posted 16 April 2005 01:48               

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We know that cyst-busting drugs do work to kill the cyst form of Lyme disease. But we also know that these drugs typically do not exact a cure. Why not? The most forthcoming answer is that the drugs work for a period of time during which the bacterial load is lowered and improvement is seen. However, there comes a time several days, weeks, or months after a cyst-busting drug is started when the infection becomes resistant to that particular drug. This is indicated by discontinuation of herx reactions and improvement which were previously experienced when taking this drug.

One obvious solution to this problem is to begin taking a different cyst-busting drug when resistance develops. Ideally, there would be dozens of safe and effective cyst-busting drugs available. However as we know this is not the case. Most people are only aware of two: metronidazole (Flagyl) and tinidizole (Tindamax or Fasigyn). Plaquenil is an option but the side effects are nasty.

My purpose in writing this message is to inform that there are two other options which are rarely discussed but highly useful:

Both are in the same family as tinidizole and metronidazole (5-nitroimidazoles):

1. Secnidazole, similar in molecular structure to tinidizole, available from http://www.apothecure.com with a prescription.

2. Ornidazole, more difficult to locate than secnidazole but worth finding. Safety profile is equal to that of other 5-nitroimidazoles, but for political reasons has not been marketed in the United States. One source is a New Zealand pharmaceutical company which is a subsidiary of Roche. Can purchase without prescription via a Canadian intermediary pharmacy under brand name Tiberal: http://www.drugdelivery.ca/ .

Although these drugs are in the same family they act significantly differently and thus each drug packs a "fresh punch" against the infection.

I hope you find this information to be useful in the quest against the Lyme disease cyst.

Disclaimer: the above information is not intended to be medical advice, I'm not a doctor, this represents my personal opinion only and is for informational purposes only.

Bryan

posted 16 April 2005 02:14            

cyst forms do not lower total bacterial load. bacterial load, until effectively proven otherwise, can only be lowered when the organism is in the motile form.

the brorson article, which is referenced below, suggests that the -azole antibiotics may be able to kill spirochetal structures within the cysts. but this theory must be tried, tested and corroborated.

as well it is not resistance to the medication that is a concerne but the MIC which can be reached with higher doses of the same drug.

..................................................................................

actually the european studies have shown that the spirochetes only stay in the cyst form for a short time.

they cannot reside in that form, which the way it has been explained to me is like an acidic protein bubble, for long.

in order to thrive the borrelia organism must be motile (meaning in spirochete form) in order to replicate.

the spirochete laboratory at the university of trieste in italy wrote in one abstract that,

"Cystic forms of Borrelia burgdorferi might represent a low metabolic activity state or phase of B. burgdorferi cells that allows the spirochete to survive in a hostile environment until conditions are favourable to multiply again...

This short-term survival, however, gives borreliae an additional chance to overcome unfavourable environmental conditions (italics mine)."

but again there have only been about 6 or 7 studies concering cysts (aka spheroblasts) so not much is known.

regardless the cyst theory, which has a lot going for it, is relatively new and the use of -azole antibiotic in Lyme has been popular for less than 10 years.

there were a lot of late stage neuroborreliosis cases that have been cured without the use of the so called cystbusters long before the theory was presented and now reached a pertinent place in the Lyme community.

like everything with treating chronic Lyme it is due to emperical evidence, since no clinical trials have been done.

the latest in vitro Brorson article suggested the use of tinidazole and macrolide to simultaneously attack cystic and mobile forms. which makes farily obvious sense.

the only problem with the Brorson study is that these are in vitro enduced borrelia cysts and may differ what happens in vivo.

Brorson wrote the following :

"When cysts were exposed to TZ (tinidazole), both the spirochetal structures and core structures inside the cysts dissolved, and the production of blebs was significantly reduced.

