Borreliosis Basics

When I began my transformation from victim to activist, I had to understand the disease process. My world had just been turned upside-down by my daughter’s diagnosis. After a period of anguished grieving, my logical side took over. I knew that with the existing IDSA party line, there was little hope for mainstream medicine to acknowledge her illness, let alone treat her. So I set out to learn everything I could about this disease, with the hope that one day, if a cure was discovered, I would be at the front of the line with my sweet, beautiful, innocent child. 

Through a series of divine connections, I found my way to the LYMErix vaccine whistleblower, a former BigPharma scientist who quite honestly scared the crap out of me. In her Facebook posts she was intimidating–smart, straightforward, no bullshit. Many people interpreted her rants about sticking to the science as personal attacks. I was afraid I wasn’t smart enough to measure up, and that I risked being the object of one of these rants, but I had a feeling in my gut that I had to know this woman. 

 After studying her Website,, I wrote a summary of what I understood to be the mechanisms of the disease process. I sent it to her in a Facebook message and asked her if it was accurate. She made a few minor corrections and inserted the more technical information, but what follows is the Borreliosis Basics piece that resulted. I’m also now honored to call Kathleen my friend, and I fail to find the words to describe how much respect I have for her. She is a remarkable woman and exceptional human being. 

 Now, chew on this: 

Borreliosis is a multi-system disease caused by a spirochetal bacterium (parasite). A spirochete is a spiral-shaped parasite with a unique mechanism for movement that features a bundle of tail-like “flagella” which resides inside the cell wall.

Borreliosis is transmitted primarily through the bite of an infected tick, but also may be transmitted by insect vectors, in utero to an unborn fetus (according to Yale), and possibly via sexual intercourse. If not treated immediately with antibiotics, the infection can persist for years and cause neurological diseases such as MS, Lupus, cancer, Chronic Fatigue/Myalgic Encephalomyelitis, ALS (Lou Gehrig’s Disease) and Alzheimer’s, according to IDSA and the CDC. Thus, borreliosis is commonly referred to as “The Great Imitator” or “New Great Imitator.” 

 Borreliae parasites have the ability to shed (bleb off) their outer membrane lipoproteins to evade detection by the immune system in a mechanism commonly known as antigenic variation. These lipoproteins are called “outer surface proteins” (Osp) and “variable major proteins” (Vmp). In layman’s terms, the blebbing, or shedding, of OspA by the borreliae parasite sends the immune system after the OspA, allowing the spirochete to hide from immune attack and persist in the host. 

Additionally, several of these outer surface lipoproteins, such as OspA (the Lyme “vaccine”–LYMErix) are TLR-2 agonists or fungal antigens, meaning they essentially disable the immune system. They do this by way of tolerance to other fungal antigens (TLR2s) as well as tolerance to other antigen types, managed by other TLRs. 

See this report : “Because IRAK1 is required forTLR7/9-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

Exposure to shed borrelial lipoproteins causes fungal tolerance in the blood and the inability to get rid of mycoplasma/eperythrozoons from the blood, especially from the red blood cells (which causes fatigue). Also, there is cross-tolerance to TLR4 agonists from constant TLR2-agonism of shed borrelial antigens like OspA and vice-versa.

This creates an environment where opportunistic infections can thrive and cause chronic, disabling disease.

Additionally, TLR2-agonist tolerance apparently reactivates latent herpes viruses, particularly Epstein Barr Virus (EBV). (Reactivation occurs thru IL-10, and the inhibition of apoptosis of OspA or EBV-infected cells, the mechanism shown above re TLR2-signaling and the inhibition of IFN-I, and perhaps other unknown mechanisms.)

Chronic EBV is probably the main driver of all these New Great and Great Imitator diseases.

Categories: Lyme 101, Lyme Disease

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11 replies

  1. Thank you for explaining Kathleen’s theories… and having the brain power to figure it out. I find the overall theory quite plausible. “Chronic Lyme” is a systemic disease.

    Current methods of treatment are obviously not working, because so many people remain sick. Treating one co-infection after another does not seem to be the answer.

    These treatments have drained all my savings. So I agree w Kathleen when she believes that no one wants to find an effective treatment because the medical world is making plenty of money as it is.

    Now that we know “chronic Lyme” suppresses the immune system, sheds fungi and reactivates HHV-4, 5, and 6, how do we treat it? Any insights?

    I appreciate your vigilance!!


