From everything I've read, Bb changes its form once it doesn't like its surroundings. Flagyl and Tindimax seems to be the only drugs capable of penetrating these cyst-forms. So, if someone who is on an antibiotic-protocol, or AP, that does not include Flagyl or Tindimax, will cause Bb to morph into a cyst-form therefore making it necessary to need Flagyl or Tindimax?
Conclusion: theoretically then, won't everyone diagnosed with Lyme *need* Flagyl or Tindimax at one point or another?
posted
Your theorizing is what I have also read as fact about lyme.
IMO, which no one else will probably agree with, WE REALLY do NOT KNOW .
If that were true unequivocally, then all those who took those cyst rupturing meds, would make BIG progress significantly . I do not see or read a lot of personal experience here that validates this theory .
We all would like to think that we can find a "LLMD" who has a systematic approach with some nice powerful antibiotics that knock off the pathogens in a sensible way that begins to make us all well. Sometimes that happens .
The usual outcome ( I read about here ) is that people try LOTS and LOTS of DRUGS ( usually some cyst " busters" ) for YEARS and years and they get better. Then they relapse .
Which leads me to the point: who can say anything dogmatically about this disease ?
posted
There was some Italian research that looked at the tendency of drugs to cause cyst formation in borrelia. Some classes of drugs turned out more inclined, some less inclined. So, if this were true, some classes of drugs would perhaps have less need of being paired with a cyst buster.
This was in vitro research and I don't think anyone else has looked at this question, so not sure how much credence to give it. Sounds like someone should be researching it, along with a lot of other patient treatment related issues that are being ignored by academic medicine, which is where this kind of research gets done.
Look at the NIH grants for lyme research and you see a whole different emphasis.
Posts: 8430 | From Not available | Registered: Oct 2000
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posted
FWIW, two other meds., showing in vitro action on the cystic form of Bb.
Brorson �, Brorson SH. An In vitro study of the susceptibility of mobile and cystic forms of Borrelia burgdorferi to hydroxychloroquine . Int Microbiol. 5: 25-31, 2002
Brorson �, Brorson SH. An in Vitro Study of the Susceptibility of Mobile and Cystic forms of Borrelia burgdorferi to bRanitidine Bismuth Citrate. Int Microbiol. 4: 209-215, 2001.
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Would you assume that a strong herx reaction would indicate that the cysts are being ruptured by the ABX, herbs or rife that the patient is applying to kill them? That would seem logical to me.
If a person is treating lyme , and having NO die- off ( herx) , then isn't that the best indicator that the pathogen is in cystic form and NOT being killed ?
Marnie
Frequent Contributor (5K+ posts)
Member # 773
posted
In all fairness, I will present both pro and con documented research on Flagyl.
But...from a strictly personal perspective, several rounds of Tinidazole (3rd generation Fagyl) did NOT cure someone I know.
Neuro degeneration is not an issue in that person, but RA is.
"Metronidazole inhibits the specific enzyme in the liver that metabolizes warfarin (CYP 450 2C9).
If a patient is on warfarin and metronidazole is added, the warfarin dose should be lowered, or at the very least, the INR should be closely monitored to insure that the patient does not become
CENTRAL NERVOUS SYSTEM TOXICITY/FLAGYL Metronidazole (Flagyl) is widely used in gynecology for the treatment of Trichomonas vaginitis.
Several cases of central nervous system toxicity have been reported in recent medical literature.
A 20-year-old black woman was given antibiotics, including metronidazole, after developing a pelvic abscess. On the 18th day she became confused, disoriented as to time and place, and agitated.
An EEG showed diffuse cerebral disturbance. Antibiotics were discontinued and her mental symptoms improved over the next week.
A second patient became confused, disoriented, developed failure of muscle coordination, and speech difficulty.
A third patient had been on metronidazole for only seven days before developing depression, lack of appetite and difficulty concentrating.
Some symptoms lasted as long as four months after the medications were discontinued.
Animal studies strongly implicate metronidazole as potentially neurotoxic agent. (American Journal of Obstetrics and Gynecology 145(5)640-641, March 1, 1983) enough liver disease to inhibit processing of the medication.
Department of Chemistry, Huazhong University of Science and Technology, Wuhan 430074, China.
The effect of metronidazole (ME) on sulfate-reducing bacteria (SRB) was studied by atomic force microscopy (AFM) in this paper.
Topography images of SRB cell show that after exposure to ME
individual cell shape is sharply modified.
Topography and phase images of SRB cell wall show that
***after exposure to ME not only the roughness of the cell wall increases*** but also the physical performance of SRB surface is changed to be uniform.
