Prior to 1994, both Myalgic Encephalomyelitis (ME) and Lyme Disease (LD) were categorized as neuro-immune diseases. However, in 1994, both definitions changed and here we are decades later going backwards from a time when objective science showed that ME and LD are neurological conditions that negatively affect the immune system.
When it comes to chronic neuro-immune illnesses like LD, ME, as well as most patients diagnosed with Chronic Fatigue Syndrome (CFS), etc., patients experience a large amount of suffering both physically and mentally.
Due to the politics and controversy that surrounds these diagnoses, there are little to no social services available to help people with neuro-immune diseases cope with both the physical and mental torment they suffer from on a daily basis.
Although these diseases present themselves differently in each person individually, it’s important to understand the corruption that has led to 25+ years of unnecessary suffering to millions of people around the world.
Myalgic Encephalomyelitis and Chronic Fatigue Syndrome
Prior to (and even after) 1994, it was well documented that ME and CFS belonged to a class of neuro-immune diseases. Since the 90’s, it was well documented that ME and CFS involved the immune system and these immunologic abnormalities were published in a multitude of scientific studies.
Here are a few examples of documented scientific literature that highlights ME and CFS’s connection to immunological abnormalities, reactivated viruses, and opportunistic infections:
1. In a study done in 1989, researchers found several immunological abnormalities. They found “lymphocytosis, atypical lymphocytosis, monocytosis, elevation of hepatocellular enzymes, low levels of antinuclear antibodies, varying levels of antithyroid antibodies, partial hypergammaglobulinemia, elevated CD4:CD8 ratio, decreased cytolytic activity of natural killer cells, and low levels of immune complexes (Komaroff & Goldenberg, 1989, p. 19). In addition, “clinical and serologic studies suggest an association of CFS with all of the human herpesviruses, particularly Epstein-Barr virus (EBV) and the recently discovered human B lymphotropic virus (HBLV) or human herpesvirus 6” (Komaroff & Goldenberg, 1989, p. 19). Researchers stated that “at this time EBV and HBLV were not shown to be the cause of ME and CFS” (Komaroff & Goldenberg, 1989, p. 19). They found that these lab abnormalities also were prevalent in people who are diagnosed with Fibromyalgia (Komaroff & Goldenberg, 1989, p. 19). Like ME and CFS, the severity of Fibromyalgia is also denied by medical bodies and involves the immune system.
2. 1990 One group of researchers from the Miami Veterans Administration Medical Center, in Florida, found that in ME/CFS patients there was “an increase in the percentage of suppressor-cytotoxic T lymphocytes, CD8, and a proportionally larger increase in the number of CD8 cells expressing the class II activation marker. Most patients had an elevated number of CD2 cells which expressed the activation marker CDw26. The numbers of CD4 cells and the helper subset of CD4+CD29+ cells in patients with CFS were not different from those in controls. There was, however, a significant decrease in the suppressor inducer subset of CD4+ CD45RA+ cells” (Fletcher, Klimas, Morgan & Salvato, 1990, p. 1403). Such concrete immunological abnormalities, makes it hard to fathom that the CDC (and other agencies) deny that people with ME and CFS have impaired immune systems.
3. Before he switched to the dark side, researcher Anthony Komaroff had well documented several immunological abnormalities when it came to ME and CFS. In one study, Komaroff found that “various abnormalities revealed by laboratory studies have been reported in adults with chronic fatigue syndrome” (Buchwald & Komaroff, 1991, p. 12). Those most consistently reported include depressed natural killer cell function and reduced numbers of natural killer cells; low levels of circulating immune complexes; low levels of several autoantibodies, particularly antinuclear antibodies and antithyroid antibodies; altered levels of immunoglobulins; abnormalities in number and function of lymphocytes; and modestly elevated levels of two Epstein-Barr virus-related antibodies, immunoglobulin G to viral capsid antigen and to early antigen” (Buchwald & Komaroff, 1991, p. 12). Even to this day, elevated EBV antibodies are still used for a CFS diagnosis in several countries around the world.
