad knee. In fact, it was a fight and an argument the whole way.
Eventually the CDC officers who own patents and who were associated with the fake non-profit ALDF got their way and had their fake vaccines. And later, the bogus Klempner "study" which was based on the Dearborn case definition (the grant for this study was a "fraud on the government"), but the bad guys knew all along that the disease was post-sepsis and was caused by the fake OspA vaccines alone. Certainly Steere knew that late, chronic neurologic Lyme was like post-sepsis since he wrote about it in 1986 and 1990 as you have seen.
1998: FDA approves LymeRIX with numerous provisos.
LYMErix is declared 76% effective (says Medline). Lyme disease was first called “Lyme Borreliosis” before tick borne disease began to be commercialized after the Bayh-Dole Act came into being, and was only called “Lyme disease” after the Dearborn Conference in 1994.
LYMErix was approved for use in ages 15-70 and recommended in endemic areas. At one point they tried to get it approved for use in children; fortunately that never happened.
The provisos (contraindications) included: Pregnant or breastfeeding mothers, children younger than 15 and adults over 70.
You want to read the entire1998 FDA meeting transcript. Sikand claims Lyme is hard to diagnose and treat. Schoen says Lyme is underreported by 10-12 times, and Luft is going at these bastards over their disease definitions the entire time, as well as, says the vaccine injuries look exactly like the "protean" or multi-system disease definition and not the "bad knee only" definition.
1999: Lyme support groups begin receiving phone calls from patients who had “Lyme again” after getting LYMErix.
Not surprising, after all that we have seen in this timeline.
1999: Gary Wormser reports that OspA is immunosuppressive.
In his 1999 study (published in 2000) "Modulation of lymphocyte proliferative responses by a canine Lyme disease vaccine of recombinant outer surface protein A (OspA)," he’s talking about how OspA causes immunosuppression in dogs too. The dog vaccines only tolerize against arthritis; they do not prevent spirochetes.
"The effect of the recombinant OspA dog vaccine preparation on human lymphocyte proliferative responses was investigated. Cultures of mitogen- or antigen-stimulated normal human PBL were supplemented with the OspA vaccine preparation at various concentrations. Fig. 1A reveals a dose-dependent regulatory effect of OspA on the proliferation of ConA-stimulated PBL, as compared to controls using saline in place of OspA or unsupplemented PBL cultures. An approximately 25-35% reduction of proliferation was observed with the OspA preparation supplemented at 0.1% volume, while a maximum reduction of 50-60% (P T 0.01) was observed with supplementation at 7% or more (Fig. 1B).
2001: FDA LYMErix meeting. Whistle blown on Dearborn and OspA.
Read the transcript of this meeting, where Ben Luft talks about the "twilight zone of disconnect" between what the patients say are vaccine injury, compared to what SKB says. SKB also mentions a high rate of pregnancy failure (miscarriage) at this hearing. SKB (Yves Lobet) also makes fun of Allen Steere and calls him basically an idiot who makes no sense with his theories.
This is also the meeting where Kathleen Dickson blew the whistle on Dearborn and OspA. Her testimony is here, minus the 19 pages that Nancy Cherry "accidentally" omitted.
2001: Klempner's fake retreatment study in which 2/3 of the participants had not received prior treatment.
There were never enough participants; he used invalid methods; he was lying about his previous findings; he was also lying about finding "no DNA-positive patients" among the previously treated because he threw the DNA positive victims out of the study. Two-thirds of the patients had never been treated before; he never reported what primers he used; he did not look for commonly activated viruses in these patients that are well known to be reactivated in the presence of immune suppression; and no scientifically valid assessments of outcomes of this standard of care "study" were performed. The result was that extended treatments were not beneficial to patients.
2002: LYMErix pulled off the market via FDA ultimatum.
In the end, the FDA gave SmithKline an ultimatum- either take LYMErix off the market or they would. To this day they still lie and say that it was due to low sales. If sales were plummeting, it was due to word getting out that the vaccine was making people sick.
2003: Complaint filed with the USDOJ.
In 2003, at the advice of staff lawyers for Richard Blumenthal, who at the time was Attorney General for the state of Connecticut, our whistleblower filed a complaintwith the U.S. Department of Justice. Fourteen years later, the charges of scientific fraud and racketeering have gone unanswered, while Lyme disease morbidity and mortality has exploded unchecked by the institutions—namely, the CDC, HHS and state & local health departments— whose duty it is to protect the health of U.S. citizens.
2006: Blumenthal's antitrust investigation into IDSA.
Now Senator Richard Blumenthal sued the Cabal for AntiTrust while he was Connecticut Attorney General. He did not include the FRAUD part about Dearborn, presumably because he had no "experts" among the "LLMDs" or ILADS to help him with that. He still doesn't, since ILADS is brainless and do not care what is true.
2015: TRUTHCURES is conceived after our first DC trip to meet with legislators.
It was on this trip, in June 2015, that then-Senator Jeff Sessions' legal staff told us to convince the U.S. Senate Committee on the Judiciary to hold a hearing for referral of the Lyme Cryme to the Department of Justice.
2016: Crooks publish (again) that Lyme is an immunosuppression disease.
Lyme Cabal members Gary Wormser, Allen Steere, “CDC officer” Paul Mead, and others admit Late Lyme and LYMErix diseases are immunosuppression outcomes, saying the “TLR2/1 agonism” (immunosuppression) is probably the “more important” driver of the disease outcome, here.
“This finding suggests that there is redundancy in the ability of the innate immune system to recognize B. burgdorferi and/or that these components can activate pathways that produce anti-inflammatory cytokines……the anti-inflammatory effects might be the more important function of TLR signaling.”