Guest guest Posted October 1, 2008 Report Share Posted October 1, 2008 Hi ! ! ! I am learning a lot from you but the response about MMS killing both good and bad bugs did not feel true. Yesterday, I happened to find the following link: http://www.miraclemineral.co.nz/ And noticed this paragraph: " Activated MMS is harnessed by the immune system, to safely kill pathogens in the human body. The immune system can use this killer to only attack those germs, bacteria and viruses that are harmful to the body, and does not affect the friendly bacteria in the body nor any of the healthy cells. It can assist the immune system in combating problems as simple as a common cold; or as deadly as cancer and AIDS. " It is the phrase: " ... does not affect the friendly bacteria in the body nor any of the healthy cells. " which seems to contradict the info you gave me??? is that right? Can you clarify this for me? (I was out of town for the last day and a half, it looks like FORTY MESSAGES!!! from this list were rec'd in that time. I don't have time now to go over them, my curiousity is such that I must first ask this question in the hope I can get an answer.) seeking greater understanding, I thank you. - Marilyn - At 08:43 AM 9/29/2008 -0400, Siegel wrote: >MMS does not distinguish between the " good " bacteria and the harmful >bacteria. It is not as harsh on you as antbx. But it does still kill both. >I have had lots of yeast problems before taking the MMS. I had gotten most >of it straightened out before going on it. A few months of being on it, all >the yeast problems began to return. I had ramped up to between 10-12 drops >at that time. Since then, others have come forward to tell of similar >experiences. You can easily counter this problem by taking good quality >probiotics away from the MMS. > >Thanks for the suggestions for the yeast, but I have a whole lot of things I >use for yeast that are very effective including Neem, iodine, agricept-L, >and tons of probiotics. Since I use the MMS topically now I have been able >to repopulate my gut to large degree now and the yeast is gradually getting >better. > > > >-- Re: [ ] questions > > , > going over the first few messages I saw on the list --- > > reviewing this one, yours from Sept 16: > > how can one develop yeast issues from MMS? isn't MMS supposed to get rid >of yeast? > am really curious about this one. > > for yeast, I have a suggestion: > I did an article about 4 years ago that strangely enough (2 me, at least) >seems somewhat similar to MMS in a small way. At the time, it was one of >the most powerful health concepts I'd found. > > it should kill yeast . > go to: > http://www.dowsers.info/toronto/dec2004.htm > > as these publications are real long, search for the > SECOND instance of: > FOCUS ON HEALTH > > thanks again! > - Marilyn - > > >At 08:20 PM 9/16/2008 -0400, susan wrote: >>I have developed yeast issues from the MMS. You should absolutely take >>probiotics while on MMS. It does kill both the good and bad bacteria >>especially at the higher doses. > >>The lower doses do not seem to be prone to this problem. Also, you only >>need to take the Vit.c 2 hours away from the MMS, not 4. It is o.k. to >>swish in mouth. > >> > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 1, 2008 Report Share Posted October 1, 2008 On 9/30/2008, Marilyn Gang (mgang@...) wrote: > It is the phrase: " ... does not affect the friendly bacteria in the > body nor any of the healthy cells. " which seems to contradict the info you > gave me??? is that right? MMS is a very powerful oxidizer. Healthy cells have more protection than unhealthy cells against oxidizers. Most, BUT NOT ALL, beneficial critters are aerobic. Aerobic critters will tolerate oxidizers much better than anaerobic critters, but are not absolutely immune. So, the bottom line is, in lower doses, MMS shouldn't take too heavy a toll on the good guys, but it will get some of them. The higher the dose, the more of them it will get. When taking a break from MMS - you should take breaks for anything, even eating (fasting one or two days a week is one of the healthiest things you can eating wise) - you should be taking things to rebuild (healthy bacteria, superfoods, mineral supplements like the Fulvic Acid minerals from Vital Earth). I also highly recommend taking things to assist the body in eliminating the oxidized crud - bentonite clays and activated charcoal being some of the best ways to accomplish this, just make sure you take the clay pre-hydrated, and drink enough water, as if you don't, it can cause constipation. Lastly - keeping the bowels moving is one of the primary goals of any health/cleansing program. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 1, 2008 Report Share Posted October 1, 2008 the immune system isn't doing any harnessing and selective use of it. the immune system will attempt to defend the body against it or it won't. there are other explanations around (sorry i can't quote or link to them now) that are much more plausible but they may not be correct either. > Re: [ ] yeast andMMS: SUSAN!? > Importance: High > > > > Hi ! ! ! > > I am learning a lot from you but the response about MMS killing both > good and bad bugs did not feel true. > > Yesterday, I happened to find the following link: > http://www.miraclemineral.co.nz/ > > And noticed this paragraph: > > " Activated MMS is harnessed by the immune system, to safely kill > pathogens in the human body. The immune system can use this killer to only > attack those germs, bacteria and viruses that are harmful to the body, and > does not affect the friendly bacteria in the body nor any of the healthy > cells. It can assist the immune system in combating problems as > simple as a > common cold; or as deadly as cancer and AIDS. " Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 1, 2008 Report Share Posted October 1, 2008 Hi MArilyn, MMS is still a big experiment. Even Jim Humble has recommended taking probiotics (Living Stream) with it. I can only relate my experience having been on it over a year now off and on. I had yeast issue in the past before MMS and resolved most of them before the beginning the MMS. These symptoms including head itching, hair falling out, vaginal itching and irritation. I was fine on the MMS concerning yeast until I got up to about 10 drops. Then all these symptoms began to return. I tried taking lots of probiotics then, reducing my MMS dosage, etc. But it has not been until I began to use the MMS transdermally that I am making progress with the yeast. For me, it definitely affected the balance good bacteria in my intestines. I have had feedback from others who have responded similarly. It does not seem to get bad until you get to a certain dosage, though. It may not ring true for you for any number of reasons: you may not have yeast to the extent I did, your system may be able to handle it better, your immune system may be stronger, etc. Everyone is different and their reactions will differ as well. But I still would recommend that for anyone taking MMS they should be on a probiotic. It won't hurt you and is good to be taking anyway. Hope that helps clarify where I am coming from. -- Re: [ ] yeast andMMS: SUSAN!? Hi ! ! ! I am learning a lot from you but the response about MMS killing both good and bad bugs did not feel true. Yesterday, I happened to find the following link: http://www.miraclemineral.co.nz/ And noticed this paragraph: "Activated MMS is harnessed by the immune system, to safely kill pathogens in the human body. The immune system can use this killer to only attack those germs, bacteria and viruses that are harmful to the body, and does not affect the friendly bacteria in the body nor any of the healthy cells. It can assist the immune system in combating problems as simple as a common cold; or as deadly as cancer and AIDS." It is the phrase: "... does not affect the friendly bacteria in the Body nor any of the healthy cells." which seems to contradict the info you gave me??? is that right? Can you clarify this for me? (I was out of town for the last day and a half, it looks like FORTY MESSAGES!!! from this list were rec'd in that time. I don't have time now to go over them, my curiousity is such that I must first ask this question in the hope I can get an answer.) seeking greater understanding, I thank you. - Marilyn - Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 1, 2008 Report Share Posted October 1, 2008 if you have bartonella -- some how it hides & the immune system doesnot work on it. some think that bartonella is missed by most dr. http://www.personal consult.com/ articles/ bartonellabook. html roger From: bob Larson <bobList@...