For those who can't go to the link, here is the text. It is long.
Cyst busters? We had it wrong all along.
Research from Dr. Zhang’s lab at JH shatters many iconic beliefs about Lyme therapies.
We know that Lyme disease, or rather the causative organism, Borrelia burdorferi, is very difficult eradicate. In vitro (in a test tube) it took a combination of 3 antibiotics to accomplish the task. Doxycycline was a requirement. The other drugs are either unavailable or prohibitively expensive, (cefoperazone and daptomycin).
Persistent viability of the spirochete relates to its ability to form round body forms and other pleomorphic variants and to from aggregates of spirochetes protected by a muccopolysaccharide covering. Rather that the terms: L forms, cyst forms and biofilm colonies, Dr. Zhang simplifies: there are two groups,rapidly dividing forms (spirochetes) and stationary forms (persisters). Cocktails of drugs are needed to eradicate the organism. At this point we know little about the synergy of various combinations.
First off, this is not new, but Lyme does not form L-forms. L forms are bacterial lacking a cell wall, like mycoplasma. Alternatively, some gram negative bacteria, treated with antibiotics shed their cells walls transforming into L forms. L forms cannot survive outside the milieu of the intracellular cytoplasm of the host cells. Lyme spirochetes are encased in a dual membrane, not a cell wall. Although the bacteria may have an intracellular location they are primarily extracellular. Cell wall drugs work because the Lyme spirochetes have something like an internal skeleton comprised of cell wall material, peptidoglycans. Lyme does not form true cysts. The terms round body form and pleomorphic variants is more accurate.
I don’t like the term cyst busters (always reminds me of ghost busters). It may be easier to consider Lyme as a dichotomy of spirochetes and persisters.
I am sorry that I have bored you so far. The rest may be of greater interest.
Doxycycline remains the first line when it comes to treating spirochete forms. Doxy has no impact on stationary forms. You already knew this.
New facts:
Flagyl is not a “cyst buster.” It does not kill stationary forms any better than doxycycline. ( you probably did not know this) This also true for amoxicillin. Ceftin does have the ability to kill both active and stationary forms of Lyme. Rifampin does not kill Lyme by itself but confers persister killing effects to doxycycline and amoxicillin.
I was sure that Tindamax must kill stationary forms. It works so well in the clinical setting. So I asked Dr. Zhang and he responded. Unpublished data show that Tindamax is ineffective against stationary form of Lyme, perhaps slightly better than Flagyl. How could I be so wrong?
Then there is a long list of drugs that kill Lyme better than currently used drugs, at least in a test tube. Two drugs stand out: Diflucan and Artemisinin.
Why do Flagyl and Tindamax work so well? These drugs have excellent penetration into tissues and into the brain. Perhaps this property and synergy explain clinical effectiveness. Tindamax (one of my favorites) is known to concentrate in bodily fluids and tissues extremely well.
Doctors have added Flagyl and Tindamax to Omnicef and Ceftin – for decades, because they are “cyst busters.” These doctors had wrong the whole time. It was always the other way around.
Ceftin remains a highly touted Lyme drug. It is said to be the only second generation cephalosporin that penetrates the blood brain barrier. Omnicef is a third generation cephalosporin, like Rocephin. All third generation drugs can pass through the BBB. Early studies cited in the literature proved that Ceftin was effective in treating early Lyme patients with EM rash. It was not studied for late state Lyme disease, unlike doxycycline.
All cephalosporins do a poor job of getting into the brain. They only penetrate the brain when there is active inflammation in the meninges (lining around the brain). Oral drugs like Ceftin and Omnicef have poor uptake into the brain in patients with chronic Lyme encephalopathy. Tindamax and Flagyl may not kill persisters better than the others but they penetrate hard to reach places including the brain.
Amoxicillin, which like Ceftin/Omnicef does not kill persisters but amoxicillin has slightly better penetration into the brain/central nervous system. I have found it more effective in most patients.
Then we are left with the question: how do we kill Lyme persisters in the brain?
IV Rocephin, with adequate brain penetration does have anti-persister properties. Perhaps IV Ceftin (cefuroxime) Zinacef, works better – worth a try.
Obvioiusly we can’t order IV antibiotics for everybody.
Rifampin crosses the BBB well and should boost the anti-persister effectiveness of drugs such as doxycycline. I have found this clinically to be the case.
Test tube results to not always translate into clinical results. Sulfa drugs kill persister and penetrate well into the brain; clinical efficacy in my practice has been lacking.
What about Diflucan? penetrates well into the brain and kills persisters. Role in Lyme to be determined.
Artemisinin? This drug has a short half-life. This is why a derivative combined with a longer acting agent (Coartem) has greater efficacy for malaria/babesiosis. Artemisinin has fair brain penetration. It has activity against Lyme persisters. Clinical use for Lyme unknown. We had a lot of stuff wrong but new doors have been opened as the search for the best way to treat Lyme goes on.
