Topic: What Treatments Cause Borrelia to Go Into Cyst Form?
SForsgren
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Member # 7686
posted
I'd like to make a list of treatments/products that cause Lyme to go into a cyst form and those that do not. Would appreciate any feedback from folks here.
To start:
ABX - do (except for cyst-busters like Flagyl, Tinidazone, etc) Rife - does not Microcurrent - does not Samento - ? Colloidal Silver - ?
Any pointers to information on these and other commonly used treatments and whether or not they push Lyme into a defensive cyst form, would be appreciated.
-------------------- Be well, Scott Posts: 4617 | From San Jose, CA | Registered: Jul 2005
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posted
bicillin is supposed to induce cyst formation. search med.abstracts, this site, for one abstract stating this.
one paper talked of bicillin and tinidazole together, the rationale being to get the spiro, and cystic forms.
while i don't recall the source, one or more of the tetracycline class of abx is supposed to prevent a morphing from the spiro-form into one or more non-helical forms.
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robi
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From what I have learned from others on this site cephlosporins cause the spirochete to go in to cyst form ......... I have no documentation on this though.
I have not done any cephlosporins and I am now doing tini (cyst buster) and I am definately feeling worse...... so something caused my keets to go in to cyst form..... 'caus it feels like they are openeing now.
robi
-------------------- Now, since I put reality on the back burner, my days are jam-packed and fun-filled. ..........lily tomlin as 'trudy' Posts: 2503 | From here | Registered: Apr 2004
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SForsgren
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posted
Are there any ABX that do NOT cause it to go into cyst form? What about Samento or CS? Any references on those? Thanks
-------------------- Be well, Scott Posts: 4617 | From San Jose, CA | Registered: Jul 2005
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There's no research on colloidal silver so I can't post anything to back this up BUT, no, silver acts very different from traditional abx. The silver ions should attach itself to any form Bb takes. I would be very surprised otherwise. Wish we had more research on this!!!
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bpeck
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SF:
I'm not sure where you're getting your information. How do you know micro currents don't push a variant?
The cyst form (also call L or S form) is the Bb variant- and that's the form it takes in the csfluid - I imagine there are many substances that push this bacteria into it's variant.
In Vitro Tetracycline will inhibit the classical form from morphing into a variant, and is the reason Donta uses it as the initial abx. But remember Bb is notorious for not behaving in vivo the same as it does in vitro.
If you make your list, please include all referenced citations... No guessing please. Thankyou. Barb
-------------------- Barb Peck (Elder LymeNet user). Lyme since 1975 Transfusion Posts: 1882 | From VT | Registered: Oct 2002
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You can check Jeff's small study on the lyme and rife site about Samento. They seemed to think it caused it to go into the cyst form.
All My Best, Scott
-------------------- BTW - I am NOT a medical professional - just speaking from MY own personal experience. Posts: 266 | From Philadelphia | Registered: May 2005
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posted
I have been taking cephlosporin on its own for a couple of months now and have been told by my doc to now introduce Flagyl for the cysts forms - I'm starting cephlosporin for five days and Flagyl for two.
About a couple of weeks into taking the cephlosporins I started to feel better and had about three weeks of feeling great but then I got worse again. Don't ketes have a life cycle of about four weeks where they come out of their 'cyst' form? I know that my symptoms have about a four week cycle that just about follows my own cycle....
Do symptoms get better or worse when they are in their cyst form?
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WildCondor
Unregistered
posted
Good question! I wish we had more research available on this. I'm curious as to the effects of combined IV antibiotics like Zithromax and Rocephin used along with monoplace Hyperbaric Oxygen. Let's open a research facility!!!!
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oxygenbabe
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There's just not enough good research, especially in vivo, to know. We'd have to have good animal studies with all the antibiotics.
I would only wager that everything is likely to send it into cyst form. Any attack and it is likely to form some kind of dormant stage--perhaps granules, too, like syphilis does--
Bacteria have been around so long. They've learned how to survive.
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SForsgren
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posted
But we must have some ideas about which things cause more likelihood/propensity towards cysting. For example, it seems that almost all ABX do this whereas I have not read that Rife or Microcurrent do this since they are not 24x7 in the body. Good discussions... Thanks
-------------------- Be well, Scott Posts: 4617 | From San Jose, CA | Registered: Jul 2005
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SForsgren
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posted
There are several LLMDs that pulse ABX - in theory for that reason I believe.