>Subject: RE: [ ] yeast andMMS: SUSAN!? Date: Wednesday, October 1, 2008, 6:41 AM the immune system isn't doing any harnessing and selective use of it.the immune system will attempt to defend the body against it or it won't.there are other explanations around (sorry i can't quote or link to themnow) that are much more plausible but they may not be correct either.> Re: [miracle_mineral_ supplement] yeast andMMS: SUSAN!?> Importance: High>>>> Hi ! ! !>> I am learning a lot from you but the response about MMS killing both> good and bad bugs did not feel true.>> Yesterday, I happened to find the following link:> http://www.miraclem ineral.co. nz/>> And noticed this paragraph:>> "Activated MMS is harnessed by the immune system, to safely kill> pathogens in the human body. The immune system can use this killer to only> attack those germs, bacteria and viruses that are harmful to the body, and> does not affect the friendly bacteria in the body nor any of the healthy> cells. It can assist the immune system in combating problems as> simple as a> common cold; or as deadly as cancer and AIDS." Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 5, 2008 Report Share Posted October 5, 2008 >MMS is a very powerful oxidizer.< In the podcast with Adam Abraham (MMS: What you need to know), Jim Humble specifically said MMS is a weak oxidizer. Is he wrong? He also says MMS won't touch anything that is alkaline. It seems like beneficial bacteria would be alkaline. -- Re: [ ] yeast andMMS: SUSAN!? On 9/30/2008, Marilyn Gang (mgangdowsers (DOT) info) wrote:> It is the phrase: "... does not affect the friendly bacteria in the> body nor any of the healthy cells." which seems to contradict the info you> gave me??? is that right?MMS is a very powerful oxidizer.Healthy cells have more protection than unhealthy cells against oxidizers.Most, BUT NOT ALL, beneficial critters are aerobic.Aerobic critters will tolerate oxidizers much better than anaerobiccritters, but are not absolutely immune.So, the bottom line is, in lower doses, MMS shouldn't take too heavy atoll on the good guys, but it will get some of them. The higher thedose, the more of them it will get.When taking a break from MMS - you should take breaks for anything, eveneating (fasting one or two days a week is one of the healthiest thingsyou can eating wise) - you should be taking things to rebuild (healthybacteria, superfoods, mineral supplements like the Fulvic Acid mineralsfrom Vital Earth).I also highly recommend taking things to assist the body in eliminatingthe oxidized crud - bentonite clays and activated charcoal being some ofthe best ways to accomplish this, just make sure you take the claypre-hydrated, and drink enough water, as if you don't, it can causeconstipation.Lastly - keeping the bowels moving is one of the primary goals of anyhealth/cleansing program. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 5, 2008 Report Share Posted October 5, 2008 About the oxidizing part, I don't know. I would go with Jim Humble's opinion as he has the most experience with it. As far as beneficial bacteria, I can only tell you MY experience, and that has been that using it orally killed my good bacteria at the higher doses. It does not seem to do this when used topically, and I have been able to slowly rebuild my flora using it this way. Jim Humble does recommend using a probiotic with it. This is prudent advice as probiotics can only be beneficial and may prevent some of the problems I encountered. -- Re: [ ] yeast andMMS: SUSAN!? >MMS is a very powerful oxidizer.< In the podcast with Adam Abraham (MMS: What you need to know), Jim Humble specifically said MMS is a weak oxidizer. Is he wrong? He also says MMS won't touch anything that is alkaline. It seems like beneficial bacteria would be alkaline. -- Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 5, 2008 Report Share Posted October 5, 2008 >The immune system can use this killer to onlyattack those germs, bacteria and viruses that are harmful to the body, anddoes not affect the friendly bacteria in the body nor any of the healthycells. < Marilyn and , I have done a little research regarding the yeast issue due to a family member having a serious case of it. I pasted below a series of abstracts discussing candida and biofilm. What I gathered from these abstracts is that yeast grows a layer of biofilm rather quickly. When you release it from biofilm, if you don't get it out of the gut in a hurry, more biofilm grows. I helped my family member overcome his yeast by dosing the MMS regularly throughout the day, sometimes every two hours. It was sort of a "shock and awe" approach in the hopes that we could release the yeast, kill it, and move it out before new biofilm formed. It worked. It also worked for strep, and in the process, his chronically loose BMs improved. I don't think any beneficial bacteria were harmed, though he was also taking probiotics. -- 0: Antimicrob Agents Chemother. 2006 Nov;50(11):3839-46. Epub 2006 Aug 21. Candida albicans biofilms produce antifungal-tolerant persister cells.LaFleur MD, Kumamoto CA, K.Department of Biology, Northeastern University, 360 Huntington Ave., 134 Mugar Hall, Boston, MA 02115, USA.Fungal pathogens form biofilms that are highly recalcitrant to antimicrobial therapy. The expression of multidrug resistance pumps in young biofilms has been linked to increased resistance to azoles, but this mechanism does not seem to underlie the resistance of mature biofilms that is a model of in vivo infection. The mechanism of drug resistance of mature biofilms remains largely unknown. We report that biofilms formed by the major human pathogen Candida albicans exhibited a strikingly biphasic killing pattern in response to two microbicidal agents, amphotericin B, a polyene antifungal, and chlorhexidine, an antiseptic, indicating that a subpopulation of highly tolerant cells, termed persisters, existed. The extent of killing with a combination of amphotericin B and chlorhexidine was similar to that observed with individually added antimicrobials. Thus, surviving persisters form a multidrug-tolerant subpopulation. Interestingly, surviving C. albicans persisters were detected only in biofilms and not in exponentially growing or stationary-phase planktonic populations. Reinoculation of cells that survived killing of the biofilm by amphotericin B produced a new biofilm with a new subpopulation of persisters. This suggests