Biofilm dissolving and cyst busting is key!
Posted by tcw (Member # 15698) on :
Bb can tranform from spirochetal form to L-form in a matter of hours, and they are not effected by beta-lactam abx during that phase. This includes penicillins, cephalosporins, - cell wall inhibitors. It seems to be unclear if Bb can reproduce as an L-form.
Different strains of Bb have different natural resistance to various abx, but without a culture you may not know which strain you have. In that case you have to take the hard path - try different abx and see what works.
Acquiring new capabilities from other bacteria (horizontal plasmid tranfer) should be possible, but my guess is that it is not a big issue for most infected patients.
Acquiring new capabilities via random mutations in the genome of Bb seems less likely yet - Bb does not grow very fast (by bacterial standards) and they have a very small genome (set of DNA).
My feeling is that the persistence of the infection is mostly due to the intracellular location (hard to get abx inside cells in large doses), the L-form (which makes cell-wall abx useless) and slow metabolic rate of Bb (protein inhibiting abx take longer to work).
Posted by Marnie (Member # 773) on :
Less than 20 minutes to go into a cyst form in "hostile conditions".
Take a straw and pretend it is Bb. Roll it up.
See a picture here (page 2 right side) *Coiled* spirochetal structure inside cyst:
If we can get MgCl2 into the cell to displace NaCl, then there should be a change in the osmotic pressure which may impact the CWD form. (?)
[ 05-06-2009, 03:52 PM: Message edited by: Marnie ]
Posted by eagle (Member # 19278) on :
So should be constantly be on a cyst-buster? Or at least be pulsing cyst-busters throughout treatment?
Do cyst-busters dissolve biofilms?
Posted by Marnie (Member # 773) on :
Look closely at HOW THE cyst busters are supposed to WORK.
About biofilms:
In nature, a large fraction of bacteria are found to be associated with surfaces. Bacteria attached to a surface form a biofilm (O'toole et al., 2000; Sauer, 2003) that protects the bacteria from harsh physical conditions and forces. Biofilms also provide protection from attack by antibiotics and the immune system.
Bb we KNOW, binds to our plasminogen (near the middle of this cross shaped protein) which -> plasmin which Bb uses as it's second "cloak" to evade the immune system.
The first protein "cloak" Bb comes from the tick's saliva. It is called SALP 15 and that protein disrupts calcium fluxes and allows invasion of Bb initially.
Bb has a PKC *inhibitor*. It is PREVENTING a calcium activated transfer of phosphates.
P= protein K= kinase (these transfer phosphates) C = calcium ACTIVATED
It has a gene to transport Ca OUT of the cell.
Posted by Keebler (Member # 12673) on :
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If allicin is used along side, it can help prevent resistance - and allicin also helps against biofilm. By shifting your protocol around a bit every so often, that also helps.
Andrographis is another herb that can be rotated. Coptis, too.
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Posted by VB (Member # 16824) on :
does andro help with biofilm?
Also, what abx get the intracellular forms?
How about L-forms?
If they're not all being addressed simulatneously (meaning multiple antibiotics that addresses ALL forms at once), is the bacteria just converting to a form that isn't currently being treated?
Posted by Marnie (Member # 773) on :
Antibiotics do not hit/destroy CWD forms (= L forms).
Antibiotics work by either destroying the cell wall or preventing it from forming in the first place.
Once CWD...
That is where osmotic pressure changes comes into play (beneficial).
Or ultrasound.
Or, I suspect, barometric pressure changes (O2 levels change).
Posted by eagle (Member # 19278) on :
quote:Originally posted by Marnie: Antibiotics do not hit/destroy CWD forms (= L forms).
Antibiotics work by either destroying the cell wall or preventing it from forming in the first place.
Once CWD...
That is where osmotic pressure changes comes into play (beneficial).
Or ultrasound.
Or, I suspect, barometric pressure changes (O2 levels change).
Marnie, Are you saying that no antibiotics can touch the L-form?
What exactly is the L-form? Isn't it still unknown if or how the L-form differs from the cyst form?
Do you think the "cyst-busters" work? From your other post above its sounds like you don't?
What's a brain-fogged layperson like me to do? Posted by VB (Member # 16824) on :
Also, can anyone answer if andrographis touches biofilms at all? I thought I gathered that from a post above, but I'm not quite sure if I read that correctly.
Posted by tcw (Member # 15698) on :
quote:Antibiotics do not hit/destroy CWD forms (= L forms).
Antibiotics work by either destroying the cell wall or preventing it from forming in the first place.
Marnie, I have not seen any evidence that protein synthesis inhibitors are not effective on L forms. If the L forms are metabolically active, they need to transcribe proteins from DNA, and most abx other than beta-lactams work this way. Whether the action is at the ribosome, mRNA or via folate synthesis inhibition - if the bacteria is metabolically active it needs these functions.
If the L form is more of an inert form, then abx would not work, but in that case the Bb is not spreading either.
Janice70 - sorry about derailing the thread, I guess this is not directly related to resistance, at least not acquired resistance.
Posted by Vermont_Lymie (Member # 9780) on :
If you read Pam Weintraub's great book, Cure Unknown, she writes that Dr. B took ceftin the first time for 22 months!
That corresponds to what other llmds have told me and what I have experienced; fortunately, compared to other quicker growing bacteria, Bb does not seem to develop resistance to some (many? all?) treatments or combos of treatments.
It is why many of us are able to take one abx for months, stop, and then go back to it after a couple of months and it still works.
Of course, more research is needed, but the IDSA idiots have pretty much stopped/limited the necessary research in the US.
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