These observations may be valuable in the treatment of resistant infections caused by B. burgdorferi, and suggest that a combination of TZ and a macrolide antibiotic could eradicate both cystic and mobile forms of B. burgdorferi (italics mine)."

the Trieste spirochete lab did find that in vitro beta-lactum abx did enduce cyst at a far greater rate than tetracycline or macrolides.

one in vivo examination (in mice) was done at a microbiology lab in Slovenia by inoculating the mice with water distilled cystic forms of b. garinni.

"The aim of this study was to determine whether motile B. garinii could develop from cystic forms, not only in vitro but also in vivo, in cyst-inoculated mice.

The cysts prepared in distilled water were able to reconvert into normal motile spirochetes at any time during in vitro experiments, lasting one month, even after freeze-thawing of the cysts.

Motile spirochetes were successfully isolated from 2 out of 15 mice inoculated intraperitoneally with cystic forms, showing the infectivity of the cysts."

so the situation is aporetic and far from certain.

in recalcitrant Lyme it is certainly worth entertaining the employment of 'cyst busters' but abatement of symptoms or remission may be reached without it as clearly has been clinically shown by thousands of late stage patients who recovered without the use of azole antibitiotics.

posted 16 April 2005 07:23               

I am a little concerned in that it sounds like your are looking to identify a 'cure' with "certainty" as you described. Why would patients not integrate the -azole into the mix of abx that has become a preference of so many LLMDs?

I don't think we know enough to pinpoint other specific protocols to move away from this. I didn't sleep much last night, so maybe I am missing something important, but I would like to hear from you that.

I need to ask for a small favor. I am out of town for the next week...could you please copy your reply to my home email? rpactwa@hotmail.com

posted 16 April 2005 09:45            

in order to thrive the borrelia organism must be motile (meaning in spirochete form) in order to replicate

Again, this is inaccurate. In fact, studies by the Brorsons have shown (with photos) that Bb can replicate INSIDE the cysts.

posted 16 April 2005 11:37            

but to replicate the spirochetes MUST be motile. that much is known. hence cyst forms only serve one purpose which is an evasion technique, like a turtle in its shell.

whether or not they may lay dormant in regard to relapse, etc is totally inknown. of course it is plausible that they may lay dormant for a long time.

by deduction it could be an explanation for asymptomology in the treated patient and subsequent relapse. definitley worth thinking about and investigating.

in the latter sense it may be prudent for an LLMD to use the cyst 'buster' antimicrobials to be on the safe side. and obvioulsy the LLMD should know more about this and whether it is necessary than you are I (i hope anyhow )

but just as easily the bacterium may be residing in deep tissue or other niches and they come out to "play" and cause relapses.

and to be honest i know almost nothing of L forms. haven't spend any time researching it.

the microbiology of the borrelium spirochete, especially to the lay person, is baffling. i look forward from a point of interest and consternation to see how this develops in my life time.

posted 16 April 2005 11:40            

This information is not ubiquitously accurate. The end of a "herx" by no means implies that a drug is no longer working, antibiotic, azole, or otherwise. And a lack of improvement also does not imply this. For example, some people do not improve until after the medication is discontinued.

Of course a drug may no longer work, but these metrics you suggest are not the "foolproof" method implied by these statements.

posted 18 April 2005 01:07            

I made one of my best strides in improvement using first a short course tinidazole and then a short course of flagyl--in tandem.

Major break-through in neurol. Sx. It took 3-6 weeks. It was intense.

One break through was in my emotional reactions to 'stimuli'(nice cryptic description); before TZ and flagyl, they were instantneious and intense; the instantaneousness of "detonations," as the late Dr.Bleiweiss would say, disappeared.
Without these, I'd think I would've been dead, and are part of the reason for why I'm here posting.

I'm very, very pleased with my results.

On, I think,http://www.arthritistrust.org,
one doctor,either used secnidazole, and nimorizole, or mentioned their use in rheumatiod arth. He definitely used flagyl and tinidazole, alone, and/or as part of a combination of agents, such as allopurinol.