that C. albicans persisters are not mutants but phenotypic variants of the wild type. Using a stain for dead cells, rare dark cells were visible in a biofilm after amphotericin B treatment, and a bright and a dim population were physically sorted from this biofilm. Only the dim cells produced colonies, showing that this method allows the isolation of yeast persisters. Given that persisters formed only in biofilms, mutants defective in biofilm formation were examined for tolerance of amphotericin B. All of the known mutants affected in biofilm formation were able to produce normal levels of persisters. This finding indicates that attachment rather than formation of a complex biofilm architecture initiates persister formation. Bacteria produce multidrug-tolerant persister cells in both planktonic and biofilm populations, and it appears that yeasts and bacteria have evolved analogous strategies that assign the function of survival to a small part of the population. In bacteria, persisters are dormant cells. It remains to be seen whether attachment initiates dormancy that leads to the formation of fungal persisters. This study suggests that persisters may be largely responsible for the multidrug tolerance of fungal biofilms.Publication Types: Research Support, N.I.H., Extramural PMID: 16923951 1: Antimicrob Agents Chemother. 2008 Mar;52(3):1127-32. Epub 2008 Jan 7. Synergistic effect of calcineurin inhibitors and fluconazole against Candida albicans biofilms.Uppuluri P, Nett J, Heitman J, Andes D.Department of Molecular Genetics and Microbiology, Duke University Medical Center, Durham, North Carolina 27710, USA.Calcineurin is a Ca2+-calmodulin-activated serine/threonine-specific protein phosphatase that governs multiple aspects of fungal physiology, including cation homeostasis, morphogenesis, antifungal drug susceptibility, and virulence. Growth of Candida albicans planktonic cells is sensitive to the calcineurin inhibitors FK506 and cyclosporine A (CsA) in combination with the azole antifungal fluconazole. This drug synergism is attributable to two effects: first, calcineurin inhibitors render fluconazole fungicidal rather than simply fungistatic, and second, membrane perturbation by azole inhibition of ergosterol biosynthesis increases intracellular calcineurin inhibitor concentrations. C. albicans cells in biofilms are up to 1,000-fold more resistant to fluconazole than planktonic cells. In both in vitro experiments and in an in vivo rat catheter model, C. albicans cells in biofilms were resistant to individually delivered fluconazole or calcineurin inhibitors but exquisitely sensitive to the combination of FK506-fluconazole or CsA-fluconazole. C. albicans strains lacking FKBP12 or expressing a dominant FK506-resistant calcineurin mutant subunit (Cnb1-1) formed biofilms that were resistant to FK506-fluconazole but susceptible to CsA-fluconazole, demonstrating that drug synergism is mediated via direct calcineurin inhibition. These findings reveal that calcineurin contributes to fluconazole resistance of biofilms and provide evidence that synergistic drug combinations may prove efficacious as novel therapeutic interventions to treat or prevent biofilms.Publication Types: Research Support, N.I.H., Extramural PMID: 18180354 [PubMed - in process] PMCID: PMC2258509 2: Antimicrob Agents Chemother. 2008 Jan;52(1):357-60. Epub 2007 Oct 15. Differential activities of newer antifungal agents against Candida albicans and Candida parapsilosis biofilms.Katragkou A, Chatzimoschou A, Simitsopoulou M, Dalakiouridou M, Diza-Mataftsi E, Tsantali C, Roilides E.Laboratory of Infectious Diseases, Third Department of Pediatrics, Aristotle University, Hippokration Hospital, 54642 Thessaloniki, Greece.The activities of voriconazole, posaconazole, caspofungin, and anidulafungin against Candida albicans and Candida parapsilosis biofilms were evaluated. In contrast to planktonic cells, the MICs for voriconazole and posaconazole for the biofilms of the two species were high (>or=256 and >64 mg/liter, respectively) but relatively low for the echinocandins caspofungin and anidulafungin (<or=1 and <or=2 mg/liter, respectively).Publication Types: Research Support, Non-U.S. Gov't PMID: 17938192 [PubMed - indexed for MEDLINE] PMCID: PMC2223899 3: Eukaryot Cell. 2007 Nov;6(11):2046-55. Epub 2007 Sep 14. Requirement for Candida albicans Sun41 in biofilm formation and virulence.Norice CT, FJ Jr, Solis N, Filler SG, AP.Department of Microbiology, Columbia University, New York, NY, USA.The cell wall of Candida albicans lies at the crossroads of pathogenicity and therapeutics. It contributes to pathogenicity through adherence and invasion; it is the target of both chemical and immunological antifungal strategies. We have initiated a dissection of cell wall function through targeted insertional mutagenesis of cell wall-related genes. Among 25 such genes, we were unable to generate homozygous mutations in 4, and they may be essential for viability. We created homozygous mutations in the remaining 21 genes. Insertion mutations in SUN41, Orf19.5412, Orf19.1277, MSB2, Orf19.3869, and WSC1 caused hypersensitivity to the cell wall inhibitor caspofungin, while two different ecm33 insertions caused mild caspofungin resistance. Insertion mutations in SUN41 and Orf19.5412 caused biofilm defects. Through analysis of homozygous sun41Delta/sun41Delta deletion mutants and sun41Delta/sun41Delta+pSUN41-complemented strains, we verified that Sun41 is required for biofilm formation and normal caspofungin tolerance. The sun41Delta/sun41Delta mutant had altered expression of four cell wall damage response genes, thus suggesting that it suffers a cell wall structural defect. Sun41 is required for inducing disease, because the mutant was severely attenuated in mouse models of disseminated and oropharyngeal candidiasis. Although the mutant produced aberrant hyphae, it had no defect in damaging endothelial or epithelial cells, unlike many other hypha-defective mutants. We suggest that the sun41Delta/sun41Delta cell wall defect is the primary cause of its attenuated virulence. As a small fungal surface protein with predicted glucosidase activity, Sun41 represents a promising therapeutic target.Publication Types: Research Support, N.I.H., Extramural PMID: 17873081 [PubMed - indexed for MEDLINE] PMCID: PMC2168420 4: Eukaryot Cell. 2007 Nov;6(11):2056-65. Epub 2007 Sep 28. Candida albicans Sun41p, a putative glycosidase, is involved in morphogenesis, cell wall biogenesis, and biofilm formation.Hiller E, Heine S, Brunner H, Rupp S.Fraunhofer Institute for Interfacial Engineering and Biotechnology, Nobelstrasse 12, 70569 Stuttgart, Germany.The SUN gene family has been defined in Saccharomyces cerevisiae and comprises a fungus-specific family of proteins which show high similarity in their C-terminal domains. Genes of this family are involved in different cellular processes, like DNA replication, aging, mitochondrial biogenesis, and cytokinesis. In Candida albicans the SUN family comprises two genes, SUN41 and SIM1. We demonstrate that C. albicans mutants lacking SUN41 show similar defects as found for S. cerevisiae, including defects in cytokinesis. In addition, the SUN41 mutant showed a higher sensitivity towards the cell wall-disturbing agent Congo red, whereas no difference was observed in the presence of calcofluor white. Compared to the wild type, SUN41 deletion strains exhibited a defect in biofilm formation, a reduced adherence on a Caco-2 cell monolayer, and were unable to form hyphae on solid medium