4. In this study, researchers found that “peripheral blood mononuclear cells collected from 13 patients with chronic fatigue syndrome and 13 healthy controls were analyzed for the presence of human herpesvirus 6 (HHV‐6) DNA by variant‐specific polymerase chain reaction and dot blot hybridization”(Kitani et al, 1994, p. 587). Results showed that “HHV‐6 DNA was detected in 7 of 13 (53%) patients, and of those 7 patients, 4 were positive for HHV‐6 variant A DNA and 3 were for variant B. No HHV‐6 DNA was detected in the controls”(Kitani et al, 1994, p. 587). The date in this study revealed that “serum antibody titers to the late antigen and antibody prevalence to the early antigen of HHV‐6 were significantly higher in the patient group” (Kitani et al, 1994, p. 587). In the end, “these results suggest active replication of HHV‐6 in patients with chronic fatigue syndrome” (Kitani et al, 1994, p. 587). HHV-6, like other herpes viruses can become reactivated due to the cross-tolerance caused by damage to TLR 7/9.
5. In this study, researchers “selected a well‐defined group of CFS patients and a group of age‐, sex‐ and ethnicity‐matched controls” (Bansal, Ford & Bradley, 2013, p. 73). The findings detected “no difference in the immunoglobulin concentrations. However, compared to the HC, the CFS cohort had significantly greater proportions of transitional B cells, naive B cells and reduced proportions of plasmablasts expressed as a percentage of B cells” (Bansal, Ford & Bradley, 2013, p. 73). Furthermore, they found that, “CFS patients may have some unusual, unrecognized autoimmune disease, or it is possible that CFS patients are unable to control lymphotrophic viral infections due to some defect of B cell memory or T cell dysfunction” (Bansal, Ford & Bradley, 2013, p. 73). Nonetheless, “it is also possible that CFS patients may be producing more BAFF to allow the survival of these increased proportions of naive B cells” (Bansal, Ford & Bradley, 2013, p. 73). Ultimately, researchers felt that “one explanation for reduced plasmablasts in the CFS cohort is that increased numbers of transitional B cells and naive B cells may overwhelm the B cell maturation process, which may consequently become suboptimal. Alternatively, T cell help provided by cytokines may not support naive B cells to develop into plasmablasts” (Bansal, Ford & Bradley, 2013, p. 73). This study displayed that many people who have CFS inhibits apoptosis. The study showed that “defective apoptotic genes increase B cell life‐spans, allowing survival of self‐reactive B cell clones, leading to the potential of autoantibody production and possible autoimmune disease” (Bansal, Ford & Bradley, 2013, p. 73). Researchers in this study “have observed patients with moderate CFS to have increased proportions of transitional and naive B cells and reduced plasmablasts” (Bansal, Ford & Bradley, 2013, p. 73). As an organization, May12.org believes that the data in this study is one of the most overlooked pieces in all neuro-immune diseases and is why the CDC changed the definitions of several neuro-immune conditions.
6. In this study, researchers compared an EBV load in blood immune cells (Baehr et al, 2014). They found “more frequently EBER-DNA but not BZLF-1 RNA in CFS patients compared to healthy controls suggesting more frequent latent replication. Taken together, our findings give evidence for a deficient EBV-specific B- and T-cell memory response in CFS patients and suggest an impaired ability to control early steps of EBV reactivation. In addition, the diminished EBV response might be suitable to develop diagnostic markers in CFS (Baehr et al, 2014, p. 1). In most studies, EBV (and other herpes viruses) are common in ME and CFS because the immune system becomes tolerant to infections managed by these particular Toll-Like Receptors (TLR).
7. In 2015, researchers in this study found that “perturbations in immune processes play an important role in chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME), a multifactorial disorder mainly characterized by severe and prolonged fatigue and typically affecting a variety of bodily systems including the immune system” (Baehr et al, 2015, p. 903). Researchers claim “that Recent reports have shown that CFS/ME is an inflammatory disorder may be associated with autoimmune responses, mainly characterized by reduced functional activity of most immune cells, including neutrophils, natural killer cells, monocytes/macrophage and dendritic cells, together with dysregulations in cytokine levels, responsible for changes in the adaptive immune system” (Baehr et al, 2015, p. 903).
Furthermore, they found that the “interactions between gut microorganisms and host immune function have been shown to contribute to aberrant inflammation in CFS/ME patients. Commensal and/or pathogen-associated molecular patterns detected by Toll-like receptors (TLRs) expressed on intestinal epithelial cells appear to trigger inflammatory signaling cascade leading to neuroinflammation and neurodegeneration” (Baehr et al, 2015, p. 903). When you see such concrete data on how ME and CFS involves the immune system, it’s hard to fathom the denial and unnecessary suffering victims face today.