-------------------- Be well, Scott Posts: 4617 | From San Jose, CA | Registered: Jul 2005
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oxygenbabe
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posted
I think pulsing, and/or rotating, abx may help avoid resistance.
Check out Carl Zimmer's current article on his blog about antimicrobial peptides.
Bacteria are built to evolve resistance, and they have many mechanisms.
Borrelia is so complex it almost seems like a little animal creature nonetheless, other bacteria are not so different. They form biofilms. They exchange genes and information. They switch virulence on and off. They evolve resistance. They go into L-forms. In turn, fungi have spores. Etc.
I am not so certain for instance that azoles are a cyst buster (metro, tini). ANd look, maybe other azoles work on it too (diflucan).
There's a lot we don't know.
Posts: 2276 | From united states | Registered: Jun 2004
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posted
Some Italians have researched this. Two abstracts pasted below. But might want to take this with a grain of salt since it was in vitro studies.
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APMIS. 2004 Jan;112(1):57-62.
Induction of cystic forms by different stress conditions in Borrelia burgdorferi.
Murgia R, Cinco M.
Spirochete Laboratory, Dipartimento di Scienze Biomediche, Universita' degli Studi di Trieste, Via Fleming 22, 34127 Trieste, Italy.
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. In this study we evaluated the rate of cyst formation induced by oxidative stress, pH variations, and heating, reconversion of cysts to vegetative forms, and some aspects of their metabolic activity. We observed cyst formation in the presence of extreme pH values, and at high temperature, but the best production of cystic forms was observed in the presence of H2O2. When transferred to BSK II medium, the cystic forms reconverted to spirochetes in relation to their age and type of induction treatment. Furthermore, we demonstrated a low metabolic activity of cystic forms by measuring amino acid incorporation. Overall, these data suggest that the phenomenon of conversion to cysts by B. burgdorferi provides a limited survival potential. This short-term survival, however, gives borreliae an additional chance to overcome unfavourable environmental conditions.
PMID: 14961976 [PubMed - indexed for MEDLINE] ----------------------------------------------
Wien Klin Wochenschr. 2002 Jul 31;114(13-14):574-9.
Cystic forms of Borrelia burgdorferi sensu lato: induction, development, and the role of RpoS.
Murgia R, Piazzetta C, Cinco M.
Dipartimento di Scienze Biomediche, sez. Microbiologia, Universita degli Studi di Trieste, Trieste, Italy.
It has been demonstrated recently that cells of Borrelia burgdorferi sensu lato, the etiological agent of Lyme disease, transform from mobile spirochetes into nonmotile cystic forms in the presence of certain unfavourable conditions, and that cystic forms are able to reconvert to vegetative spirochetes in vitro and in vivo. The purpose of this study was to investigate the kinetics of conversion of borreliae to cysts in different stress conditions such as starvation media or the presence of different antibiotics. Using the same experimental conditions we also investigated the possible role in cyst formation of RpoS, an alternative sigma factor that controls a regulon in response to starvation and transition to stationary phase. We observed that beta-lactams penicillin G and ceftriaxone, the antibiotics of choice in Lyme borreliosis treatment, favoured the production of cysts when used with serum-depleted BSK medium. In contrast, we observed a low level of cyst formation in the presence of macrolides and tetracyclines. In order to elucidate the role of the rpoS gene in cyst formation we analyzed the reaction of the rpoS mutant strain in comparison with its wild-type in different conditions. Under the same stimuli, both the wild-type borrelia and the rpoS knock-out isogenic strain produced cystic forms with similar kinetics, thus excluding the participation of the gene in this phenomenon. Our findings suggest that cyst formation is mainly due to a physical-chemical rearrangement of the outer membrane of Borrelia burgdorferi sensu lato leading to membrane fusion and controlled by different regulation mechanisms.
PMID: 12422604 [PubMed - indexed for MEDLINE]
Posts: 8430 | From Not available | Registered: Oct 2000
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Effects of penicillin, ceftriaxone, and doxycycline on morphology of Borrelia burgdorferi.
Kersten A, Poitschek C, Rauch S, Aberer E.
Department of Dermatology, University of Vienna, Austria.
