You can’t plead to the CDC but you can plead to a crowd.

­     The CDC wants to project an image which says “we listen,” “we will work with you,” “we care“. The patients in the trenches know that’s not the way it is. The CDC wants to maintain a positive image. One thing they do to improve that image is to create events where patient advocates can go and speak. The advocates give advice and the CDC can take the advice or not. History provides ample evidence that they rarely adopt these recommendations. The events are more about the appearance of listening rather than providing a real opportunity to create solutions. These meetings have too many restrictions. The advocates have no power at these events. We have no vote at the table, no guarantee of print space, and no authority. They wouldn’t have it any other way. The advocates who attend have good intentions and work hard for the patient community, but all those efforts can come at a cost. When an advocate goes and speaks to the CDC, the advocate improves the CDC’s image. If the advocates accomplish something meaningful then they deserve a lot of credit. Remember though, what comes out of a meeting is only the first step. Success comes if the CDC ultimately includes that information in any final work and that rarely happens. If the advice is removed from the final work, then the hard work and efforts were in vain. The CDC gets the image boost it wants from the meeting but the patients rarely get anything positive. When the CDC’s image improves it becomes harder to convince the public they are harming us. It is not a neutral result. It is a negative result for the community.

The truth behind the image is far worse than these meetings imply. They create a shiny opaque veneer on an ugly truth. They have millions of skeletons in their closet and they don’t want them revealed. The CDC has engaged in widespread medical abuse of patients for decades. Thirty years abusing ME patients. Thirty years abusing CFS patients. Thirty five years abusing Lyme disease patients. Thirty years abusing Morgellons patients and there are more. The combined patients have put up with over a century of shared abuse, shared pain, and shared losses. The CDC is powerful. Their authority dictates the way doctors must treat us. Patients have heard for decades, “We won’t treat you for this.” “We won’t cover you for that.” “All you need is a psychiatrist.” Doctors won’t treat the patients for these diseases but many doctors will bully them. The system will make a fortune off the patients’ fading health which can last decades. Doctors will also convince friends and family that they are crazy when they actually have a brutal disease. The patients life slowly falls apart as their medical condition worsens due to the non-treated disease. Many lose their job then their home. Many eventually lose their friends and families who expect them to quit faking it because they believe some doctor that said it. Eventually the patient will become severely ill, an empty shell of who they once were. This goes on until the patients health has been totally bled dry and no more procedures can be done. When there is no more money to be made from them they are totally abandoned by the medical system and can go die.
This patient hell has been going on for thirty five years now. Thirty five years of the CDC hearing it and doing nothing. There are people in the community who still believe we can talk to them. We shouldn’t expect a 35 year abuser to change anytime soon. Most people are not aware of this widespread abuse because the medical industry is good at keeping this off of mass media. PR efforts will keep the industries image and doctors image intact. Meetings with advocates is one thing which help perpetuate a false positive image. People believe the CDC couldn’t possibly be so uncaring if they listen to patient advocates. They would certainly correct it. These meetings convey the message that the CDC listens, they work with the patient, they care. The advocates work hard to try and create something good from these meetings but nothing changes. They just don’t have any power there and that is how the CDC wants it.

We can replace attending these events with other kinds of advocacy.

  • The public needs to know we are done with the CDC’s 35 year charade. All they have done is perpetuate the widespread medical abuse of millions of patients. When they schedule a meeting, let the world outside the abused patient community know why you don’t want to attend. Advocacy groups and individuals can do this. We need to talk to the public not the CDC. Researchers such as Dr. Alan Steere and Suzanne Vernon (CDC) and Dr. Barbara Johnson (CDC) need to be called out on their bogus research.
  • A gallop poll showed 67% of the public gave doctors high marks for honesty and ethics. The top jobs are in the medical field. Why do they need to change anything if most people think they are truthful? Dismantling the CDC’s and doctors false positive image is a valid and important goal.
  • Taking it to Congress and the courtrooms as well because the law is more powerful than the medical industry.
  • Marches in the streets. Events like May We March For Lyme is one coming up in May.

Lyme disease leads to immunosuppression.


It is very clear that Lyme disease is a disease of immunosuppression for a vast majority of Lyme patients. The so-called “Lyme arthritis” only effects a minority of patients and is the only kind of Lyme officially recognized. Immune suppression is the most damaging symptom of Lyme and is not being addressed by ANY infectious disease organization. It allows other infections to become active and remain chronic.  It is primarily other viruses and bacterial infections which does the majority of damage.