He emphasized 5-nitro-imidazoles, his reason given in his paper.

IMO, worth trying.
These 5-nitro-imids. increase in size, starting with flagyl being the smallest in molecular size,followed by tinidazole.

pq

posted 18 April 2005 20:45            

Hatchlings...eggs...

Those frequencies don't work?

Most Americans (even those without Lyme) are acidic all the time...Proof that the cysts can't last for a long time? Where? Please DOCUMENT your research, comments.

posted 18 April 2005 23:40            

quote:

---

Originally posted by Marnie:

Proof that the cysts can't last for a long time? Where? Please DOCUMENT your research, comments.

I'm betting they can stick around a long time...and wait.

---

every published abstract has shown that in vitro borrelia cysts are short lived. i showed them above.

the one in vivo experiment (trieste - referenced above) showed that in mice without treatment who had borrelia induced cysts had reverted to motile or spirochete form.

can they (sperhoblasts) stick around for a long time?

possible, but i wouldn't think at a high rate since it is a defense mechanism. the borrelia must be in motile spirochete form to replicate.

if not under attack from antibiotics (or any other theoretical unfavorable condition) the bacteria has no apparent need to be in cystic form.

again, there has been only a handful of studies on this and the situation is far, far from certain.

but with the info that is available i think it is more plausible that recalcitrant lyme and relapsese are related to deep tissue and CNS infection than cysts form.

posted 19 April 2005 08:12               

They know it works on this one and others thats why ther using it in lyme cyst stage.

Atkinson-Barr has done a small study on Metronidazole Therapy in the Treatment of Chronic Lyme Disease. He used to work for the company that makes it, however, the Brorson's (see just below) have also done a study on metronidazole (flagyl) which verifies his work. Flagyl has an effect on the cyst shaped life cycle of lyme and other spirochetes. Atkinson-Barr's personal web site is no longer up. Tinidazole supposedly has less side effects and is supposed to be more effective on some strains than metronidazole. As far as I know there have been no studies on this. It is used more often in Europe and I think in South America

Dr B
Metronidazole (Flagyl) is commonly used in select patients with treatment resistant, chronic Lyme. When present in a hostile environment, such as growth medium lacking some nutrients, or spinal fluid, or serum with certain antibiotics added, Bb will change into a cystic form. This cyst seems to be able to remain dormant, but when placed into an environment more favorable to its growth, the cyst can open, and an intact spirochete emerges. The conventional antibiotics used for Lyme, such as the penicillins, cephalosporins, etc. do not kill the cystic form of Bb. Furthermore, the cyst lacks the usual surface antigens found on the spirochete (these are the markers detected by ELISAs and western blots). This may be another reason for the chronically sick Lyme patient remaining seronegative.

Discussion
Cysts were significantly associated with MS patients using each of the three different methods. This multi-method approach strengthens the association between CSF cysts and MS in a well-defined coastal area of southern Norway. There are two possible explanations for the association between MS and CSF cysts: the cystic structures are either the agents causing MS or they have appeared in the CSF as a consequence of MS.
The positive reaction with antispirochetal antiserum, the similarity of the cystic structures with cystic forms of spirochetes and the similarities between the cysts in the erythema migrans patient and the MS patients suggest that the patients were infected with a spirochete. The appearance of rod-like,slightly curved bacteria and spirochetes after culturing two of the CSF samples in BSK-H medium suggests the same. Spirochetes may vary in appearance and may sometimes emerge as rod-like structures [18]. The fact that only two spinal fluids gave rise to spirochete-like structures after culturing may be caused by the fact that cystic forms of spirochetes may often be difficult to convert to normal bacteria {11) and the BSK-H medium is not necessarily optimal for this possible unknown spirochete.

