Discussion in 'Infections: Lyme, Candida, EBV ...' started by Tom Kindlon, Jul 25, 2019.
Is this the Allen Steere thing? I cannot access the article/study. I'm thinking this is Allen Steere's umpteenth attempt at trying to prove it really ain't persistent Lyme that's causing all those pesky persistent symptoms. Rheumatologists...Go figure.
Some of my favorite people....
If it ain't the knees or facial palsy, it ain't there. And even when it is, it's likely nonviable remnants, so it really isn't.
Of course, it's full court press time now that the draft of the new Lyme Guidelines is out.
Let's see, in the last two weeks articles have surfaced in the NY Times, WaPo, The Guardian, the New York somethingoranother. I know I'm missing some.
Just a short note of explanation to any who might wonder.
A problem within the Lyme community is that frequently only overt signs are given any degree of serious scrutiny by some researchers. Swollen knees, facial palsy, EM or - in Europe - ACA. Things that the researcher can see.
If someone cannot see it, then you as a patient are not suffering with it - or only imagine you are.
So when someone CAN see it, and they are still striving to deny what's behind what even they cannot refuse to admit is blatantly there, well, it can drive a patient to cynicism.
Weird. No one is saying that. The bacteria is definitely cleared up, no one disputes that. Symptoms remain, that's the puzzle and obviously they would be a consequence of the infection but not the bacteria itself.
The answer to one's question is rarely a solution to the problem. Good example here. Like Wessely proudly boasting that after 3 decades of hard work they can confidently say that mood is not a predictive factor in ME, a question no one who understands the first thing about this disease has ever asked and quite frankly a completely pathetic thing to boast about.
Is the emperor's new butt flap purple or beige? Let's put it to the test! The answer will shock you. More at Buzzfeed Science.
No, that is inaccurate. Many dispute that. Northeastern University's Kim Lewis, Tulane's Monica Embers, Johns Hopkins' Zhang... Many more. These and other's have published within the past few years that Bb persisters happen despite IDSA-recommended treatment protocol.
Indeed, there has been a concerted push to discover and test new protocols because of these findings.
Do you know what's the hypothesis on where the bacteria would be hiding? Or how they could be hiding? I'm sure bacteria can evolve to fool the immune system but we should still be able to find them in lab tests. A decade or so ago, certainly, but we have the resolution for it now.
So is that a different approach than post-lyme? Stealth lyme? Mustachioed-and-fake-glasses lyme? Is that a thing, bacteria that can remain hidden? Viruses, sure, but bacteria aren't as good at the ninja thing.
@rvallee, a lot to unpack in your questions, but the short answer is Yes, if you are asking in general. Let me see if I can get my hands and computer to comply and let me copy and paste each of your questions with some short answers. Sorry for brevity; these are fair and good questions, and I could devote a chapter to each. I won't, though.
Yes, in privileged sites like brain tissue, heart muscles, tendons, lymph nodes, biofilms, etc - things that would involve invasive procedures to find - and even then it's hit or miss since the testing isn't geared toward direct culture, and neither is the spirochete.
Sure, with mechanisms like antigenic variation and morphing into different forms like L-forms and round bodies.
No, sorry, we cannot. We can sometimes culture the derma aspects, right? Like the bulls-eye rash and ACA in Europe. Once in a while we get lucky with synovial fluid. But other than that, it's pretty much a crap shoot. You've got some PCR capabilities, but the good ones get shot down by the CDC (at least one did), and most everything else is indirect. The notable exceptions are post-mortem exams. There is a running list of case studies where they examine corpses and find spirochetes despite treatment, sometimes protracted treatments. Happens frequently in animal studies as well, including primates like Rhesus monkeys. Once in a while you get lucky and a Lyme patient survives a catastrophic attack and survives, and because of the circumstances they are able to culture the spirochete. This happened to Neil Spector a Duke researcher who almost died from Bb-induced heart attack.
Yes, it is different than post-lyme. Bacteria that can remain hidden happens. Think syphilis, also a spirochete. Borrelia Burgdorferi is considered one of the most complex bacteria known to man, some argue the most complex. Bb evades, successfully, the immune system and most of our attempts to capture it in real time, in vivo, once it has disseminated and progressed to late stage.
The paper was first published June 17th. This was one of the first news articles reported on that date
What's interesting is something similar was discussed for Q-Fever during the Q&A at the Emerge Australia ME/CFS conference. Apparently many years ago an Australian researcher reported finding fragments of the Q-Fever bacteria in bone marrow........... researcher has since passed away.
This is another article on the topic (highlighted at the time by ME researcher Derya Unutmaz in a tweet)
@wigglethemouse and @rvallee , this has been part of the conventional Lyme narrative since circa 1990.