In 1994, the Centers for Disease Control and Prevention (CDC) officer Dr. Keiji Fukuda changed the ME case definition in a way that discounts the organic (opportunistic infections and reactivated viruses) causes and immune dysfunction outcomes of the disease.
As a result of Fukuda changing the case definition of ME and CFS in 1994, the new definition portrays what was once a serious neuro-immune disease as a condition that is somatic by nature.
MEadvocacy is a project of May12.org, a 501(c)(3) not-for-profit corporation whose mission is to raise global awareness and education for complex immunological and neurological diseases. Activists in both May12.org and MEadvocacy believe that the Fukuda definition implies that ME is “is not a disease but a symptom of fatigue rather than an acquired disease with immune abnormalities” (MEadvocacy, 2016, p. 1). However, since the Fukuda definition was put forward 1994, the severity of the disease has been largely undermined.
The Fukuda criteria was created purposely “so that those with somatoform disorders would fit under the demeaning “CFS” Fukuda criteria and be diagnosed as CFS” (MEadvocacy, 2016, p. 1). In addition, the National Institute of Health (NIH) worked in congruence with the CDC to rewrite the origin of the disease (MEadvocacy, 2016).
Firstly, they altered the definition of the disease in a way that implies that “it is not a disease but a symptom of fatigue rather than an acquired disease with immune abnormalities as seen in the Lake Tahoe outbreak” (MEadvocacy, 2016). Making ME and CFS about fatigue was just the beginning of how the CDC and NIH worked together to water down the severity of the disease.
As they downplayed the severity of ME and CFS, the CDC and NIH began to define “the disease with overly broad and faulty criteria so the psychologists/psychiatrists can now diagnose those with depression and somatoform disorders as “CFS” (MEadvocacy, 2016, p. 1).
Furthermore, the “NIH’s Dr. Straus and CDC’s Dr. Fukuda purposefully created the currently used Fukuda criteria so that those with somatoform disorders would fit under the CFS Fukuda criteria and be diagnosed as CFS” (ME advocacy, 2016, p. 1).
As a result, the CDC and NIH have muddied “the cohort even further and resulting in confusing and unreliable research under the name CFS” (MEadvocacy, 2016, p. 1). Since the implementation of Fukuda’s fake case definition in 1994, ME and CFS have been portrayed to the public as a disease of the mind.
Similarly to ME and CFS, 1994 was the year that the definition of Lyme Disease was changed to omit the fact that it is also a serious neuro-immune condition. Prior to 1994, members of the CDC published several studies that demonstrated LD as a chronic disease that affected people’s immune systems and caused neurological complications. Although the CDC has shut down independent researchers since they changed the definition, there have been other scientists who have published literature on the severity of LD.
Here are some examples of researchers (including the CDC) who have published data on the neuro-immune effects of Borreliae.
1. In a article titled Clinical Manifestations of Lyme Disease by Steere et al (electronically published in 2011), they describe LD in three distinct stages:
In the first stage, Steere et al (2011) state that LD “typically begins with a unique skin lesion, erythema chronicum migrans (ECM) (p.1). Although we know now, that many people who acquire LD do not get this rash in the beginning. Researchers also state that “patients with this lesion may also have headache, meningeal irritation, mild encephalopathy, multiple annular secondary lesions, malar or urticarial rash, generalized lymphadenopathy and splenomegaly, migratory musculoskeletal pain, hepatitis, sore throat, non-productive cough, conjunctivitis, periorbital edema, or testicular swelling” (Steere et al, 2011, p. 1). After a few weeks to months, people progress into a second stage of LD.
In the second stage, patients “develop frank neurologic abnormalities, including meningitis, encephalitis, cranial neuritis (including bilateral facial palsy), motor or sensory radiculoneuritis, mononeuritis multiplex, or myelitis. At this time, about 8% of patients develop cardiac involvement — AV block, acute myopericarditis, cardiomegaly, or pancarditis. Throughout this stage, many patients continue to experience migratory musculoskeletal pain in joints, tendons, bursae, muscle, or bone” (Steere et al, 2011, p. 1). Months to years later, LD progresses into its final stage.