Immune suppression from Lyme disease was defined out of existence through research fraud in designing the Dearborn two-tier test.


    Now 20 studies which reveal the widespread immune suppression from Lyme disease. Remember, if you have Lyme disease, a vaccination is dangerous to you. You cannot mount an adequate immune response. Your doctor will deny this is true because he simply does what he is told. It is highly unlikely that he reads peer-reviewed research like these studies here.



1994 Feb – Antigens of Lyme disease of spirochaete Borrelia burgdorferi inhibits antigen or mitogen-induced lymphocyte proliferation.
“These results have demonstrated an immune suppressive mechanism of B. burgdorferi. The magnitude of host immune responses may be dependent on the degree of suppression which is related to the spirochaete quantity and their length of presence in the host.”



1998 Jun – Borrelia burgdorferi Stimulates the Production of Interleukin-10 in Peripheral Blood Mononuclear Cells from Uninfected Humans and Rhesus Monkeys
“These results demonstrate that B. burgdorferi can stimulate the production of an antiinflammatory, immunosuppressive cytokine in naive cells and suggest that IL-10 may play a role both in avoidance by the spirochete of deleterious immune responses and in limiting the inflammation that the spirochete is able to induce.”



2000 Jul – Modulation of lymphocyte proliferative responses by a canine Lyme disease vaccine of recombinant outer surface protein A (OspA).
Gary Wormser, lead author of the Lyme disease guideline opinions is admitting OspA, the antigen in the Lyme vaccine and a surface protein, induces immunosuppression in a canine model of Lyme disease.
“…OspA interferes with the response of lymphocytes to proliferative stimuli including a blocking of cell cycle phase progression. … Future studies designed to delete the particular region or component of the OspA molecule responsible for this effect may lead to improved vaccine preparations.”
lymphocytes – immune system white blood cells.
cell cycle phase progression – replication.



2000 Dec – Early induction of gamma interferon and interleukin-10 production in draining lymph nodes from mice infected with Borrelia burgdorferi.
“The differential effect of IL-10 on IFN-gamma production in C57BL/6J and C3H/HeJ mice suggests that IL-10 is probably involved in the regulation of IFN-gamma production by LN cells during infection and may be at the root of the differential susceptibility to Lyme arthritis in these two strains of mice.”



2003 Jul – Borrelia burgdorferi-induced tolerance as a model of persistence via immunosuppression. Summary
“…we characterized tolerance induced by B. burgdorferi, describing a model of desensitization which might mirror the immunosuppression recently attributed to the persistence of Borrelia in immunocompetent hosts.”



2003 Sep – Interaction of Borrelia burgdorferi sensu lato with Epstein-Barr virus in lymphoblastoid cells.
“Since the possibility of interruption of latent Epstein-Barr virus infection has been suggested by the induction of the lytic virus cycle with chemical substances, other viruses, and by immunosuppression, we hypothesized that the same effect might happen in B. burgdorferi sensu lato infection as happens in Lyme disease patients with positive serology for both agents. … Demonstration of such findings must be interpreted cautiously, but may prove a mixed borrelial and viral cause of severe neurological disease.”



2006 Mar 15 – Borrelia burgdorferi lipoprotein-mediated TLR2 stimulation causes the down-regulation of TLR5 in human monocytes.
“We show that stimulation of human monocytes with B. burgdorferi lysate, lipidated outer surface protein A, and triacylated lipopeptide Pam3CysSerLys4 results in the up-regulation of both TLR2 and TLR1 but the down-regulation of TLR5, the receptor for bacterial flagellin, and that this effect is mediated via TLR2. … In addition, TLR2 stimulation rendered cells hyporesponsive to a TLR5 agonist. …”



2006 Jun – Borrelia burgdorferi Induces TLR1 and TLR2 in human microglia and peripheral blood monocytes but differentially regulates HLA-class II expression.
IMPORTANT: The difference in HLAs cause the two types of Lyme. The hypersensitivity type ( the “Lyme arthritis” ), and immunosuppressed type. Dr Alan Steere completely denied the existence of the immunosuppressed outcome by deliberately designing the Lyme two-tier test ( Dearborn criteria ) so the neurological outcome would test negative. Those patients are sent off to psychiatrists and told they are crazy.
“These results show that signaling through TLR1/2 in response to B. burgdorferi can elicit opposite immunoregulatory effects in blood and in brain immune cells, which could play a role in the different susceptibility of these compartments to infection.”