under the conditions tested. Interestingly, Sun41p was found to be secreted in the medium of cells growing as blastospores as well as those forming hyphae. Our results support a function of SUN41p as a glycosidase involved in cytokinesis, cell wall biogenesis, adhesion to host tissue, and biofilm formation, indicating an important role in the host-pathogen interaction.Publication Types: Research Support, Non-U.S. Gov't PMID: 17905924 [PubMed - indexed for MEDLINE] PMCID: PMC2168408 5: Biol Pharm Bull. 2007 Sep;30(9):1813-5. Candida albicans biofilms produce more secreted aspartyl protease than the planktonic cells.Mendes A, Mores AU, Carvalho AP, RT, Samaranayake LP, EA.Laboratory of Stomatology, Faculty of Dentistry, Pontifical Catholic University of Paraná, Brazil.By using a simple, low-cost system of polystyrene centrifuge tubes we compared the secreted aspartyl proteases (Saps) secretion during the biphasic growth modes of Candida albicans using twenty-one clinical isolates. Our results indicate that biofilms of C. albicans consistently secrete more Saps than their planktonic counterparts.Publication Types: Research Support, Non-U.S. Gov't PMID: 17827747 [PubMed - indexed for MEDLINE] 6: Appl Environ Microbiol. 2007 Aug;73(15):4940-9. Epub 2007 Jun 8. Metal ions may suppress or enhance cellular differentiation in Candida albicans and Candida tropicalis biofilms.on JJ, Ceri H, Yerly J, Rabiei M, Hu Y, uzzi R, RJ.Department of Biological Sciences, University of Calgary, Calgary, Canada.Candida albicans and Candida tropicalis are polymorphic fungi that develop antimicrobial-resistant biofilm communities that are characterized by multiple cell morphotypes. This study investigated cell type interconversion and drug and metal resistance as well as community organization in biofilms of these microorganisms that were exposed to metal ions. To study this, Candida biofilms were grown either in microtiter plates containing gradient arrays of metal ions or in the Calgary Biofilm Device for high-throughput susceptibility testing. Biofilm formation and antifungal resistance were evaluated by viable cell counts, tetrazolium salt reduction, light microscopy, and confocal laser scanning microscopy in conjunction with three-dimensional visualization. We discovered that subinhibitory concentrations of certain metal ions (CrO(4)(2-), Co(2+), Cu(2+), Ag(+), Zn(2+), Cd(2+), Hg(2+), Pb(2+), AsO(2)(-), and SeO(3)(2-)) caused changes in biofilm structure by blocking or eliciting the transition between yeast and hyphal cell types. Four distinct biofilm community structure types were discerned from these data, which were designated "domed," "layer cake," "flat," and "mycelial." This study suggests that Candida biofilm populations may respond to metal ions to form cell-cell and solid-surface-attached assemblages with distinct patterns of cellular differentiation.Publication Types: Research Support, Non-U.S. Gov't PMID: 17557844 [PubMed - indexed for MEDLINE] PMCID: PMC1951024 7: Antimicrob Agents Chemother. 2007 Jul;51(7):2454-63. Epub 2007 May 14. Role for cell density in antifungal drug resistance in Candida albicans biofilms.Perumal P, Mekala S, Chaffin WL.Department of Microbiology and Immunology, Texas Tech University Health Sciences Center, Lubbock, TX 79430, USA.Biofilms of Candida albicans are less susceptible to many antifungal drugs than are planktonic yeast cells. We investigated the contribution of cell density to biofilm phenotypic resistance. Planktonic yeast cells in RPMI 1640 were susceptible to azole-class drugs, amphotericin B, and caspofungin at 1 x 10(3) cells/ml (standard conditions) using the XTT [2,3-bis(2-methoxy-4-nitro-5-sulfophenyl)-2H-tetrazolium-5-carboxanilide sodium salt] assay. As reported by others, as the cell concentration increased to 1 x 10(8) cells/ml, resistance was observed with 10- to 20-fold-greater MICs. Biofilms that formed in microtiter plate wells, like high-density planktonic organisms, were resistant to drugs. When biofilms were resuspended before testing, phenotypic resistance remained, but organisms, when diluted to 1 x 10(3) cells/ml, were susceptible. Drug-containing medium recovered from high-cell-density tests inhibited low-cell-density organisms. A fluconazole-resistant strain showed greater resistance at high planktonic cell density, in biofilm, and in resuspended biofilm than did low-density planktonic or biofilm organisms. A strain lacking drug efflux pumps CDR1, CDR2, and MDR1, while susceptible at a low azole concentration, was resistant at high cell density and in biofilm. A strain lacking CHK1 that fails to respond to the quorum-sensing molecule farnesol had the same response as did the wild type. FK506, reported to abrogate tolerance to azole drugs at low cell density, had no effect on tolerance at high cell density and in biofilm. These observations suggested that cell density has a role in the phenotypic resistance of biofilm, that neither the drug efflux pumps tested nor quorum sensing through Chk1p contributes to resistance, and that azole drug tolerance at high cell density differs mechanistically from tolerance at low cell density.Publication Types: Research Support, N.I.H., Extramural PMID: 17502416 [PubMed - indexed for MEDLINE] PMCID: PMC1913227 8: J Med Microbiol. 2007 May;56(Pt 5):645-9. Enhancement of the in vitro activity of amphotericin B against the biofilms of non-albicans Candida spp. by rifampicin and doxycycline.El-Azizi M.Department of Microbiology and Biotechnology, German University in Cairo-GUC, New Cairo City, Egypt. mohamed.el-aziziguc (DOT) edu.egThe in vitro activity of amphotericin B (AMB) alone and in combination with rifampicin (RIF) and doxycycline (DOX) was tested against the biofilms of 30 clinical isolates of non-albicans Candida (NAC) species namely, Candida parapsilosis, Candida krusei and Candida glabrata. The killing activity of AMB at 10 x MIC was significantly increased in combination with either antibiotic. With RIF, the killing activity increased by 20.6, 23.5 and 14 % against the biofilms of C. parapsilosis, C. krusei and C. glabrata, respectively; with DOX, the killing activity increased by 30.64, 35.28 and 31.13 %, respectively. Pre-exposure of the isolates to the same combinations significantly reduced the number of colonized cells in the biofilms by 20, 25.14 and 13.07 % with RIF for C. parapsilosis, C. krusei and C. glabrata, respectively, and by 18.94, 24.52 and 29.15 % with DOX, respectively. The data showed that combination of RIF or DOX with AMB enhanced the killing activity of the antifungal agent against biofilms of NAC species. Whether such an effect operates against biofilm-associated infections needs to be clarified by further in vivo studies.PMID: 17446287 [PubMed - indexed for MEDLINE] 9: Infect Immun. 