In late stage LD, Steere et al claim that “60% of patients develop frank arthritis, which may be intermittent or chronic (p.1). In addition, researchers found “evidence suggests that Lyme disease may also be associated with chronic neurologic or skin involvement” (Steere et al, 2011, p. 1).
The CDC clearly articulated in this study that “Lyme disease occurs in stages with different clinical manifestations at each stage, but the course of the illness in each patient is highly variable” (Steere et al, 2011, p. 1). It’s important to note the head researcher in this study is the key contributor in the 1994 definition change of LD.
2. In an article titled Clinical Pathologic Correlations of Lyme Disease by Stage written in 1998, the CDC described how the immature immune system of a child potentially played a role in the reason that inflammatory cells are so sparse in children who acquire maternally.
This study found that Spirochetes can be recovered or seen in the infant’s tissues including the brain, spleen and kidney (Duray & Steere, 1988, p. 77). Researchers found that the chronic villi of the placenta show an increase in Hofbauer cells as in luetic placentitis. Inflammatory changes of fetal or neonatal changes are not as pronounced as in the adult, but cardiac abnormalities, including intracardiac septal defects, have been seen (Duray & Steere, 1988, p. 77).
Steere and Durray stated that “It is clear that B. burgdorferi can be transmitted in the blood of infected pregnant women across the placenta into the fetus (Duray & Steere, 1988, p. 77). Steere and Duray (1988) reiterate that “this has now been documented with resultant congenital infections and fetal demise” (p.77).
In another part of this study, Steere states that soon after the onset of ECM “there is lymphoid hyperplasia of the lymph nodes and spleen consisting of prominent germinal centers and numerous perifollicular lymphocytes, with proliferation of plasma cell precursors and mature plasma cells. The plasma cell precursors are large, appear tumor-like, and can resemble Reed-Sternberg cells” (Duray & Steere, 1988, p. 67).
Researchers concluded in this study, that “it is not known why inflammatory cells are so sparse from maternal transmission, but it is possible that an immature immune system plays a role” (Duray & Steere, 1988, p. 77).
Since these studies were done in the 80’s there has been evidence that OspA may cause adults to have immature immune cells that produce inefficient antibodies to manage certain pathogens.
3. In 1990, Karen Klinger, an author from the United Press International, interviewed CDC officer Allen Steere in regards to LD. In that article. Steere states that “in a manner that is ‘like what occurs in syphilis, we found Lyme infection can have long periods of latency and then cause slowly progressive disease’ leading to chronic problems including memory loss, fatigue, sleep disorders, numbness and spinal pain, Steere said” (Klinger 1990, p. 1).
Steere went on to talk about a new study that they had worked on. Steere said “the 14 men and 13 women in the new study, who ranged in age from 25 to 72, developed neurological abnormalities an average of 26 months after the initial infection. However, the range of time spanned from one month to 14 years” (Klinger 1990, p. 1). Steere said “24 of them developed a mild form of encephalopathy, a brain disease characterized by memory loss” (Klinger 1990, p. 1). Steere noted that these people “forgot names, missed appointments, or misplaced objects” (Klinger 1990, p. 1). He stated, “to compensate, they often made daily lists, the researchers said. Ten patients also had symptoms of depression and five had subtle symptoms of a language disturbance, with difficulty finding words” (Klinger 1990, p. 1). Steere told Klinger (1990) that “those who showed no improvement, Steere said it is possible they suffered irreversible brain damage or that their symptoms were not caused by live bacteria susceptible to antibiotics (p.1). Around this time, is when Steere and the CDC started to discover that Osps shed by Lyme Disease were causing irreversible damage to the immune system.
4. Stricker & Winger (2001) state that “although immunologic abnormalities appear to play a role in this disease, specific immunologic markers of chronic LD have not been identified” (p.43). In their study, “they evaluated 73 patients with chronic LD for lymphocyte subset abnormalities using flow cytometry (Stricker & Winger, 2001, p. 43). They found that “53 patients had predominant musculoskeletal symptoms, while 20 patients had predominant neurologic symptoms” (Stricker & Winger, 2001, p. 43).
The “estimated duration of infection ranged from 3 months to 15 years, and all patients had positive serologic tests for B. burgdorferi (Stricker & Winger, 2001, p. 43). Ten “patients with acute LD (infection less than 1 month) and 22 patients with acquired immunodeficiency syndrome (AIDS) served as disease controls” (Stricker & Winger, 2001, p. 43). The results clearly displayed a significant difference between LD patients and the control group.