2006 Oct – Interleukin-10 anti-inflammatory response to Borrelia burgdorferi, the agent of Lyme disease: a possible role for suppressors of cytokine signaling 1 and 3.
“… Because it is known that cytokine signaling are induced by IL-10 and that B. burgdorferi and its lipoproteins most likely interact via TLR2 or the heterodimers TLR2/1 and/or TLR2/6, we hypothesized that cytokine signaling are induced by IL-10 and B. burgdorferi and its lipoproteins in macrophages and that cytokine signaling may mediate the inhibition by IL-10 of concomitantly elicited cytokines. We report here that mouse J774 macrophages incubated with IL-10 and added B. burgdorferi spirochetes (freeze-thawed, live, or sonicated) or lipidated outer surface protein A (L-OspA) augmented their SOCS1/SOCS3 mRNA and protein expression, with SOCS3 being more abundant. Pam(3)Cys, a synthetic lipopeptide, also induced SOCS1/SOCS3 expression under these conditions, but unlipidated OspA was ineffective…”



2007 Jan – Decreased up-regulation of the interleukin-12Rbeta2-chain and interferon-gamma secretion and increased number of forkhead box P3-expressing cells in patients with a history of chronic Lyme borreliosis compared with asymptomatic Borrelia-exposed individuals.
“… In addition, regulatory T cells might also play a role, by immunosuppression, in the development of chronic Lyme borreliosis.”



2008 Mar – Viable Borrelia burgdorferi Enhances Interleukin-10 Production and Suppresses Activation of Murine Macrophages
“B. burgdorferi induces IL-10 in vivo … Together, these results suggest that viable B. burgdorferi can suppress early primary macrophages Mφ responses during infection by causing increased release of IL-10.”



2010 – Our experience with examination of antibodies against antigens of Borrelia burgdorferi in patients with suspected lyme disease.
“RESULTS: All patients had specific antiborrelial antibodies confirmed by using the westernblot in spite of negative ELISA. Immunological investigations revealed a deficiency of cellular immunity in all patients and in a part of them (15.6%) a deficiency of humoral immunity was also found. The presence of different types of autoantibodies was detected in 17 (53.1%) patients.
CONCLUSION: In patients with persisting difficulties that could be associated with Lyme disease, it is necessary to use the westernblot test which could prove the presence of specific antibodies. It is probably due to the very low production of specific antibodies caused also by the status of immune deficiency detected in all our patients (Tab. 1, Ref. 11).”



2011 May 26 – PLOS Pathogens: Lymphoadenopathy during Lyme Borreliosis Is Caused by Spirochete Migration-Induced Specific B Cell Activation
“Together, these findings suggest a novel evasion strategy for B. burgdorferi: subversion of the quality of a strongly induced, potentially protective borrelia-specific antibody response via B. burdorferi’s accumulation in lymph nodes.”



2011 Dec – Interleukin-10 alters effector functions of multiple genes induced by Borrelia burgdorferi in macrophages to regulate Lyme disease inflammation.
“Our data show that IL-10 alters effectors induced by B. burgdorferi in macrophages to control concomitantly elicited inflammatory responses. Moreover, for the first time, this study provides global insight into potential mechanisms used by IL-10 to control Lyme disease inflammation.”



2012 Feb 1 – TLR2 signaling depletes IRAK1 and inhibits induction of type I IFN by TLR7/9.
“The inhibitory effect of TLR2 was not dependent on new protein synthesis or intercellular signaling. IL-1R-associated kinase 1 (IRAK1) was depleted rapidly (within 10 min) by TLR2 agonist, but not until later (e.g., 2 h) by TLR9 agonist. Because IRAK1 is required for TLR7/9-induced IFN-I production, we propose that TLR2 signaling induces rapid depletion of IRAK1, which impairs IFN-I induction by TLR7/9. This novel mechanism, whereby TLR2 inhibits IFN-I induction by TLR7/9, may shape immune responses to microbes that express ligands for both TLR2 and TLR7/TLR9, or responses to bacteria/virus coinfection.”