AFM frictional loops show that after exposure to ME, SRB surface friction is increased remarkably.
PMID: 16701623
(Me: Many pathogens are now resistant to Flagyl Clostridium difficile is but one.)
In all FAIRNESS...here is an abstract that indicates Flagyl works:
Eur J Med Res. 2004 Jul 30;9(7):334-6.
Clinical effects of fluconazole in patients with neuroborreliosis.
had been treated with 200 mg fluconazole daily for 25 days after an unsuccessful therapy with antibiotics.
At the end of treatment eight patients had no borreliosis symptoms and remained free of relapse in a follow-up examination one year later.
In the remaining four patients, symptoms were considerably improved.
(My note here - 8+4=12, not 11)
At the end of therapy immune reactivity (IgM+) disappeared in three patients. Since borrelia spp. are almost exclusively localised intracellular, they may depend on certain metabolites of their eucaryotic host cell. Inhibition of P450 and other cytochromes by fluconazole may incapacitate Borrelia upon longterm exposure.
PMID: 15337633
AND...this maybe another reason why Flagyl COULD help:
``Human cytochrome P450 2C9 (CYP2C9) is a member of the monooxygenase superfamily of enzymes involved in drug metabolism and the
***synthesis of cholesterol*** (blocking?)
steroids, and other lipids''
I suspect pathogen LOAD plays a huge part OR the particular STRAIN of Bb OR whether it was still expressing OspC, not OspA and OspB.
All spirochetes ferment sugar to ethanol/alcohol. Bb moves away from alcohol. Obviously , Bb doesn't want its cell wall damaged.
Now...
Alcohol (ethanol) is broken down by liver enzymes within minutes.
Conversion of ethanol to acetaldehyde requires the enzyme alcohol dehydrogenase.
Acetaldehyde is then transformed to acetic acid ("vinegar") by
the enzyme aldehyde dehydrogenase.
If individuals can't break down alcohol easily, problems may occur if alcohol is consumed.
Patients with these problems appear to be partially deficient in aldehyde dehydrogenase, resulting in high levels of accumulated acetaldehyde.
Acetaldehyde has been blamed for asthmatic reactions to alcohol in up to half of Japanese asthma patients.
Now...aldehyde dehygrogenase is also known as aldehyde oxidase!
Is it already deficient?
Acetaldehyde accumulation is bad, really really bad.
Initially lyme patients respond to Bb's OspC protein expression. Later, if RA is the main symptom, the patient is responding to OspA and OspB. IF one continues to respond to OspC...then, the heart, lungs and brain are impacted, it appears.
In another post, I mentioned the possibility of NO (nitric oxide) and ASA - aspirin - as potentially helping to rid Bb.
NO dilates the blood vessels and is a strong antibacterial. ASA thins the blood.
What it looks like is we need to keep the vessels dilated and the blood thin so that our own nutrients (esp. oxygen) can reach the infection areas.
This, I found today:
``Enhancement of alcohol dehydrogenase activity in vitro by acetylsalicylic acid.''
(Even in the presence of ethanol. It helps with step 1 in breaking down alcohol. Only step 1.)
This all has to do with PDE1 and PDE4 enzymes as well as PKC (protein) and Calmodulin-dependent cyclic nucleotide phosphodiesterase (PDE1)- an enzyme. There is a signalling between these.
Bb has a PKC...protein kinase C inhibitor according to genetic research. These inhibitors normally trigger cell death. Tamoxifen is a man-made PKC inhibitor to treat breast cancer (kill the infected cells).
The body would logically respond by increasing PFK...to prevent major sudden cell die-off. This looks to upregulate PDE1 and PDE4, depending on whether or not Bb is still expressing OspC or is back to OspA and OspB.
This gets incredibly complex, I know!
Posts: 9481 | From Sunshine State | Registered: Mar 2001
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posted
Could someone explain what the cyst form is please? Does it mean you get cysts on you so you can see them, or are they internal and you can't see them?
Thanks.
Posts: 67 | From UK | Registered: Jan 2007
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[I know nothing about the validity of the salt/C protocol.]
-------------------- --Lymetutu-- Opinions, not medical advice! Posts: 96239 | From Texas | Registered: Feb 2001
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bejoy
Frequent Contributor (1K+ posts)
Member # 11129
posted
Theoretically, I have heard that strong doses of protease enzymes are syst busters as well. I have not tried them yet, nor have I heard from anyone who has. Have you?
-------------------- bejoy!