They found that “all 31 chronic LD patients who were tested prior to antibiotic treatment had significantly decreased CD57 lymphocyte counts (mean, 30+/-16 cells per microl; normal, 60-360 cells per microl, P<0.001) (Stricker & Winger, 2001, p. 43). Nineteen “of 37 patients (51%) who were tested after initiating antibiotic therapy had decreased CD57 levels (mean, 66+/-39 cells per microl), and all five patients tested after completing antibiotic treatment had normal CD57 counts (mean, 173+/-98 cells per microl) (Stricker & Winger, 2001, p. 43).
In contrast, “all 10 patients with acute LD and 82% of AIDS patients had normal CD57 levels, and the difference between these groups and the pre-treatment patients with chronic LD was significant (P<0.001) (Stricker & Winger, 2001, p. 43).
Patients “with chronic LD and predominant neurologic symptoms had significantly lower mean CD57 levels than patients with predominant musculoskeletal symptoms (30+/-21 vs. 58+/-37 cells per microl, P=0.002) (Stricker & Winger, 2001, p. 43). In the end, researchers in this study found that “A decrease in the CD57 lymphocyte subset may be an important marker of chronic LD (Stricker & Winger, 2001, p. 43). In recent years, new research has shown that those who have <100 on their CD57 test have been exposed to immune suppressing pathogen such as LD.
5. In an article published in the New York Times in 1990, Steere did an interview where he described the effects of LD. Steere told the reporter that “Some victims of Lyme Disease may suffer memory loss, mood changes, tingling sensations, shooting pains and other signs of nerve damage that strike years after the initial tick bite and may not disappear with antibiotic therapy” (New York Times, 1990, p. 1). Steere described “the doctors studied 27 patients with chronic neurological symptoms that typically began a year or two after the start of their infections” (New York Times, 1990, p. 1).
Steere went on to describe their symptoms. He stated that “all but three of them had signs of mild brain disease, or encephalopathy. These included memory problems, like forgetting names, missing appointments and misplacing objects. Others felt very sleepy during the day or were troubled by extreme irritability, growing angry over what would ordinarily be minor annoyances” (New York Times, 1990, p. 1).
Steere said that LD is “is similar to syphilis” (New York Times, 1990, p. 1). Steere went on to tell reporters “although the neurological symptoms and consequences are different, in both diseases there are long periods of latent infection followed by a variety of neurological disorders” (New York Times, 1990, p. 1). Steere mentioned to the reporter that “the other major category of disorder was polyneuropathy, a disorder of the nerves outside the brain (New York Times, 1990, p. 1). Steere said that People often had back aches with shooting pains, tingling sensations and lack of feeling in their hands and feet (New York Times, 1990, p. 1). Steere said that researchers “found that a two-week course of antibiotic injections significantly improved the way the patients felt. But six months later, more than a third had either relapsed or were no better” (New York Times, 1990, p. 1). Most likely due to the immunosuppressive effects of lipoproteins shed Lyme spirochetes.
6. In a more recent article titled Suppression of Long-Lived Humoral Immunity Following Borrelia Burgdorferi Infection, Baumgarth, Elsner, Hastey & Olsen (2015) published a study that described how LD affects the immune system (p. 1). Researchers in this study state that “similar to many other infections, infection with B. burgdorferi results in strong antibody response induction, which can be used clinically as a diagnostic measure of prior exposure” (Baumgarth, Elsner, Hastey & Olsen, 2015, p. 1).
However, they found that “clinical studies have shown a sometimes-precipitous decline of such antibodies shortly following antibiotic treatment, revealing a potential deficit in the host’s ability to induce and/or maintain long-term protective antibodies” (Baumgarth, Elsner, Hastey & Olsen, 2015, p. 1).
This is further supported by reports of frequent repeat infections with B. burgdorferi in endemic areas. The data in this study displayed that “B. burgdorferi infected mice show a similar rapid disappearance of Borrelia-specific antibodies after infection and subsequent antibiotic treatment” (Baumgarth, Elsner, Hastey & Olsen, 2015, p. 1).
They found that “this failure was associated with development of only short-lived germinal centers, micro-anatomical locations from which long-lived immunity originates” (Baumgarth, Elsner, Hastey & Olsen, 2015, p. 1).