    • Hello! Thanks for reading and commenting. That’s the next question everyone asks. I am not a medical professional, so none of my comments should be construed as medical advice. What we are seeing is that the NIH agrees with this model. Here is a recent post from Kathleen:

      Please share this information around (4 reports, all new) and see that the treatments for HLA-associated sepsis outcomes (MS, Lupus, maybe RA,… and is reactivated herpesviruses), is the same as
      non-HLA-linked sepsis (Chronic Fatigue, Chronic Lyme, ibromyalgia, … and is also reactivated herpesviruses and etc, like the NIH says here, pneumonia) outcomes in terms of treatment.
      Stem cells, immune boosters, B cell depletion (Rituximab)
      some say add antivirals…
      The NIH also says all these occurs as a result of exposure to TLR2-agonist like fungi, like Lyme and LYMErix… The NIH says in the NYTimes that Chronic Lyme is really about reactivated EBV/similars, summer of 2013. And Paul Duray was also an NIH employee, which, as you can see in the header graphic for this group, speaks about Lyme causing something like a leukemia (“EBV-transformed cells”).
      The last report (new) shows the same dynamic in parallel in
      oral infections.
      FROM THE NIH, Dec, 2014
      ”Stem cell transplants may halt
      progression of multiple sclerosis”
      Three-year outcomes from an ongoing clinical trial suggest that high-dose immunosuppressive therapy followed by transplantation of a person’s own blood-forming stem cells may induce sustained remission in some people with relapsing-remitting multiple sclerosis (RRMS). RRMS is the most common form of MS, a progressive autoimmune disease in which the immune system attacks the
      brain and spinal cord. The trial is funded by the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health, and conducted by the NIAID-funded Immune Tolerance Network (ITN) .
      Three years after the treatment, called high-dose immunosuppressive therapy and autologous hematopoietic cell transplant or HDIT/HCT, nearly 80 percent of trial participants had survived without experiencing an increase in disability, a relapse of MS symptoms or new brain lesions. Investigators observed few serious early complications or unexpected side effects, although many participants experienced expected side effects of high-dose immunosuppression, including infections and gastrointestinal problems. The three-year findings are published
      in the Dec. 29, 2014, online issue of JAMA Neurology.
      “These promising results support the need for future studies to further evaluate the benefits and risks of HDIT/HCT and directly compare this treatment strategy to current MS therapies,” said NIAID Director Anthony S. Fauci, M.D. “If the findings from this study are confirmed, HDIT/HCT may become a potential therapeutic option for people with this often-debilitating disease, particularly those who have not been helped by standard treatments.”
      “Preventing Secondary
      “Some people who survive sepsis can develop secondary infections days or even months later. A research team
      that included Richard Hotchkiss, Jonathan Green and Gregory Storch of Washington University School of Medicine in St. Louis suspected that this is because sepsis might cause lasting damage to the immune system. To test this hypothesis, the scientists compared viral activation in people with sepsis, other critically ill people and healthy individuals. The researchers looked for viruses like Epstein-Barr and herpes simplex that are often dormant in healthy
      people but can reactivate in those with suppressed immune systems. [Sepsis Has Long-Term Impact for Older Adults, Study Finds]
      ***** Of the three study groups, people with sepsis had much higher levels of these viruses, suggesting reactivation due to compromised immune responses. Immune suppression could make it difficult
      to defend against the reactivated viruses as well as new infections like pneumonia. The team now plans to test whether immune-boosting drugs can prevent deaths in sepsis survivors.****
      This Inside Life Science
      article was provided to Live Science in cooperation with the National
      Institute of General Medical Sciences, part of the National Institutes of Health.…
      Older Patients have the same kind of immune system as people
      with Lyme or LYMErix disease since Old People’s immune systems are
      CHARACTERIZED by crappy TLR2-agonist responses…
      NEW, Upenn, Oral infections…
      Notice this dynamic is identical to the one we propose with
      OspA/shed fungal antigens from Borrelia (TLR2-agonists) turn off the immune response, allowing the secondary infections (in our case, EBV, etc) to do all the damage (and not always inflammation, BTW);
      And it is the same as the NIH’s Sepsis dynamic in the above
      3 articles…
      Clearly points to something like OspA as the culprit
      “P. gingivalis uses this connection between C5aR and TLR2 to
      disarm and dissociate the MyD88 pathway, which normally protects the host from infection, from the proinflammatory and immune-evasive pathway mediated by Mal and PI3K,” Hajishengallis said.…/gum-disease-bacteria-…


  2. “pressed” it to reblog – and tweeted it too – awesome job on these two 🙂

    Liked by 1 person


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