Antibiotic therapy with penicillin, doxycycline, and ceftriaxone has proven to be effective for the treatment of Lyme borreliosis. In some patients, however, it was noticed that borreliae can survival in the tissues in spite of seemingly adequate therapy. For a better understanding of this phenomenon, we investigated the different modes of degeneration of Borrelia burgdorferi suspensions during a 96-h exposure to various antibiotics. By dark-field microscopy and ultrastructural investigations, increasing blebbing and the gradual formation of granular and cystic structures could be followed during the exposure time. Although antibiotic concentrations at the MIC at which 90% of organisms are inhibited after 72 h were 80% or even greater, motile organisms were still present after incubation with penicillin and doxycycline but not after incubation with ceftriaxone. By transmission electron microscopy, intact spirochetal parts, mostly situated in cysts, were seen up to 96 h after exposure with all three antibiotics tested. According to experiences from studies with other spirochetes it is suggested that encysted borreliae, granules, and the remaining blebs might be responsible for the ongoing antigenic stimulus leading to complaints of chronic Lyme borreliosis.
PMID: 7625800
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
Microbiology. 2000 Jan;146 ( Pt 1):119-27.
Serum-starvation-induced changes in protein synthesis and morphology of Borrelia burgdorferi.
Alban PS, Johnson PW, Nelson DR.
Department of Biochemistry, Microbiology, and Molecular Genetics, University of Rhode Island, Kingston 02881, USA.
It has been demonstrated previously that motile Borrelia burgdorferi cells transform into non-motile cyst-forms when incubated for several weeks in BSKII (a complex medium) lacking rabbit serum. B. burgdorferi cells cannot synthesize fatty acids de novo and serum is thought to provide a source of fatty acids and lipids. When B. burgdorferi cells were serum-starved in defined RPMI medium, -90% of the cells formed spherical cysts within 48 h. Cyst formation was inhibited by tetracycline. Cyst opening and recovery of vegetative cells was rapidly induced by the addition of either BSKII or rabbit serum. The percentage of viable cells recovered from cysts ranged from 2.9% to 52-5%. Viability was inversely proportional to cyst age. Protein synthesis by B. burgdorferi during serum starvation was examined by labelling cells with Tran35S-Label and analysing the labelled proteins by two-dimensional gel electrophoresis and fluorography. The synthesis of over 20 proteins was induced during serum starvation. Western blots of proteins from vegetative cells and cysts probed with sera from either B. burgdorferi-infected humans or monkeys revealed that several cyst proteins were antigenic. These data suggest that cells of B. burgdorferi, although possessing a small genome and extremely limited biosynthetic capabilities, rapidly respond to conditions of serum starvation by inducing changes in protein synthesis and cell morphology. This study may help explain how cells of B. burgdorferi can survive periods of nutrient deprivation in different hosts and host tissues.
PMID: 10658658 [PubMed - indexed for MEDLINE]
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ Int Microbiol. 2004 Jun;7(2):139-42.
An in vitro study of the susceptibility of mobile and cystic forms of Borrelia burgdorferi to tinidazole.
Brorson O, Brorson SH.
Department of Microbiology, Vestfold Sentralsykehus, Tonsberg, Norway.
The susceptibility of mobile and cystic forms of Borrelia burgdorferi to tinidazole (TZ) was examined. The minimal bactericidal concentration (MBC) of TZ against the mobile spirochetes was >128 microg/ml at 37 degrees C in micro-oxic atmosphere when incubated for 14 days. TZ significantly reduced the conversion of mobile spirochetes to cystic forms during incubation. The MBC for older (10-months-old) cysts at 37 degrees C in a micro-oxic atmosphere was >0.5 microg/ml, but >0.125 microg/ml for young (1-day-old) cysts. Acridine orange staining, dark-field microscopy and transmission electron microscopy revealed that, when the concentration of TZ was > or = MBC, the contents of the cysts were partly degraded, core structures did not develop inside the young cysts, and the amount of RNA in these cysts decreased significantly. When cysts were exposed to TZ, 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.
PMID: 15248163 [PubMed - indexed for MEDLINE] ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
Int Microbiol. 2002 Mar;5(1):25-31. Related Articles, Links
An in vitro study of the susceptibility of mobile and cystic forms of Borrelia burgdorferi to hydroxychloroquine.
Brorson O, Brorson SH.
Department of Microbiology, Vestfold Sentralsykehus, Tonsberg, Norway.
