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» LymeNet Flash » Questions and Discussion » Medical Questions » How long does it take for Lyme spirochetes to become resistant to a drug?

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Author Topic: How long does it take for Lyme spirochetes to become resistant to a drug?
Janice70
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Or do they become resistant at all?
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gemofnj
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I really dont know the exact answer, it does a few things that are really sneaky:

1. create a coating, called biofilm which is a protein that protects it from getting killed by abx

2. hops into healthy cells and hides out and stays dormant for indefinite periods (intracellular)

3. creates a bubble around itself (cyst or L Form) so that it can live in a protected environment

other folks may have a bit more information too. Dr. B's guidelines may explain a little bit about this.

http://www.lymediseaseresource.com/BurrGuide2008.pdf

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Buster
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Biofilm dissolving and cyst busting is key!
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tcw
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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).

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Marnie
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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:

http://www.lymeinfo.net/medical/LDAdverseConditions.pdf

See how hard it would be to penetrate/destroy that cell wall?

And even if/when its cell walls are "oxidized", Bb is capable of rebuilding that cell wall.

Now...if successful, all we have left is the CWD forms which is when abx and our own antibodies don't work.

Step 2 is needed.

*Osmotic changes* or ultrasound (or I think even barometric pressure changes) to "finish the job".

Osmotic pressure tutorial for kids here:

http://www.wisc-online.com/objects/index_tj.asp?objID=NUR4004

There is a difference in the "osmotic pressure" of NaCl and MgCl2.

http://www.owlnet.rice.edu/~bios352/Bios352/exam/ExamII2007answers.pdf

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 ]

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eagle
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So should be constantly be on a cyst-buster? Or at least be pulsing cyst-busters throughout treatment?

Do cyst-busters dissolve biofilms?

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Marnie
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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.

Is plasmin Bb's "biofilm"?

What could halt this?

http://www.abbs.info/fulltxt/39-06/39060406.htm

Okay, I'll help:

"Human tissue factor pathway inhibitor-2 (hTFPI-2) is a Kunitz-type serine protease inhibitor that

*inhibits* trypsin, *plasmin*, cathepsin G, plasma kallikrein, *and* promatrix *metalloproteinases (MMPs)*

Now...find the connection between the ERK/MAPK Pathway and the Activity of the Human Tissue Factor Pathway Inhibitor-2 ...

Bb's toxin cleaves MAPKK-1.
Mg activates ERK-2 (extracellular signal)

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.

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Keebler
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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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VB
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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?

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Marnie
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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).

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eagle
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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? [dizzy]

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VB
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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.
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tcw
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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.

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Vermont_Lymie
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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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