At first, I was a bit irritated at this exercise of parsing out this "chronic" Vs."late" terminology. But now I see that it is extremely relevant and important and, really, is at the heart of the debate and the very center of the whole Lyme controversy. So thank you, X-member, for bringing it up - and keeping at it!Chronic or Late Lyme Neuroborreliosis: Analysis of Evidence Compared to Chronic or Late Neurosyphilis
Importantly, the existence of late Lyme disease is approved by all official guidelines in the U.S., Canada and Europe. The terms “late” and “chronic” Lyme disease, as in syphilis, are synonymous and define tertiary Lyme disease. The use of “chronic” Lyme disease as a different entity is inaccurate and confusing.
So, one question to ask would be: Are all late-Lyme infections chronic and incurable?
We really have 2 problems here: One is a late-Lyme infection that may or may not be possible to completely eradicate. And the other is the question of permanent (or temporary) brain (or nerve, spine, joint, etc.) damage. Or, of course, both of these issues may be happening at the same time.
This difference is really important to me due to my inability to take further antibiotics in such case that I may still be actively infected. Would you agree that these two possibilities would call for vastly different treatments from one another?
This next statement by X-member is a whole separate issue and should probably have its own thread:
Does a late Lyme infection always indicate a disseminated infection? Whenever I see a picture of the classic bulls-eye rash, I always wonder why it is shaped that way? Why is it not a solid circle of inflammation radiating outward from the bite evenly in all directions? Why is there a center red spot surrounded by a ring of no inflammation that is then followed by another red ring of inflaming, reacting antibodies?I don't agree that a disseminted infection is the same thing as a late borrelia infection.
(I believe there has been some work on this question, but I can't remember or gather my thoughts about it coherently. I would greatly appreciate any info. I did find this picture -
https://ocimc.files.wordpress.com/2013/ ... hanism.jpg
It seems Salp15 prevents antibodies from binding to the spirochete along with some OspA and OspC switching. But then, this is a subject for yet another entire thread!)
How does this happen? And why does this happen? Does it somehow aid the spirochetes in their dissemination? If that is so, then you could say that as soon as the spirochetes enter the body, the infection is immediately disseminated. So, perhaps, all Lyme - acute and otherwise - can be considered a disseminated Lyme infection?