In this work the susceptibility of mobile and cystic forms of Borrelia burgdorferi to hydroxychloroquine (HCQ) was studied. The minimal bactericidal concentration (MBC) of HCQ against the mobile spirochetes was > 32 microg/ml at 37 degrees C, and > 128 microg/ml at 30 degrees C. Incubation with HCQ significantly reduced the conversion of mobile spirochetes to cystic forms. When incubated at 37 degrees C, the MBC for young biologically active cysts (1-day old) was > 8 microg/ml, but it was > 32 microg/ml for old cysts (1-week old). Acridine orange staining, dark-field microscopy and transmission electron microscopy revealed that the contents of the cysts were partly degraded when the concentration of HCQ was > or = MBC. At high concentrations of HCQ (256 microg/ml) about 95% of the cysts were ruptured. When the concentration of HCQ was > or = MBC, core structures did not develop inside the cysts, and the amount of RNA in these cysts decreased significantly. Spirochetal structures inside the cysts dissolved in the presence of high concentrations of HCQ. When the concentration of HCQ was > or = MBC, the core structures inside the cysts were eliminated. These observations may be valuable in the treatment of resistant infections caused by B. burgdorferi, and suggest that a combination of HCQ and a macrolide antibiotic could eradicate both cystic and mobile forms of B. burgdorferi.
PMID: 12102233 [PubMed - indexed for MEDLINE] ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ APMIS. 1999 Jun;107(6):566-76. Related Articles, Links
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.
Formation and cultivation of Borrelia burgdorferi spheroplast-L-form variants.
Mursic VP, Wanner G, Reinhardt S, Wilske B, Busch U, Marget W.
Max von Pettenkofer-Institut, Ludwig-Maximilians-Universitat Munchen, Germany.
As clinical persistence of Borrelia burgdorferi in patients with active Lyme borreliosis occurs despite obviously adequate antibiotic therapy, in vitro investigations of morphological variants and atypical forms of B. burgdorferi were undertaken. In an attempt to learn more about the variation of B. burgdorferi and the role of atypical forms in Lyme borreliosis, borreliae isolated from antibiotically treated and untreated patients with the clinical diagnosis of definite and probable Lyme borreliosis and from patient specimens contaminated with bacteria were investigated. Furthermore, the degeneration of the isolates during exposure to penicillin G in vitro was analysed. Morphological analysis by darkfield microscopy and scanning electron microscopy revealed diverse alterations. Persisters isolated from a great number of patients (60-80%) after treatment with antibiotics had an atypical form. The morphological alterations in culture with penicillin G developed gradually and increased with duration of incubation. Pleomorphism, the presence of elongated forms and spherical structures, the inability of cells to replicate, the long period of adaptation to growth in MKP-medium and the mycoplasma-like colonies after growth in solid medium (PMR agar) suggest that B. burgdorferi produce spheroplast-L-form variants. With regard to the polyphasic course of Lyme borreliosis, these forms without cell walls can be a possible reason why Borrelia survive in the organism for a long time (probably with all beta-lactam antibiotics) [corrected] and the cell-wall-dependent antibody titers disappear and emerge after reversion.
Comparison of in vitro activities of ketolides, macrolides, and an azalide against the spirochete Borrelia burgdorferi.
Hunfeld KP, Wichelhaus TA, Rodel R, Acker G, Brade V, Kraiczy P.
Institute of Medical Microbiology, University Hospital of Frankfurt, D-60596 Frankfurt/Main, Germany. [email protected]
Two ketolides, three macrolides, and one azalide were tested in vitro against 17 isolates of the B. burgdorferi s.l. complex. As measured in micrograms per milliliter, activity was highest for cethromycin (MIC at which 90% of the tested isolates were inhibited [MIC(90)], 0.0019 micro g/ml) and telithromycin (MIC(90), 0.0078 micro g/ml). Electron-microscope analysis and time-kill studies also supported enhanced effectiveness of both ketolides.
In vitro susceptibility testing of four antibiotics against Borrelia burgdorferi: a comparison of results for the three genospecies Borrelia afzelii, Borrelia garinii, and Borrelia burgdorferi sensu stricto.
Sicklinger M, Wienecke R, Neubert U.
Department of Dermatology, Ludwig-Maximilians University of Munich, D-80337 Munich, Germany.