-------------------- Bite date ? 2/10 symptoms began 5/10 dx'd, after 3 months numerous test and doctors
IgM Igenex +/CDC + + 23/25, 30, 31, 34, 41, 83/93
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Currently at around 95% +/- most days. Posts: 3134 | From Massachusetts | Registered: May 2010
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Judie
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posted
Wow, great stuff. Thanks!
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Keebler
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- Thanks so much for posting this, very interesting. -
Posts: 48021 | From Tree House | Registered: Jul 2007
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It might be my brain fog, but I still don't quite get it.
So is he saying that, while Tindamax and Flagyl don't bust cysts, they do, in fact, help with the tissue penetration/BBB crossing of drugs like Ceftin and Omnicef?
In other words: Ceftin/Omnicef etc. do the killing of persisters and Tindamax/Flagyl just support these drugs, helping with deeper tissue/brain penetration ...?
Hope this makes sense ... lots of brain fog,
N.
-------------------- I appreciate all your replies. If it takes me a while to respond, it is either because I'm too sick or because I am unable to log in. From European servers, Lymenet is very frequently inaccessible for days at a time ... Posts: 235 | From Europe | Registered: Jul 2012
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posted
Artemisinin is a Lyme drug? So when we take it, and feel we have a Babs herx, we might actually be dealing with a Lyme herx ... What the heck?
It does seem like this is ground-breaking new research!
-------------------- I appreciate all your replies. If it takes me a while to respond, it is either because I'm too sick or because I am unable to log in. From European servers, Lymenet is very frequently inaccessible for days at a time ... Posts: 235 | From Europe | Registered: Jul 2012
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bcb1200
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posted
Remember folks, this is all done in a test tube and what happens out of the body (in vitro) doesn't always equate to what happens in the body (in vivo).
But it is good info nonetheless.
-------------------- Bite date ? 2/10 symptoms began 5/10 dx'd, after 3 months numerous test and doctors
IgM Igenex +/CDC + + 23/25, 30, 31, 34, 41, 83/93
Currently on:
Currently at around 95% +/- most days. Posts: 3134 | From Massachusetts | Registered: May 2010
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posted
So I'm currently on Tindomax. Does this mean I should stop taking it, b/c it doesn't work?
Posts: 79 | From Austin | Registered: Jun 2015
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TF
Frequent Contributor (5K+ posts)
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posted
Some quotes from the blog that say that Tindamax and flagyl are very useful:
"Why do Flagyl and Tindamax work so well? These drugs have excellent penetration into tissues and into the brain. Perhaps this property and synergy explain clinical effectiveness. Tindamax (one of my favorites) is known to concentrate in bodily fluids and tissues extremely well."
"Tindamax and Flagyl may not kill persisters better than the others but they penetrate hard to reach places including the brain."
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bcb1200
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Member # 25745
posted
quote:Originally posted by me: I see this doc and he is amazing. I saw him yesterday. He is keeping me on the Tindamax. Therefore, I'm ASSUMING that it depends on the individual.
NO! Stay on all meds per your DOC. This doesn't mean it isn't working! It just means it could be working in a different way than we expected.
-------------------- Bite date ? 2/10 symptoms began 5/10 dx'd, after 3 months numerous test and doctors
IgM Igenex +/CDC + + 23/25, 30, 31, 34, 41, 83/93
Currently on:
Currently at around 95% +/- most days. Posts: 3134 | From Massachusetts | Registered: May 2010
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Tincup
Honored Contributor (10K+ posts)
Member # 5829
posted
bcd said.. "Remember folks, this is all done in a test tube and what happens out of the body (in vitro) doesn't always equate to what happens in the body (in vivo)."
I agree 100%. In fact, some test tube results can be non-effective in humans and/or even dangerous.
The info in the article came mostly from Johns Hopkins studies (VERY LIMITED amount of studies) and the researchers do NOT recommend treating humans using that info. A LOT more research needs to be done first.
Tincup
Honored Contributor (10K+ posts)
Member # 5829
posted
As for no "L-forms"? There appears to be a difference of opinion between Johns Hopkins and Dr. S of ILADS in CA.
"Cell wall-deficient (CWD) bacterial forms were first described in 1935 by Klieneberger, who named them L-forms after the Lister Institute where she worked.74
Subsequent research by Dienes showed that various bacteria could form CWD colonies and then revert back to bacillary morphology under appropriate conditions.75
An extensive review by Domingue and Woody highlighted the extent of CWD morphology in many bacterial strains and the potential role of these mutant bacteria to produce persistent infection and chronic diseases.76
The confusing terminology used to describe CWD bacteria has hindered work in this field. While the term ‘L-form’ or ‘spheroplast’ describes CWD morphology in coccobacillary organisms, the term ‘cyst’ or ‘round body’ has been used to describe similar morphology in spirochetes.76"
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