Figure 4a [Unable to display image] A cyst from an MS patient which is immunogold labeled with anti-Bonelia. There is a distinct and specific immunolabelng along the envelope of the cyst. TEM. Bar = 500 nm. Figure 4b. Larger magnification of the envelope of the cyst to illustrate the immunogold labeling. TEM. Bar = 200 nm.

It could be argued that the damage which MS caused in the brains of the patients had made them more vulnerable to spirochetal infection. But this does not seem a probable explanation. since all the MS patients had these cystic structures in their CFS. Other researchers have proposed that spirochetes could be the agents responsible for MS [5, 6, 8, 9]. For instance. Steiner [6] found spirochetes and granular bodies in brain autopsies of MS patients. These were proposed to belong to the genus BorreIia and were named Spirochaeta myelophthora [6].

We previously studied spirochetes (B. burgdorferi) that have converted from spirochetes to cystic forms in CSF in vitro using the same methods as mentioned above [11]. With all these methods used in this study (TEM, AO, DF), the cystic structures observed in the CSF of the MS patients are morphologically similar to cystic forms of spirochetes. We found that cysts which are produced by inoculating B. burgdorferi in CSF at 37 C can be PCR negative using conventional DNA extraction and OspA primers (unpublished observation). This is either because the cyst wall inhibits the entrance to the genome or because the genomes of spirochetes have been changed. We have also to keep in mind that PCR detection of B. burgdorferi spirochetes often may give false-negative results [19).

The positive IgG index associated with MS in our patient cohort proves that the patients had an active inflammatory process in the CNS (Table 1). Inflammatory processes in the b~ and spinal cord of virtually any cause are usually less intense than inflammation in peripheral tissues and some microbiological agents, including spirochetes, provoke a very gentle inflammatory response [20, 21 ]. Considering the nature of MS, this disease could very well be a chronic infection and the clinical picture of MS has repeatedly been confused with neuroborreliosis [22-26). Therefore, we have both microbiological and some clinical support for the hypothesis that the cystic structures found in the CSF of the MS patients may originate from spirochetes which could be the causative agents of MS.

They have used flagyl and other (*****dazole's) in cyst treatments a long time.

Heres some other cyst stuff. http://www.lymenet.de/literatur/cystsl.htm

An in vitro study of the susceptibility of mobile and cystic forms of Borrelia burgdorferi to metronidazole.

Brorson O, Brorson SH.

Department of Microbiology, Vestfold Sentralsykehus, Tonsberg, Norway.

The aim of this study was to examine the susceptibility of mobile and cystic forms of Borrelia burgdorferi to metronidazole. Because B. burgdorferi is a microaerobic bacterium like Helicobacter pylori, metronidazole (MZ) was chosen in the susceptibility test. For both microaerobic and aerobic incubation the normal mobile spirochetes were resistant to this antibiotic with an MBC > or = 512 microg/ml. Conversion of mobile spirochetes to cystic forms was not observed when they were incubated with MZ. When they were incubated under microaerobic conditions, the biologically active cystic forms had an MBC > or = 4 microg/ml, but the MBC was > or = 32 microg/ml with aerobic incubation at 37 degrees C. Staining with acridine orange (AO), dark field microscopy (DFM), and transmission electron microscopy (TEM) revealed that the contents of the cysts were degraded when the concentration of MZ was > or = MBC. Some cysts were also ruptured. When incubated with a sufficient concentration of MZ, core structures did not develop inside the cysts, and AO revealed less RNA in the cysts. Our observations may help efforts to treat resistant infections caused by B. burgdorferi with a combination of MZ and other antibiotics in order to eradicate both cystic and mobile forms of B. burgdorferi. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10379684&dopt=Abstract

posted 19 April 2005 09:56            

but the MS and CSF cyst correlation is extremely interesting, especially when juxtaposed to the statement by burrascano directly above.

posted 19 April 2005 10:28               

tinidazole, metronidazole,

nitroimidazoles,secnidazole,quinacrine, furazolidone, ornidazole,benzimidazole, albendazole,mebendazole,
nocodazole,oxfendazole,
thiabendazole,fenbendazole.