The data “showed structural abnormalities and failed to induce memory B cells and long-lived plasma cells for months after the infection, rendering the mice susceptible to reinfection with the same strain of B. burgdorferi (Baumgarth, Elsner, Hastey & Olsen, 2015, p. 1).
The inability to induce long-lived immune responses was not due to the particular nature of the immunogenic antigens of B. burgdorferi, as antibodies to both T-dependent and T-independent Borrelia antigens lacked longevity and B cell memory induction” (Baumgarth, Elsner, Hastey & Olsen, 2015, p. 1).
In conclusion, researchers stated that their studies “show that B. burgdorferi-infection results in targeted and temporary immunosuppression of the host and bring new insight into the mechanisms underlying the failure to develop long-term immunity to this emerging disease threat” (Baumgarth, Elsner, Hastey & Olsen, 2015, p. 1). Although the immunosuppression in this study was not a result of the immunogenic antigens shed by spirochetes, it displays the need to explore how LD affects the immune system.
7. In one of the most recent studies done on LD and the immune system, researchers examined “four hundred and thirty-two human serum samples organized into seven categories followed CDC two-tier Lyme disease (LD) diagnosis guidelines and Infectious Diseases Society of America (IDSA) guidelines for post-treatment Lyme disease syndrome” (Croucher et al, 2018, p. 1).
Furthermore, “all patient categories were tested for their immunoglobulin M (IgM) and G (IgG) responses against 20 microbes associated with TBD” (Croucher et al, 2018, p. 1). Researchers in this study recognized “that microbial infections in patients suffering from TBDs do not follow the one microbe, one disease Germ Theory as 65% of the TBD patients produce immune responses to various microbes” (Croucher et al, 2018, p. 1). Date in this study “established a causal association between TBD patients and TBD associated co-infections and essential opportunistic microbes following Bradford Hill’s criteria” (Croucher et al, 2018, p. 1).
This study “indicated an 85% probability that a randomly selected TBD patient will respond to Borrelia and other related TBD microbes rather than to Borrelia alone” (Croucher et al, 2018, p. 1). Researchers concluded that “a paradigm shift is required in current healthcare policies to diagnose TBD so that patients can get tested and treated even for opportunistic infections” (Croucher et al, 2018, p. 1). Given the information provided in the examples above, it’s almost disturbing that both the CDC and ILADS continue to neglect studying how LD affects the immune system.
Dearborn, Michigan – 1994
Understanding what happened at the “Dearborn” conference can make it easier for people to understand why the CDC have not only halted any further research on the true Lyme disease case definition, they are also responsible for ignoring an entire class of immunosuppressive diseases.
All that said, this is the true disease mechanism that all of us people suffering have in common. Although antibiotics and natural remedies may help people feel better from the accumulated infections that accompany Lyme disease it doesn’t fix the damage caused to the immune system by Borelliae.
Since the CDC knew that Osp’s can cause immune suppression, what were they thinking when they decided to inject a vaccine that contained OspA into people as a preventative measure against Lyme disease?
Whether you are sick from a tick bite or the LYMErix vaccine, it’s the same disease. Donald Marks, MD, PhD, former lab director for Cannaugh stated that “the company has masked serious causally-related adverse events behind qualifiers, such as “…and which may have no causal relationship with the vaccine” and “…cannot be distinguished from the natural history of the underlying disease,” all the while knowing these are confusing the issue” (Marks, 2009, p. 2).
Both LYMErix and Borreliae spirochetes contain OspA. A triacyl lipoprotein that causes immunosuppression, an antibody deficiency in its victim’s. Even the criminal Allen Steere himself published a study on how deformed B- cells caused by OspA were later shown to be an outcome of LYMErix.
In the end, CDC officers and others who were involved in the commercialization of OspA (American Lyme Disease Foundation (ALDF), Mayo Clinic, Yale’s L2 Diagnostics, Corixa, Imugen, SmithKline) knew all of this during (and likely prior to) the phase I and II trials of the OspA “vaccine” patented by Yale University (5,747,294) (Persing, 1996).
In the patent, Persing mentioned that OspA can be harmful and has immunological effects. Prior to 1994, members of the CDC also published studies describing the immunological effects of OspA.
So let me get this straight; first, you have members of the CDC who published research on how Lyme disease shed’s immune altering Osp’s.
