Monday, 4 October 2010


Evolution and Distribution of the ospC Gene, a Transferable Serotype Determinant of Borrelia burgdorferi

Alan G. Barbour and Bridgit Travinsky

The full article is available through the above link and something I felt was highly important was

'Nevertheless, we doubt that the observed antigenic diversity of OspC is merely epiphenomenal to functional differences between proteins. The range of pairwise sequence distances among family of surface proteins of the relapsing fever agent ospC alleles nearly matches that of the highly polymorphic Borrelia hermsii immunity (4). Possibly, both immune and niche selective forces are in play, but their relative contributions remain to be determined.'

I was alerted to this through the comments from

Microbe World

Lyme Disease Bacterium Collaborates with Accomplices to Evade Immune System

submitted by Merry Buckley on September 29, 2010

Warning: the bacterium behind Lyme disease is collaborating with its accomplices to construct a gene that can defeat your immune defenses.

Although this work supports much that Ben Luft has been studying for some years and has been found by other researchers over the last 20 years, the significance as I see it is that Barbour an IDSA doctor has long since supported the IDSA Guideline Authors stance and this very clearly is a move towards what ILADS doctors have been saying for years.

Are we at last at that long awaited tipping point in the science surrounding this emerging disease?

I previously posted the Tom Grier lectures, links in my side bar an extract from lecture number 4 below shows that Pachner had already published on similar findings.


1) Normal uninfected mice are inoculated with Borrelia burgdorferi in the tail vein.

2) One month later, blood is isolated from the tail of the same mouse, and the bacteria are isolated for tests.

3) The bacteria are also isolated from the brain of the same mouse, and kept completely separate for testing.

4) The antibodies from the mouse’s blood recognize and attack the bacteria that were isolated from the blood of the mouse.

5) The same antibodies fail completely to recognize the bacteria that were isolated from the same mouse’s brain; it is as if these bacteria were completely invisible to the mouse’s immune system.

What has happened to the bacteria in the mouse brain?

Once the bacteria were isolated within the brain, it was then cut off from the peripheral immune system.

This allowed the bacteria to change with each new bacterial division, and without the mouse’s immune system recognizing the changes; it is just like a criminal getting a face-lift and wearing a disguise.

The immune system kept up with the bacteria trapped in the blood, but could not make antibodies to the Lyme bacteria trapped within the brain.

The antibodies that were being produced no longer recognized the bacteria because it was still looking for the original strain, and what were now in the mouse’s brain were several generations away from the strain that Dr. Andrew Pachner started with.

Basically in crude terms, the Lyme bacteria that became isolated within the brain, mutated.

The Lyme spirochete we started with that was originally injected into the tail, is no longer the same isolate that Dr. Andrew Pachner found in the brain of the same mouse.

You now begin to see how current Lyme tests that are created using a laboratory strain of bacteria; a strain not even found in nature, can hardly be expected to keep up with the over 200,000 possible variations that Borrelia are capable of producing.

These findings give reasons for:-

the problems with seronegativity,

the problems in finding effective vaccines

the reasons why the immune system and antibiotics combined have difficulty eradicating the infection especially the longer it is allowed to get established.

Public awareness and Doctor awareness is an immediate concern to prevent others un-necessarily being infected and allowed to progress into a chronic health problem for which there is no known definitive treatment cure.

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