2007 May;75(5):2612-20. Epub 2007 Mar 5. Interaction of Candida albicans with adherent human peripheral blood mononuclear cells increases C. albicans biofilm formation and results in differential expression of pro- and anti-inflammatory cytokines.Chandra J, McCormick TS, Imamura Y, Mukherjee PK, Ghannoum MA.Center for Medical Mycology, University Hospitals Case Medical Center, Cleveland, OH, USA.Monocytes and macrophages are the cell types most commonly associated with the innate immune response against Candida albicans infection. Interactions between the host immune system and Candida organisms have been investigated for planktonic Candida cells, but no studies have addressed these interactions in a biofilm environment. In this study, for the first time, we evaluated the ability of C. albicans to form biofilms in the presence or absence of adherent peripheral blood mononuclear cells (PBMCs; enriched for monocytes and macrophages by adherence). Our analyses using scanning electron and confocal scanning laser microscopy showed that the presence of PBMCs enhanced the ability of C. albicans to form biofilms and that the majority of PBMCs were localized to the basal and middle layers of the biofilm. In contrast to the interactions of PBMCs with planktonic C. albicans, where PBMCs phagocytose fungal cells, PBMCs did not appear to phagocytose fungal cells in biofilms. Furthermore, time-lapse laser microscopy revealed dynamic interactions between C. albicans and PBMCs in a biofilm. Additionally, we found that (i) only viable PBMCs influence Candida biofilm formation, (ii) cell surface components of PBMCs did not contribute to the enhancement of C. albicans biofilm, (iii) the biofilm-enhancing effect of PBMCs is mediated by a soluble factor released into the coculture medium of PBMCs with C. albicans, and (iv) supernatant collected from this coculture contained differential levels of pro- and anti-inflammatory cytokines. Our studies provide new insight into the interaction between Candida biofilm and host immune cells and demonstrate that immunocytes may influence the ability of C. albicans to form biofilms.Publication Types: Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't PMID: 17339351 [PubMed - indexed for MEDLINE] PMCID: PMC1865760 10: Antimicrob Agents Chemother. 2007 Feb;51(2):510-20. Epub 2006 Nov 27. Putative role of beta-1,3 glucans in Candida albicans biofilm resistance.Nett J, Lincoln L, Marchillo K, Massey R, Holoyda K, Hoff B, VanHandel M, Andes D.Department of Medicine, University of Wisconsin Electron Microscopy Facility, Madison 53792, USA.Biofilms are microbial communities, embedded in a polymeric matrix, growing attached to a surface. Nearly all device-associated infections involve growth in the biofilm life style. Biofilm communities have characteristic architecture and distinct phenotypic properties. The most clinically important phenotype involves extraordinary resistance to antimicrobial therapy, making biofilm infections very difficulty to cure without device removal. The current studies examine drug resistance in Candida albicans biofilms. Similar to previous reports, we observed marked fluconazole and amphotericin B resistance in a C. albicans biofilm both in vitro and in vivo. We identified biofilm-associated cell wall architectural changes and increased beta-1,3 glucan content in C. albicans cell walls from a biofilm compared to planktonic organisms. Elevated beta-1,3 glucan levels were also found in the surrounding biofilm milieu and as part of the matrix both from in vitro and in vivo biofilm models. We thus investigated the possible contribution of beta-glucans to antimicrobial resistance in Candida albicans biofilms. Initial studies examined the ability of cell wall and cell supernatant from biofilm and planktonic C. albicans to bind fluconazole. The cell walls from both environmental conditions bound fluconazole; however, four- to fivefold more compound was bound to the biofilm cell walls. Culture supernatant from the biofilm, but not planktonic cells, bound a measurable amount of this antifungal agent. We next investigated the effect of enzymatic modification of beta-1,3 glucans on biofilm cell viability and the susceptibility of biofilm cells to fluconazole and amphotericin B. We observed a dose-dependent killing of in vitro biofilm cells in the presence of three different beta-glucanase preparations. These same concentrations had no impact on planktonic cell viability. beta-1,3 Glucanase markedly enhanced the activity of both fluconazole and amphotericin B. These observations were corroborated with an in vivo biofilm model. Exogenous biofilm matrix and commercial beta-1,3 glucan reduced the activity of fluconazole against planktonic C. albicans in vitro. In sum, the current investigation identified glucan changes associated with C. albicans biofilm cells, demonstrated preferential binding of these biofilm cell components to antifungals, and showed a positive impact of the modification of biofilm beta-1,3 glucans on drug susceptibility. These results provide indirect evidence suggesting a role for glucans in biofilm resistance and present a strong rationale for further molecular dissection of this resistance mechanism to identify new drug targets to treat biofilm infections.PMID: 17130296 [PubMed - indexed for MEDLINE] PMCID: PMC1797745 11: Antimicrob Agents Chemother. 2006 Oct;50(10):3488-91. Protein O-mannosyltransferase isoforms regulate biofilm formation in Candida albicans.Peltroche-Llacsahuanga H, Goyard S, d'Enfert C, Prill SK, Ernst JF.Institut für Medizinische Mikrobiologie, RWTH Aachen, Germany.Five isoforms of protein mannosyltransferase (Pmt) O-mannosylate secretory proteins in Candida albicans. pmt mutants were differentially defective for biofilm formation on plastic in static and flow-through systems, and a Pmt inhibitor blocked early stages of biofilm formation. Conceptually, Pmt inhibition may prevent surface anchoring and biofilm-dependent resistance of fungal pathogens.Publication Types: Research Support, Non-U.S. Gov't PMID: 17005840 [PubMed - indexed for MEDLINE] PMCID: PMC1610076 Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 5, 2008 Report Share Posted October 5, 2008 On 10/5/2008, Poole Family (lipoole@...) wrote: > In the podcast with Adam Abraham (MMS: What you need to know), Jim > Humble specifically said MMS is a weak oxidizer. Is he wrong? He also > says MMS won't touch anything that is alkaline. It seems like > beneficial bacteria would be alkaline. A little googling shows you to be correct... I had forgotten that, and in my mind confused 'powerful therapy' with its oxidation strength/potential. Thanks for the correction. there are actually two aspects to oxidation... oxidation 'strength/potential', and oxidation capacity. MMS has a much lower oxidation *strength* than chlorine or ozone, but more oxidative capacity (ozone has even more) Not all beneficial critters are alkaline, just as not all beneficial critter are aerobic (flourish in an oxygen rich environment). Here's a good link which mentions all three (but focused on Chlorine Dioxide): http://www.lenntech.com/chlorine_dioxide.htm Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 13, 2008 Report Share Posted October 13, 2008 I have been taking mangosteen which is an antimicrobial. I buy it at Costco for $17 a bottle and it last me about a month. I take two tablespoons a day. I have been feeling okay as of late and have returned to work but it is a long path to recovery for what I have. Sharon > > >The immune system can use this killer to only > attack those germs, bacteria and viruses that are harmful to the body, and > does not affect the friendly bacteria in the body nor any of the healthy > cells. < > > Marilyn and , > > I have done a little research regarding the yeast issue due to a family member having a serious case of it. I pasted below a series of abstracts discussing candida and biofilm. What I gathered from these abstracts is that yeast grows a layer of biofilm rather quickly. When you release it from biofilm, if you don't get it out of the gut in a hurry, more biofilm grows. I helped my family member overcome his yeast by dosing the MMS regularly throughout the day, sometimes every two hours. It was sort of a " shock and awe " approach in the hopes that we could release the yeast, kill it, and move it out before new biofilm formed. It worked. It also worked for strep, and in the process, his chronically loose BMs improved. I don't think any beneficial bacteria were harmed, though he was also taking probiotics. > > -- > > 0: Antimicrob Agents Chemother. 