Then, these same scientists decide to use humans as lab rats and inject them with OspA which gave many recipients late stage “chronic Lyme disease” (Berland, Fikrig & Flavell, 1992). Which begs to question that maybe it was because of this vaccine, that CDC officers decided to manipulate the LD case definition and testing in Dearborn, Michigan in 1994.
Just prior to the Dearborn conference, Allen Steere published research in which he:
1) developed fraudulent diagnostic testing that left out OspA and OspB despite those being highly immunogenic, primary diagnostic antigens (Dickson, n.d.); and
2) added an ELISA to be used as a “screening” test, to exclude the immune suppressed cases from diagnosis (Dickson, n.d.).
This was in direct opposition to his own 1986 research which was the basis for the original, 1990 case definition, and also stated that only Western blot band 41 (flagellin) was necessary to diagnose Lyme borreliosis (Patent #5,618,533) (Berland, Fikrig & Flavell, 1992). This flagellin based test, was one of the most accurate tests on LD ever created. This particular test was suppressed by Yale doctors, and never made it to market. However, that patent has recently run out. Perhaps International Lyme and Associated Diseases Society (ILADS) should look into repeating this test, so that more people can get a proper LD diagnosis.
The diagnostic standard was changed from one that reflected the persistence of spirochetes and their variable surface antigens (few changing antibodies based on Steere’s 1986 report), to one that reflects only the hypersensitivity response or the production of many antibodies.
The labs that were invited to participate did not agree with the change, and reported an average accuracy rate of 15% (Dickson, n.d.). This “two-tier” testing protocol is still the only testing accepted and used by the CDC, insurance industry and medical societies, despite not meeting FDA standards for method validation (specificity, sensitivity, etc.) (Dickson, n.d.).
In the end, this was all done so that they could make money by commercializing tick-borne diseases, test kits, and vaccines. One can only assume that if they narrowed the case definition, then they could say: “Hey, we have an 85% effective vaccine!”.
We have suffered enough abuse. We have lost everything. It’s time to end the suffering and psychiatric abuse that children, women and men face on a daily basis on account of these fraudulent case definitions. If we don’t band together and fight back, we will continue to suffer. We will be left with the physical and/or psychological long-term effects from an AIDS-like disease.
HIV is a virus that affects T-cells; whereas, ME, CFS, and LD affect the immune system and can inhibit apoptosis in B-cells. As a result, the B-cell maturation is often stunted. Consequently, B-cells remain immature and unable to produce efficient antibodies to manage reactivated viruses and opportunistic infections. That’s why patients remain ill, and some go in and out of remission.
It’s time for the CDC to acknowledge the organic outcomes of these illnesses. Also, it is time to bring these neuro-immune outcomes to the forefront of activism! The causes and presentations of these diseases may differ. However, the evidence of neurological and immunological mechanisms of the disease unites us all.
We may never unite or agree on how each disease should be defined, but one thing we should be uniting for is the corruption, fraud, human rights violations, and color of law abuse that accompanies each of these conditions.
Baehr, V. V., Strohschein, K. G., Giannini, C. undefined, Koelsch, U. undefined, Bauer, S. undefined, Doebis, C. undefined, … Scheibenbogen, C. undefined. (2015). Deficient EBV-Specific B- and T-Cell Response in Patients with Chronic Fatigue Syndrome. PLoS ONE, 9(1). doi: 10.1371/journal.pone.0085387