The "small but significant number of people with Lyme disease continue to suffer..." is widely acknowledged to be 10-20 percent of infected individuals. At currently around 400,000 cases per year in the US alone, that's a staggering amount of people still sick since, say, 1975. (Of course, there weren't that many cases per annum back 45 years ago)
"Lyme arthritis, the most common feature of late stage disease..." also is part of that narrative. They need to qualify that with "observable". Most Lyme advocates would argue that Lyme arthritis is far removed from being the most common feature of late-stage Lyme.
Edit to add: This is all predicated on the idea they insist on nonviable spirochete remnants to be the culprit. They are going out of their way to say, "Hey look! No hands!" and they aren't even riding a bike.
OK that was the puzzling thing since it's implied by post- that the initial infection has to be ended.
Damn the limits of our knowledge. Human behavior is still just as irrational about things in the shadows, and seemingly almost random.
An assumptive close, typically.
ETA: This gets really complicated real fast. Truth be told, persistent symptoms may in fact be due to an immune malfunction, which may involve debris. We don't know. Neither side has been demonstrated conclusively, persistently.
Where I draw the line is how they attack patients and demean them, and it makes me ask why. And why no NIH research into late stage diagnostics? And why all the contradictory positions until right before the 1994 diagnostic consensus criteria - which never received a true consensus - and the concerted move toward vaccine revenues?
But attempting to discredit or marginalize patients...What researchers do that to patients in their own discipline? Why would they?
The Lyme Disease active agent is a spirochaete, as is Syphilis. Which is well known for hiding for years (post initial infection) and then becoming active again bringing ruin, insanity and death (at least in historical times!). And it's another of the great medical imitators, showing lots of different signs and symptoms. Mimicking lots of diseases.
I wonder if looking where (untreated) Syphilis spirochaetes commonly hide might be the kind of place to look for Borrelia burgdorferi persisting? I've no idea if this kind of research has been done on either disease, and don't have the energy right now to try and find out - bad PEM after outing 2 days ago.
This post may well be off topic, but I'm so PEM-ed I can't work out if it is or isn't.
If you're interested you might want to check out the work of Dr. Judith Miklossy. She's published a lot in the area of spirochetes. I cannot remember is she is out of Austria or Switzerland or...Regardless, she makes comparisons between different spirochetal infections and draws pretty sharp inferences.
Thanks ever so much @duncan, I'm really not up to it at present, but I've bookmarked and hope to get back. I may be gone for some time, as family (Kids) including the dreaded Grandkids are arriving tomorrow... Limits time on internet a bit, but it's the sensory envelopment that really does me in. But it's fab to see them. They're here for 2 weeks. Mix of and !
This looks huge. If confirmed, perhaps this could be a major breakthrough.
If I understand correctly, they focused on peptidoglycan (PG), an essential component of bacterial cell envelopes. Apparently, the PG of B. burgdorferi, the bacterium that causes Lyme disease, has an unusual chemical composition. And because the B. burgdorferi genome lacks proteins required to recycle components of PG, the authors suspected these might be dumped into the local environment, something that was confirmed when they tested it by radiolabelling the components.
They then showed that patients with Lyme arthritis (LA) had B. burgdorferi PG material, not in their blood, but in synovial fluid which is found in the cavities of our joints. So it was in the location where patients were having symptoms and it was still there after full antibiotic treatment, suggesting that B. burgdorferi PG material persists long after the Lyme bacterium is eradicated.
The authors also showed that most LA synovial fluid samples contained significant levels of antibodies against B. burgdorferi PG, whereas control samples from patients with other forms of arthritis did not. Furthermore, the antibodies in LA patients were specific for PG; there was little to no reactivity to PGs from other bacteria - in contrast to the controls with other forms of arthritis.
The LA patients also had upregulation of virtually all major proinflammatory markers in the synovial fluid (think: IL-1, TNFα, IL-6, IL-8). They then showed that B. burgdorferi PG alone can elicit these proinflammatory cytokines when tested in human peripheral blood mononuclear cells. Finally, they demonstrated that injecting B. burgdorferi PG into the veins of mice causes acute arthritis symptoms such as swelling of the joints.
So the authors seem to have demonstrated a mechanism by which Lyme infection can cause symptoms after the B. burgdorferi and the infection have been eradicated by antibiotic treatment. This was about Lyme arthritis but the authors suggest something similar might be true for "other Lyme disease manifestations". I don't have the knowledge and skills to evaluate the technical aspects of the paper and it is sometimes unclear how many samples and patients they used in each of their experiments, but it all sounds quite impressive. Would be interesting to hear what more experienced science-minded forum members think of this.
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