2006 Nov;50(11):3839-46. Epub 2006 Aug 21. > > > > Candida albicans biofilms produce antifungal-tolerant persister cells. > > LaFleur MD, Kumamoto CA, K. > > Department of Biology, Northeastern University, 360 Huntington Ave., 134 Mugar Hall, Boston, MA 02115, USA. > > Fungal pathogens form biofilms that are highly recalcitrant to antimicrobial therapy. The expression of multidrug resistance pumps in young biofilms has been linked to increased resistance to azoles, but this mechanism does not seem to underlie the resistance of mature biofilms that is a model of in vivo infection. The mechanism of drug resistance of mature biofilms remains largely unknown. We report that biofilms formed by the major human pathogen Candida albicans exhibited a strikingly biphasic killing pattern in response to two microbicidal agents, amphotericin B, a polyene antifungal, and chlorhexidine, an antiseptic, indicating that a subpopulation of highly tolerant cells, termed persisters, existed. The extent of killing with a combination of amphotericin B and chlorhexidine was similar to that observed with individually added antimicrobials. Thus, surviving persisters form a multidrug-tolerant subpopulation. Interestingly, surviving C. albicans persisters were detected only in biofilms and not in exponentially growing or stationary-phase planktonic populations. Reinoculation of cells that survived killing of the biofilm by amphotericin B produced a new biofilm with a new subpopulation of persisters. This suggests that C. albicans persisters are not mutants but phenotypic variants of the wild type. Using a stain for dead cells, rare dark cells were visible in a biofilm after amphotericin B treatment, and a bright and a dim population were physically sorted from this biofilm. Only the dim cells produced colonies, showing that this method allows the isolation of yeast persisters. Given that persisters formed only in biofilms, mutants defective in biofilm formation were examined for tolerance of amphotericin B. All of the known mutants affected in biofilm formation were able to produce normal levels of persisters. This finding indicates that attachment rather than formation of a complex biofilm architecture initiates persister formation. Bacteria produce multidrug-tolerant persister cells in both planktonic and biofilm populations, and it appears that yeasts and bacteria have evolved analogous strategies that assign the function of survival to a small part of the population. In bacteria, persisters are dormant cells. It remains to be seen whether attachment initiates dormancy that leads to the formation of fungal persisters. This study suggests that persisters may be largely responsible for the multidrug tolerance of fungal biofilms. > > Publication Types: > a.. Research Support, N.I.H., Extramural > > PMID: 16923951 > > > 1: Antimicrob Agents Chemother. 2008 Mar;52(3):1127-32. Epub 2008 Jan 7. > > > > Synergistic effect of calcineurin inhibitors and fluconazole against Candida albicans biofilms. > > Uppuluri P, Nett J, Heitman J, Andes D. > > Department of Molecular Genetics and Microbiology, Duke University Medical Center, Durham, North Carolina 27710, USA. > > Calcineurin is a Ca2+-calmodulin-activated serine/threonine- specific protein phosphatase that governs multiple aspects of fungal physiology, including cation homeostasis, morphogenesis, antifungal drug susceptibility, and virulence. Growth of Candida albicans planktonic cells is sensitive to the calcineurin inhibitors FK506 and cyclosporine A (CsA) in combination with the azole antifungal fluconazole. This drug synergism is attributable to two effects: first, calcineurin inhibitors render fluconazole fungicidal rather than simply fungistatic, and second, membrane perturbation by azole inhibition of ergosterol biosynthesis increases intracellular calcineurin inhibitor concentrations. C. albicans cells in biofilms are up to 1,000-fold more resistant to fluconazole than planktonic cells. In both in vitro experiments and in an in vivo rat catheter model, C. albicans cells in biofilms were resistant to individually delivered fluconazole or calcineurin inhibitors but exquisitely sensitive to the combination of FK506-fluconazole or CsA-fluconazole. C. albicans strains lacking FKBP12 or expressing a dominant FK506- resistant calcineurin mutant subunit (Cnb1-1) formed biofilms that were resistant to FK506-fluconazole but susceptible to CsA- fluconazole, demonstrating that drug synergism is mediated via direct calcineurin inhibition. These findings reveal that calcineurin contributes to fluconazole resistance of biofilms and provide evidence that synergistic drug combinations may prove efficacious as novel therapeutic interventions to treat or prevent biofilms. > > Publication Types: > a.. Research Support, N.I.H., Extramural > > PMID: 18180354 [PubMed - in process] > PMCID: PMC2258509 > > > -------------------------------------------------------------------- ------------ > > 2: Antimicrob Agents Chemother. 2008 Jan;52(1):357-60. Epub 2007 Oct 15. > > > > Differential activities of newer antifungal agents against Candida albicans and Candida parapsilosis biofilms. > > Katragkou A, Chatzimoschou A, Simitsopoulou M, Dalakiouridou M, Diza-Mataftsi E, Tsantali C, Roilides E. > > Laboratory of Infectious Diseases, Third Department of Pediatrics, Aristotle University, Hippokration Hospital, 54642 Thessaloniki, Greece. > > The activities of voriconazole, posaconazole, caspofungin, and anidulafungin against Candida albicans and Candida parapsilosis biofilms were evaluated. In contrast to planktonic cells, the MICs for voriconazole and posaconazole for the biofilms of the two species were high (>or=256 and >64 mg/liter, respectively) but relatively low for the echinocandins caspofungin and anidulafungin (<or=1 and <or=2 mg/liter, respectively). > > Publication Types: > a.. Research Support, Non-U.S. Gov't > > PMID: 17938192 [PubMed - indexed for MEDLINE] > PMCID: PMC2223899 > > > -------------------------------------------------------------------- ------------ > > 3: Eukaryot Cell. 2007 Nov;6(11):2046-55. Epub 2007 Sep 14. > > > > Requirement for Candida albicans Sun41 in biofilm formation and virulence. > > Norice CT, FJ Jr, Solis N, Filler SG, AP. > > Department of Microbiology, Columbia University, New York, NY, USA. > > The cell wall of Candida albicans lies at the crossroads of pathogenicity and therapeutics. It contributes to pathogenicity through adherence and invasion; it is the target of both chemical and immunological antifungal strategies. We have initiated a dissection of cell wall function through targeted insertional mutagenesis of cell wall-related genes. Among 25 such genes, we were unable to generate homozygous mutations in 4, and they may be essential for viability. We created homozygous mutations in the remaining 21 genes. Insertion mutations in SUN41, Orf19.5412, Orf19.1277, MSB2, Orf19.3869, and WSC1 caused hypersensitivity to the cell wall inhibitor caspofungin, while two different ecm33 insertions caused mild caspofungin resistance. Insertion mutations in SUN41 and Orf19.5412 caused biofilm defects. Through analysis of homozygous sun41Delta/sun41Delta deletion mutants and sun41Delta/sun41Delta+pSUN41-complemented