Why do blebs matter?
Blebs outnumber spirochetes
Blebs, not spirochetes, cause disease
The 1994 report Target imbalance: disparity of Borrelia burgdorferi genetic material in synovial fluid from Lyme arthritis patients by a group led by David Persing of the Mayo Clinic, found that spirochetes could not be cultured from the fluid of Lyme arthritis patients' inflamed knees, but that DNA of the blebbed material from borrelia was abundantly present. They concluded that the disease process is initiated by the Outer Surface Proteins (Osps) carried by (and shed by) spirochetes.
Blebs overwhelm the immune system
The spirochetal survival mechanism of antigenic variation can easily overwhelm the immune system because the blebs, covered in toxic lipoproteins, disseminate throughout the host. Alan Barbour explained this phenomenon in his patent for OspA, which was later marketed as a vaccine. According to US Patent 6,719,983:
“An important aspect of the invention is the recognition that Borrelia VMP-like sequences recombine at the vls site, with the result that antigenic variation is virtually limitless. Multiclonal populations therefore can exist in an infected patient so that immunological defenses are severely tested if not totally overwhelmed.”
Blebs are covered in toxic lipoproteins
What Barbour explained is that the blebs released by Borreliae are covered in such widely variable antigens that the immune system cannot fight the infection. There are too many targets, they’re constantly changing, and some aren’t even attached to the offending organism!
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.