MICs and minimal bactericidal concentrations (MBCs) were evaluated for the four antibiotics azithromycin, amoxicillin, ceftriaxone, and doxycycline against the three main genospecies of Borrelia burgdorferi sensu lato. In MBC testing, statistically significant differences between the genospecies could be found in 7 out of 12 comparative evaluations (P < 0.05).
PMID: 12682190 [PubMed - indexed for MEDLINE]
I hope these few citations help in your research.
-------------------- **Eat Chocolate** Posts: 942 | From USA | Registered: Mar 2005
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bpeck
Frequent Contributor (1K+ posts)
Member # 3235
posted
Imanurse posted most of the references published regarding the variant form of Lyme.
The variant of a bacteria is the form that can revert back to what's called the classical or parent form... for example the classical or parent form of Lyme is the spirochete.. it morphs into it's variant which is called an L form, S form or cystic form when it's living conditions become harsh. In almost all cases, a bacteria's variant is not suseptible to the same abx the classical form is. That's why combo's are used for the slow replicating bacteria (like Lyme).
This is not the same as a bacteria mutating in the presence of an antibiotic, and becoming resistant to that antibiotic forever.
Barb
-------------------- Barb Peck (Elder LymeNet user). Lyme since 1975 Transfusion Posts: 1882 | From VT | Registered: Oct 2002
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It has been demonstrated recently that cells of Borrelia burgdorferi sensu lato, the etiological agent of Lyme disease, transform from mobile spirochetes into nonmotile cystic forms in the presence of certain unfavourable conditions, and that cystic forms are able to reconvert to vegetative spirochetes in vitro and in vivo. The purpose of this study was to investigate the kinetics of conversion of borreliae to cysts in different stress conditions such as starvation media or the presence of different antibiotics. Using the same experimental conditions we also investigated the possible role in cyst formation of RpoS, an alternative sigma factor that controls a regulon in response to starvation and transition to stationary phase. We observed that beta-lactams penicillin G and ceftriaxone, the antibiotics of choice in Lyme borreliosis treatment, favoured the production of cysts when used with serum-depleted BSK medium. In contrast, we observed a low level of cyst formation in the presence of macrolides and tetracyclines. In order to elucidate the role of the rpoS gene in cyst formation we analyzed the reaction of the rpoS mutant strain in comparison with its wild-type in different conditions. Under the same stimuli, both the wild-type borrelia and the rpoS knock-out isogenic strain produced cystic forms with similar kinetics, thus excluding the participation of the gene in this phenomenon. Our findings suggest that cyst formation is mainly due to a physical-chemical rearrangement of the outer membrane of Borrelia burgdorferi sensu lato leading to membrane fusion and controlled by different regulation mechanisms. _______________________________ Found this on the net: beyond my brain to fully comprehend!
-------------------- nan Posts: 2135 | From Tick Country | Registered: Oct 2000
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staying afloat
Unregistered
posted
Speaking from experience and from what my former llmd says, higher doses of minocycline will form abundant cysts. Note that the articles pointed to lower doses of tetracyclines not forming cysts, but, at higher doses, they most definitely do!
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Marnie
Frequent Contributor (5K+ posts)
Member # 773
posted
A hostile environment causes Bb and other pathogens to go into cyst form.
What's a "hostile" environment?
In nature, spores (like cysts) form when there is excessive heat or cold OR the nutrients that the pathogen needs are temporarily unavailable.
They "hibernate". It's really hard to destroy spores or cysts.
These spores or cysts can hang around for a LONG time...just waiting to emerge and gobble up whatever "food" is there.
I happen to believe that the pathogens can mutate to forms other than cysts when the right nutrients aren't there too.
For example, a pathogen that needs/wants sugar will mutate (eventually) if given Xylitol (natural sugar substitute) instead.
But when sugar is added back...it mutates BACK (eventually) to being able to utilize sugar once again. In other words...it is able to adapt faster than we can.
In the meantime...substituting Xylitol for sugar will knock off some of them for AWHILE. So switching back and forth....or taking a "medication vacation" MAY be more beneficial.
Bb doesn't like the incomplete protein...gelatin. Neither do we...we would die on only gelatin as a protein source. So much for J E L L O.
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nonetheless, other bacteria are not so different. They form biofilms. They exchange genes and information. They switch virulence on and off. They evolve resistance. They go into L-forms. In turn, fungi have spores. Etc.
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