strains, we verified that Sun41 is required for biofilm formation and normal caspofungin tolerance. The sun41Delta/sun41Delta mutant had altered expression of four cell wall damage response genes, thus suggesting that it suffers a cell wall structural defect. Sun41 is required for inducing disease, because the mutant was severely attenuated in mouse models of disseminated and oropharyngeal candidiasis. Although the mutant produced aberrant hyphae, it had no defect in damaging endothelial or epithelial cells, unlike many other hypha-defective mutants. We suggest that the sun41Delta/sun41Delta cell wall defect is the primary cause of its attenuated virulence. As a small fungal surface protein with predicted glucosidase activity, Sun41 represents a promising therapeutic target. > > Publication Types: > a.. Research Support, N.I.H., Extramural > > PMID: 17873081 [PubMed - indexed for MEDLINE] > PMCID: PMC2168420 > > > -------------------------------------------------------------------- ------------ > > 4: Eukaryot Cell. 2007 Nov;6(11):2056-65. Epub 2007 Sep 28. > > > > Candida albicans Sun41p, a putative glycosidase, is involved in morphogenesis, cell wall biogenesis, and biofilm formation. > > Hiller E, Heine S, Brunner H, Rupp S. > > Fraunhofer Institute for Interfacial Engineering and Biotechnology, Nobelstrasse 12, 70569 Stuttgart, Germany. > > The SUN gene family has been defined in Saccharomyces cerevisiae and comprises a fungus-specific family of proteins which show high similarity in their C-terminal domains. Genes of this family are involved in different cellular processes, like DNA replication, aging, mitochondrial biogenesis, and cytokinesis. In Candida albicans the SUN family comprises two genes, SUN41 and SIM1. We demonstrate that C. albicans mutants lacking SUN41 show similar defects as found for S. cerevisiae, including defects in cytokinesis. In addition, the SUN41 mutant showed a higher sensitivity towards the cell wall- disturbing agent Congo red, whereas no difference was observed in the presence of calcofluor white. Compared to the wild type, SUN41 deletion strains exhibited a defect in biofilm formation, a reduced adherence on a Caco-2 cell monolayer, and were unable to form hyphae on solid medium under the conditions tested. Interestingly, Sun41p was found to be secreted in the medium of cells growing as blastospores as well as those forming hyphae. Our results support a function of SUN41p as a glycosidase involved in cytokinesis, cell wall biogenesis, adhesion to host tissue, and biofilm formation, indicating an important role in the host-pathogen interaction. > > Publication Types: > a.. Research Support, Non-U.S. Gov't > > PMID: 17905924 [PubMed - indexed for MEDLINE] > PMCID: PMC2168408 > > > -------------------------------------------------------------------- ------------ > > 5: Biol Pharm Bull. 2007 Sep;30(9):1813-5. > > > > Candida albicans biofilms produce more secreted aspartyl protease than the planktonic cells. > > Mendes A, Mores AU, Carvalho AP, RT, Samaranayake LP, EA. > > Laboratory of Stomatology, Faculty of Dentistry, Pontifical Catholic University of Paraná, Brazil. > > By using a simple, low-cost system of polystyrene centrifuge tubes we compared the secreted aspartyl proteases (Saps) secretion during the biphasic growth modes of Candida albicans using twenty-one clinical isolates. Our results indicate that biofilms of C. albicans consistently secrete more Saps than their planktonic counterparts. > > Publication Types: > a.. Research Support, Non-U.S. Gov't > > PMID: 17827747 [PubMed - indexed for MEDLINE] > > -------------------------------------------------------------------- ------------ > > 6: Appl Environ Microbiol. 2007 Aug;73(15):4940-9. Epub 2007 Jun 8. > > > > Metal ions may suppress or enhance cellular differentiation in Candida albicans and Candida tropicalis biofilms. > > on JJ, Ceri H, Yerly J, Rabiei M, Hu Y, uzzi R, RJ. > > Department of Biological Sciences, University of Calgary, Calgary, Canada. > > Candida albicans and Candida tropicalis are polymorphic fungi that develop antimicrobial-resistant biofilm communities that are characterized by multiple cell morphotypes. This study investigated cell type interconversion and drug and metal resistance as well as community organization in biofilms of these microorganisms that were exposed to metal ions. To study this, Candida biofilms were grown either in microtiter plates containing gradient arrays of metal ions or in the Calgary Biofilm Device for high-throughput susceptibility testing. Biofilm formation and antifungal resistance were evaluated by viable cell counts, tetrazolium salt reduction, light microscopy, and confocal laser scanning microscopy in conjunction with three- dimensional visualization. We discovered that subinhibitory concentrations of certain metal ions (CrO(4)(2-), Co(2+), Cu(2+), Ag (+), Zn(2+), Cd(2+), Hg(2+), Pb(2+), AsO(2)(-), and SeO(3)(2-)) caused changes in biofilm structure by blocking or eliciting the transition between yeast and hyphal cell types. Four distinct biofilm community structure types were discerned from these data, which were designated " domed, " " layer cake, " " flat, " and " mycelial. " This study suggests that Candida biofilm populations may respond to metal ions to form cell-cell and solid-surface-attached assemblages with distinct patterns of cellular differentiation. > > Publication Types: > a.. Research Support, Non-U.S. Gov't > > PMID: 17557844 [PubMed - indexed for MEDLINE] > PMCID: PMC1951024 > > > -------------------------------------------------------------------- ------------ > > 7: Antimicrob Agents Chemother. 2007 Jul;51(7):2454-63. Epub 2007 May 14. > > > > Role for cell density in antifungal drug resistance in Candida albicans biofilms. > > Perumal P, Mekala S, Chaffin WL. > > Department of Microbiology and Immunology, Texas Tech University Health Sciences Center, Lubbock, TX 79430, USA. > > Biofilms of Candida albicans are less susceptible to many antifungal drugs than are planktonic yeast cells. We investigated the contribution of cell density to biofilm phenotypic resistance. Planktonic yeast cells in RPMI 1640 were susceptible to azole-class drugs, amphotericin B, and caspofungin at 1 x 10(3) cells/ml (standard conditions) using the XTT [2,3-bis(2-methoxy-4-nitro-5- sulfophenyl)-2H-tetrazolium-5-carboxanilide sodium salt] assay. As reported by others, as the cell concentration increased to 1 x 10(8) cells/ml, resistance was observed with 10- to 20-fold-greater MICs. Biofilms that formed in microtiter plate wells, like high-density planktonic organisms, were resistant to drugs. When biofilms were resuspended before testing, phenotypic resistance remained, but organisms, when diluted to 1 x 10(3) cells/ml, were susceptible. Drug- containing medium recovered from high-cell-density tests inhibited low-cell-density organisms. A fluconazole-resistant strain showed greater resistance at high planktonic cell density, in biofilm, and in resuspended biofilm than did low-density planktonic or biofilm organisms. A strain lacking drug efflux pumps CDR1, CDR2, and MDR1, while susceptible at a low azole concentration, was resistant at high cell density and in biofilm. A strain lacking CHK1 that fails to respond to the quorum-sensing molecule farnesol had the same response as did the wild type. FK506, reported to abrogate tolerance to azole drugs at low cell density, had no effect on tolerance at high cell density and in biofilm. These observations suggested that cell density has a role in the phenotypic resistance of biofilm, that neither the drug efflux pumps tested nor quorum sensing through Chk1p contributes to resistance, and that azole drug tolerance at high cell density differs mechanistically from tolerance at low cell density. > > Publication Types: > a.. Research Support, N.I.H., Extramural > > PMID: 17502416 [PubMed - indexed for MEDLINE] > PMCID: PMC1913227 > > > -------------------------------------------------------------------- ------------ > > 8: J Med Microbiol. 