"Do not go where the path may lead; go instead where there is no path and leave a trail." -Ralph Waldo Emerson Posts: 1918 | From Alive and Well! | Registered: Feb 2007
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posted
Thanks for your research Marnie. I'm actually following some of it! But I do numbers better than words. Did that one study really say that out of 11 patients, 8 recovered and 4 improved?
I think the Vitalzym I am taking (10/day) contains the protease enzymes along with serrapeptase. My experience is that this keeps the inflammation down. I understand from reading that these enzymes (taken on empty stomach) also keep the blood more "slippery"--whatever that means.
Since I started the reservatrol two weeks ago (still at a low dose) I'm having more inflammation symptoms. I'm wondering if more enzymes would help?
A final note: I thought I read on the forum that someone is using ?celery seed extract? as a cyst buster.
-------------------- When I lost my grip on Faith in the maze of illness, Hope gently clasped my hand and led on.
RuthRuth Posts: 478 | From California | Registered: Jan 2007
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-------------------- When I lost my grip on Faith in the maze of illness, Hope gently clasped my hand and led on.
RuthRuth Posts: 478 | From California | Registered: Jan 2007
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Rianna
Frequent Contributor (1K+ posts)
Member # 11038
posted
I had to write something for my Nurse/Health Authority to understand my llmd's Protocol - I hope this makes sense and helps, Obviously it is the treatment that I am on and to make makes the most sense of all treatments - I am also on loads of other bits - This is just the Rotational AB regime :-
1) Motile form the typical spiral-shaped bacteria form. 2) L- form the cell wall deficient (CWD). 3) Cyst form (also called spheroplasts or starvation forms) Spirochetes have a unique mode of motility that allows them to easily travel through tissues of the body. By rotating their axial filament (endoflagella) the flagellum rotates causing the spirochete to actually move in a cork-screw fashion. This mode of motility allows spirochetes to literally "screw" themselves into and through the tissues of the body. They can also contract like a spring and move through tissue as they uncoil. Spirochetes hide their flagella from the host's immune defences - which are normally antigenic and would trigger an immune response if detected. The work of Brorson and Brorson discovered that the Motile spirochete has the ability to convert into a Cyst form (considered as the organism's mode of reproduction) - then back again into a Motile spirochete. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Display&dopt=pubmed_pubmed&from_uid=9646104
Antibiotics 1) Cephalosporins and Penicillin used for the Motile Spirochetes 2) Macrolide or Tetracycline's used for the L-form Cell Wall Deficient/Intracellular Forms 3) Metronidazole and Tinidazole for the Cyst form
Therefore the protocol set by my LLMD is:-
Firstly in a Chronic Lyme patient, it is necessary to lower the spirochete load with an IV Cephalosporin (Ceftriaxone/Rocephin) and then to introduce and pulse the different antibiotics to ensure all forms are treated, over a long period of time until patient is symptom free.
After some four to six months, introduce Penicillin (ideally sustained release/Bicillin) although amoxicillin can be used, which continues to treat the Motile Spirochetes but will also push the Spirochetes into a Cyst form. Therefore, although this class of antibiotic continues to lower the Motile load, it is then necessary to rotate through the different types of antibiotics to treat the other forms.
At this stage the protocol transforms into a repeating 8 week cycle that varies every 2 weeks:
For Motile Spirochetes - Penicillin for 6 weeks and after 2 weeks add L-form/Intracellular Forms - Macrolide or Tetracycline family for 2 weeks then stop this & add For Cyst Forms - Metronidazole or Tinidazole for 2 weeks *Also use Grapefruit Seed Extract as the Brorsons discovered this was an amazing Cyst buster Rest period - 2 weeks
It is normal to have a two week break as The Brorson's also discovered that newly formed Borrelia Cysts will readily convert to the more exposed Spirochete form during this period. The cycle is then repeated over and again until the patient is symptom free - although it is often necessary to change the L-form and/or the Cyst form antibiotics (together with an increase to the advised dosages) in order to counter possible Borrelia resistance or patient intolerance. It is recommended that the two week break is extended to six weeks later in the protocol.
Herxheimers Upon commencement of treatment, it is normal for symptoms to amplify during the initial period of therapy which may prolong into weeks or even months. This is called a Jarisch-Herxheimer reaction (Herx) and is the body's response to the bacterial lipoproteins (BLP's) being released from the dying borrelia. A high/chronic infection will result in an intense and prolonged Herxheimers reaction as these BLPs stimulate the inflammatory cascade. The Herx reaction is a very helpful clinical marker that Lyme clinicians can use to determine both the success of a particular antibiotic and the severity of the disease.
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posted
I liked that last post. I guess that's why so many people don't get better, because all the different phases aren't being treated.
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