Here’s the proof: but how does Borrelia “persist”?

A controversial but thoroughly researched article has been published in a relatively small trade journal.

Raphael Stricker et al., including Lorraine Johnson, the face and soul of Lymedisease.org, use controversial terms, but they have done a very important job.

They have collected evidence from animal experiments and human studies (sometimes, unfortunately, as a result of autopsies) confirming the presence of Borrelia in tissues and serum after treatment.

Their achievements to date are enormous. I admit that I also quote some of them in my lectures and publications, but such a list is impressive. Here it is:

Animal experiments:

Human research:

My Lyme friends and I have discussed the topic, and I will summarise it briefly:

1. We do not wish to take a position in the chronic Lyme disease – post-Lyme debate, but we clearly see that the symptoms remaining after treatment are primarily due to the remaining infection. They can be cured with proper treatment.
2. It is not advisable to continue using the terms “chronic Lyme” or “post-Lyme/PTLDS”, as neither is well defined, in our opinion, but one side believes that one term is not, and the other side believes that the other term is not. There is no need to generate debate; patients need to be cured.
3. The infection does not need to hide because:
   1. the immune response can no longer effectively eliminate the new generation that appears every 3-4 weeks,
   2. Borrelia is faster than the white blood cells that would engulf it,
   3. monotherapy antibiotics cannot produce bactericidal concentrations in living humans.
4. For this reason, and in any case, it is unnecessary to discuss “persistent forms”:
   1. biofilm or “clumping” is primarily a characteristic of rapidly multiplying bacteria in an undisturbed environment, i.e. mostly in culture. I have never seen Borrelia like this in a blood sample.
   2. The L-form is a form that shows signs of irreversible destruction when antibodies successfully attack flagellin proteins: there is no escape from this.
   3. The cyst form is usually a cluster of several Borrelia bacteria, which is also uncommon.
   4. In addition, I have immunofluorescence microscopy and dark-field video footage of a single Borrelia curling up into a “gemma” form: like a small coin dropped into water, it sparkles, flashes and spins. This easily reverts once the danger has passed.
   5. Furthermore, Borrelia survives so-called coiling phagocytosis, i.e. it coils into the cell membrane, enters the cell in this way, and comes out in the same way, but then with a thicker “skin” with a double membrane, which is human tissue, i.e. “terrain-coloured”.
5. It is indeed absurd to think that the remaining peptidoglycans or genome of the pathogen are responsible for the persistence of symptoms without the pathogen itself.

Now the only question is: do we close our eyes and continue to believe that a short course of treatment will solve the problem, or do we take action? Do we treat it better and try to detect the pathogen using better methods?

https://www.scirp.org/journal/paperinformation?paperid=149133