"There is no such thing as consensus science."
~Michael Crichton
Among the medical profession there is a common belief that Lyme disease is hard to get and easy to cure. This belief represents neither the patient experience with, nor the published literature about Borrelia burgdorferi, the Lyme spirochete.
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What are spirochetes?
In basic taxonomy terms, spirochetes are their own phylum, "Spirochaetes" in the Eubacteria kingdom. The main distinction of Spirochaetes from other phyla is the unique structure and location of their mechanism of motility, their flagella.
Borrelia spirochetes have the ability through various mechanisms to avoid being killed by antibiotics and the immune system.
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How do spirochetes cause disease?
Through their mechanism of immune evasion, spirochetes shed bits of their outer surface (known as "blebs"). These blebs are far more abundant than spirochetes and can easily overwhelm the immune response. Lyme disease is caused by the lipoproteins on the blebs: not the spirochetes themselves.
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What's so bad about blebs?
The blebs that are shed by borrelia to evade the immune system are covered in Outer Surface Proteins, or Osps, such as OspA, OspB, OspC, and so on. These Osps are characterized by their chemical structure as "triacyl lipoproteins". In organic chemistry, structure equals function. Here we explain how the Osps function to cause disease.
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Lyme causes immunosuppression
Many research groups have confirmed that OspA gums up the immunity works, causes immunosuppression and inhibits apoptosis, the natural process of programmed cell death which is supposed to limit infection. Here we cite published research on the damaging effects of OspA.
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What is "Chronic Lyme"?
"Chronic Lyme" is a misnomer, but that doesn't mean people aren't terribly ill. Yes, spirochetes are permanent, but as we now know, it's the toxic lipoproteins that cause illness via immune system damage. Here we delve into downstream effects of Borrelia burgdorferi infection and immunosuppression.
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