2012 Oct – Different patterns of expression and of IL-10 modulation of inflammatory mediators from macrophages of Lyme disease-resistant and -susceptible mice.
“Neutralization of endogenously produced IL-10 increased production of inflammatory mediators, notably by macrophages of C57 mice, which also displayed more IL-10 than C3H macrophages. The distinct patterns of pro-inflammatory mediator production, along with TLR2/TLR1 expression, and regulation in macrophages from Lyme disease-resistant and -susceptible mice suggests itself as a blueprint to further investigate differential pathogenesis of Lyme disease.”



2013 Aug – IRAK4 kinase activity is not required for induction of endotoxin tolerance but contributes to TLR2-mediated tolerance.
“Prior exposure to LPS (lipopolysaccharide) induces “endotoxin tolerance” that reprograms TLR4 responses to subsequent LPS challenge by altering expression of inflammatory mediators. Endotoxin tolerance is thought to limit the excessive cytokine storm and prevent tissue damage during sepsis but renders the host immunocompromised and susceptible to secondary infections….”



2013 Dec 19 – Borrelia burgdorferi Elicited-IL-10 Suppresses the Production of Inflammatory Mediators, Phagocytosis, and Expression of Co-Stimulatory Receptors by Murine Macrophages and/or Dendritic Cells
“… The IL-10 levels appear able to block many of the immune functions of these anaphase-promoting complexes (needed for cell replication) that should be critical for controlling Bb infection. … Because macrophages (removes dead/dying cells and dibris) and dendritic (skin) cells are believed to be largely responsible for moderating the early immune responses against Bb deposited into the skin, these findings suggest this IL-10 elicitation may be largely responsible for the dysregulated early leukocyte responses and delayed adaptive responses that are believed to have a major influence in the ability of Bb to efficiently disseminate and persist … “



2015 Jan – CD4+ T cells promote antibody production but not sustained affinity maturation during Borrelia burgdorferi infection.
“The data further suggest that B. burgdorferi infection drives the humoral response away from protective, high-affinity, and long-lived antibody responses and toward the rapid induction of strongly induced, short-lived antibodies of limited efficacy.”



2015 July 2 – PLOS Pathogens: Suppression of Long-Lived Humoral Immunity Following Borrelia burgdorferi Infection
Immunosuppression is one of the worst kinds of damage one can get from an infectious disease. Eventually you contract other infections and they become active for years and decades. Infections like EBV, other herpesviruses, and mycoplasma infections slowly deplete, exhaust, and damage your entire body and mind.
“This data illustrate the potent, if temporal, immune suppression induced by Borrelia-infection. Collectively, the data reveal a new mechanism by which B. burgdorferi subverts the adaptive immune response.”

This is further information on the above study.

2015 Jul 15 – Lyme disease subverts immune system, prevents future protection
““We demonstrated that an animal infected with Borrelia burgdorferi, the corkscrew-shaped bacteria that cause Lyme disease, launches only a short-lived immune response, and that protective immunity against repeat infections quickly wanes,” said Nicole Baumgarth, a professor in the School of Veterinary Medicine and an authority on immune response to infectious diseases at the UC Davis Center for Comparative Medicine.

“This study also suggests a possible mechanism responsible for the disappearance of antibodies following infection and subsequent treatment with antibiotics,” she said.

The bacteria initially trigger a strong immune response in an infected animal, but findings from this study indicate that the bacteria soon cause structural abnormalities in “germinal centers” — sites in lymph nodes and other lymph tissues that are key to producing a long-term protective immune response.

For months after infection, those germinal centers fail to produce the specific cells — memory B cells and antibody-producing plasma cells — that are crucial for producing lasting immunity. In effect, the bacteria prevent the animal’s immune system from forming a “memory” of the invading bacteria …”



All the abused patient groups in medicine share what is essentially the same disease. Immune suppression with active opportunistic infections. The immune system is suppressed in all these diseases; Lyme disease (OspA damage) , ME/CFS, Gulf War illness (fungal contamination from expired vaccines), Fibromyalgia, post sepsis syndrome, Gardasil vaccine victims with severe fatigue, and all fungal contaminated vaccines. The symptoms are virtually interchangable.

The Dearborn Lyme test ( the 2-tier test ) was designed to test negative for the vast majority of those of us with Lyme in order to sell a bogus vaccine Lymerix. The vaccine made from OspA a surface protein actually caused the disease it was supposed to protect us from. Many who got the vaccine became sick ( immune suppressed then chronic infections ). The bogus vaccine was taken off the market. The test design is based on provable medical fraud. It is a matter of the DOJ doing its job and prosecuting those responsible.!english/c7up