Bramanti, P., Salmeri, F., Soraci, L., Soraci, G., Sofo, V., Marino, S., & Gambuzza, M. (2015). The Role of Toll-Like Receptors in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis: A New Promising Therapeutic Approach? CNS & Neurological Disorders – Drug Targets, 14(7), 903–914. doi: 10.2174/1871527314666150325235247
Kitani, T., Kuratsune, H., Yamaguchi, K., Yalcin, S., & Yamanishi, K. (1994). Prevalence of Human Herpesvirus 6 Variants A and B in Patients with Chronic Fatigue Syndrome. Microbiology and Immunology, 38(7), 587–590. doi: 10.1111/j.1348-0421.1994.tb01827.x
Bansal, A. S., Ford, B., & Bradley , A. S. (2013). Altered functional B cell subset populations in patients with chronic fatigue syndrome compared to healthy controls. Clinical & Experimental Immunology, 172(1), 73–80. doi: 10.1111/cei.12043
Baumgarth, N. A., Elsner , R. J., Hastey, C. J., & Olsen , K. (2015). Suppression of Long-Lived Humoral Immunity Following Borrelia burgdorferi Infection. PLOS Pathogens, 11(7). doi: 10.1371/journal.ppat.1004976
Berland, R., Fikrig, E., & Flavell, R. (1992, February 11). US5618533A – Flagellin-based polypeptides for the diagnosis of lyme disease. Retrieved February 11, 2020, from https://patents.google.com/patent/US5618533A/en
Buchwald, D., & Komaroff, A. L. (1991). Review of Laboratory Findings for Patients with Chronic Fatigue Syndrome. Clinical Infectious Diseases, 13(Supplement_1), 12–18. doi: 10.1093/clinids/13.supplement_1.s12
Croucher, S., Meriläinen, L., Franz, O., Pirttinen, H., Quevedo-Diaz, M., Garg , K., & Gilbert, L. (2018). Evaluating polymicrobial immune responses in patients suffering from tick-borne diseases. Scientific Reports, 8(1). doi: 10.1038/s41598-018-34393-9
Dickson , K. (n.d.). Chapter 3 of Cryme Disease-. Retrieved February 11, 2020, from http://www.actionlyme.org/CRYMEDISEASE_CHP3_B.htm
Duray, P. H., & Steere, A. (1988). Clinical Pathologic Correlations of Lyme Disease. Annals New York Academy of Sciences , 539, 65–79. doi: 10.1093/clinids/11.supplement_6.s1487
Fletcher, M. G., Klimas, N. R., Morgan, R., & Salvato, F. A. (1990). Immunologic abnormalities in chronic fatigue syndrome. Journal of Clinical Microbiology, 28(6), 1403–1410. doi: 10.1128/jcm.28.6.1403-1410.1990
Klinger , K. (1990, November 21). Lyme Disease can Remain Dormant for Years. Retrieved February 7, 2020, from https://www.upi.com/Archives/1990/11/21/Lyme-disease-can-remain-dormant-for-years/8201659163600/?fbclid=IwAR1qOERy08VDenn9yMv8AqgODK6Jl6t0K-QflRhNlf_UzpbeHBNvTYzaKPA
Komaroff , A., & Goldenberg D Search articles by ‘Goldenberg D’ Goldenberg, D. (1989). The Chronic Fatigue Syndrome: Definition, current studies and Lessons for Fibromyalgia Research. The Journal of Rheumatology, 19, 23–27. Retrieved from https://europepmc.org/article/med/2691680
Marks, D. (2009). FDA meeting 2009. Retrieved February 11, 2020, from https://www.dropbox.com/s/6t6xqzrcq4jtg1a/Marks FDA Lymerix.docx?dl=0
MEadvocacy Advisory-Committee (2016, November 6). Systemic Bias Continues at NIH. Retrieved February 7, 2020, from https://www.meadvocacy.org/systemic_bias_continues_at_nih
New York Times. (1990, November 22). Lyme Disease Shows Latent Effects. Retrieved February 7, 2020, from https://www.nytimes.com/1990/11/22/news/lyme-disease-shows-latent-effects.html
Persing , D. (1996, March 6). Method for Detecting B. burgdorferi Infection. Retrieved February 11, 2020, from http://patft1.uspto.gov/netacgi/nph-Parser?Sect1=PTO1&Sect2=HITOFF&d=PALL&p=1&u=/netahtml/PTO/srchnum.htm&r=1&f=G&l=50&s1=6045804.PN.&OS=PN/6045804&RS=PN/6045804
Steere, A. C., Bartenhagen, N. H., Craft, J. E., Hutchinson, G. J., Newman, J. H., Pachner, A. R., … Malawista, S. undefined. (2011, November 8). Clinical Manifestations of Lyme Disease. Retrieved from https://www.sciencedirect.com/science/article/abs/pii/S0176672486801237?fbclid=IwAR1zuOPwXZfk4tE7AsUnquJEgHPstNjsq5D7eWNNogwdvurUPpEwhcpVedEStricker, R. B., & Winger, E. E. (2001). Decreased CD57 lymphocyte subset in patients with chronic Lyme disease. Immunology Letters, 76(1), 43–48. doi: 10.1016/s0165-2478(00)00316-3