An In Vitro Study of the Susceptibility of Mobile and Cystic Forms
of Borrelia burgdorferi to Metronidazole
Date of Publication:
June, 1999
Source:
APMIS, 107(6):566-576
Authors:
(1) Brorson O; (2) Brorson S.
Institution:
(1) Department of Microbiology, Vestfold Sentralsykehus, Tonsberg
(2) Department of Pathology, Ulleval Hospital, Oslo, Norway
Abstract
The aim of this study was to examine the susceptibility of mobile and cystic forms of Borrelia burgdorferi
to metronidazole. Because B. burgdorferi is a microaerobic bacterium like Helicobacter pylori,
metronidazole (MZ) was chosen in the susceptibility test. For both microaerobic and aerobic incubation
the normal mobile spirochetes were resistant to this antibiotic with an MBC >=512 [micro]g/ml.
Conversion of mobile spirochetes to cystic forms was not observed when they were incubated with MZ.
When they were incubated under microaerobic conditions, the biologically active cystic forms had an
MBC >=4 [micro]g/ml, but the MBC was >=32 [micro]g/ml with aerobic incubation at 37[degrees]C.
Staining with acridine orange (AO), dark field microscopy (DFM), and transmission electron microscopy
(TEM) revealed that the contents of the cysts were degraded when the concentration of MZ was >=MBC.
Some cysts were also ruptured. When incubated with a sufficient concentration of MZ, core structures did
not develop inside the cysts, and AO revealed less RNA in the cysts. Our observations may help efforts
to treat resistant infections caused by B. burgdorferi with a combination of MZ and other
antibiotics in order to eradicate both cystic and mobile forms of B. burgdorferi.
——————————————————
Quotations From The Full-Text Article
“Serology, PCR, and cultivation are important for the conclusive diagnosis of Lyme borreliosis, but all
these techniques have shortcomings, and false-positive and false-negative results are frequent. Many
reports claim that all known antibiotics have shortcomings in the treatment of Lyme borreliosis.
B. burgdorferi has the ability to make cystic forms both in vivo and in vitro, e.g. when exposed to
antibiotics commonly used for treating Lyme borreliosis. This phenomenon, combined with the
ability of the cysts to reconvert to normal mobile spirochetes may explain a reactivation of the
disease after an illusory cure – and not a “post Lyme syndrome” as postulated by other
researchers.”
(p.566)
“Helicobacter pylori is also [like B. burgdorferi] capable of transforming to coccoid (cystoid) forms
and reversing to normal mobile forms, and for this bacterium treatment with three or more
antibiotics has been established. Therefore duel medication with MZ [metronidazole] as one of the
antibiotics could be of value, also for curing infections caused by mobile and cystic forms of B.
burgdorferi.

BRORSON's Work on Borrelia burgdorferi

posted 20 April 2005 02:48               

Bryan

posted 20 April 2005 10:38            

BRYAN WROTE:
We know that cyst-busting drugs do work to kill the cyst form of Lyme disease. But we also know that these drugs typically do not exact a cure.

BARB REPLIES:
We don't know any such thing in vivo.

BRYAN WROTE:
Why not? The most forthcoming answer is that the drugs work for a period of time during which the bacterial load is lowered and improvement is seen. However, there comes a time several days, weeks, or months after a cyst-busting drug is started when the infection becomes resistant to that particular drug. This is indicated by discontinuation of herx reactions and improvement which were previously experienced when taking this drug.

BARB REPLIES:
Oh man where do I start?? - first because your inital statements are false - then the following are not just redundant but moot.
You've started a domino effect of false statements somhow tying in the 'discontinuation of herxing' as proof of resistance.

You would have been better off just to post that were were some new AZOLES that people may not be aware of.

Sorry...
Barb