2007 May;56(Pt 5):645-9. > > > > Enhancement of the in vitro activity of amphotericin B against the biofilms of non-albicans Candida spp. by rifampicin and doxycycline. > > El-Azizi M. > > Department of Microbiology and Biotechnology, German University in Cairo-GUC, New Cairo City, Egypt. mohamed.el-azizi@... > > The in vitro activity of amphotericin B (AMB) alone and in combination with rifampicin (RIF) and doxycycline (DOX) was tested against the biofilms of 30 clinical isolates of non-albicans Candida (NAC) species namely, Candida parapsilosis, Candida krusei and Candida glabrata. The killing activity of AMB at 10 x MIC was significantly increased in combination with either antibiotic. With RIF, the killing activity increased by 20.6, 23.5 and 14 % against the biofilms of C. parapsilosis, C. krusei and C. glabrata, respectively; with DOX, the killing activity increased by 30.64, 35.28 and 31.13 %, respectively. Pre-exposure of the isolates to the same combinations significantly reduced the number of colonized cells in the biofilms by 20, 25.14 and 13.07 % with RIF for C. parapsilosis, C. krusei and C. glabrata, respectively, and by 18.94, 24.52 and 29.15 % with DOX, respectively. The data showed that combination of RIF or DOX with AMB enhanced the killing activity of the antifungal agent against biofilms of NAC species. Whether such an effect operates against biofilm-associated infections needs to be clarified by further in vivo studies. > > PMID: 17446287 [PubMed - indexed for MEDLINE] > > -------------------------------------------------------------------- ------------ > > 9: Infect Immun. 2007 May;75(5):2612-20. Epub 2007 Mar 5. > > > > Interaction of Candida albicans with adherent human peripheral blood mononuclear cells increases C. albicans biofilm formation and results in differential expression of pro- and anti-inflammatory cytokines. > > Chandra J, McCormick TS, Imamura Y, Mukherjee PK, Ghannoum MA. > > Center for Medical Mycology, University Hospitals Case Medical Center, Cleveland, OH, USA. > > Monocytes and macrophages are the cell types most commonly associated with the innate immune response against Candida albicans infection. Interactions between the host immune system and Candida organisms have been investigated for planktonic Candida cells, but no studies have addressed these interactions in a biofilm environment. In this study, for the first time, we evaluated the ability of C. albicans to form biofilms in the presence or absence of adherent peripheral blood mononuclear cells (PBMCs; enriched for monocytes and macrophages by adherence). Our analyses using scanning electron and confocal scanning laser microscopy showed that the presence of PBMCs enhanced the ability of C. albicans to form biofilms and that the majority of PBMCs were localized to the basal and middle layers of the biofilm. In contrast to the interactions of PBMCs with planktonic C. albicans, where PBMCs phagocytose fungal cells, PBMCs did not appear to phagocytose fungal cells in biofilms. Furthermore, time- lapse laser microscopy revealed dynamic interactions between C. albicans and PBMCs in a biofilm. Additionally, we found that (i) only viable PBMCs influence Candida biofilm formation, (ii) cell surface components of PBMCs did not contribute to the enhancement of C. albicans biofilm, (iii) the biofilm-enhancing effect of PBMCs is mediated by a soluble factor released into the coculture medium of PBMCs with C. albicans, and (iv) supernatant collected from this coculture contained differential levels of pro- and anti-inflammatory cytokines. Our studies provide new insight into the interaction between Candida biofilm and host immune cells and demonstrate that immunocytes may influence the ability of C. albicans to form biofilms. > > Publication Types: > a.. Research Support, N.I.H., Extramural > b.. Research Support, Non-U.S. Gov't > > PMID: 17339351 [PubMed - indexed for MEDLINE] > PMCID: PMC1865760 > > > -------------------------------------------------------------------- ------------ > > 10: Antimicrob Agents Chemother. 2007 Feb;51(2):510-20. Epub 2006 Nov 27. > > > > Putative role of beta-1,3 glucans in Candida albicans biofilm resistance. > > Nett J, Lincoln L, Marchillo K, Massey R, Holoyda K, Hoff B, VanHandel M, Andes D. > > Department of Medicine, University of Wisconsin Electron Microscopy Facility, Madison 53792, USA. > > Biofilms are microbial communities, embedded in a polymeric matrix, growing attached to a surface. Nearly all device-associated infections involve growth in the biofilm life style. Biofilm communities have characteristic architecture and distinct phenotypic properties. The most clinically important phenotype involves extraordinary resistance to antimicrobial therapy, making biofilm infections very difficulty to cure without device removal. The current studies examine drug resistance in Candida albicans biofilms. Similar to previous reports, we observed marked fluconazole and amphotericin B resistance in a C. albicans biofilm both in vitro and in vivo. We identified biofilm-associated cell wall architectural changes and increased beta-1,3 glucan content in C. albicans cell walls from a biofilm compared to planktonic organisms. Elevated beta- 1,3 glucan levels were also found in the surrounding biofilm milieu and as part of the matrix both from in vitro and in vivo biofilm models. We thus investigated the possible contribution of beta- glucans to antimicrobial resistance in Candida albicans biofilms. Initial studies examined the ability of cell wall and cell supernatant from biofilm and planktonic C. albicans to bind fluconazole. The cell walls from both environmental conditions bound fluconazole; however, four- to fivefold more compound was bound to the biofilm cell walls. Culture supernatant from the biofilm, but not planktonic cells, bound a measurable amount of this antifungal agent. We next investigated the effect of enzymatic modification of beta-1,3 glucans on biofilm cell viability and the susceptibility of biofilm cells to fluconazole and amphotericin B. We observed a dose-dependent killing of in vitro biofilm cells in the presence of three different beta-glucanase preparations. These same concentrations had no impact on planktonic cell viability. beta-1,3 Glucanase markedly enhanced the activity of both fluconazole and amphotericin B. These observations were corroborated with an in vivo biofilm model. Exogenous biofilm matrix and commercial beta-1,3 glucan reduced the activity of fluconazole against planktonic C. albicans in vitro. In sum, the current investigation identified glucan changes associated with C. albicans biofilm cells, demonstrated preferential binding of these biofilm cell components to antifungals, and showed a positive impact of the modification of biofilm beta-1,3 glucans on drug susceptibility. These results provide indirect evidence suggesting a role for glucans in biofilm resistance and present a strong rationale for further molecular dissection of this resistance mechanism to identify new drug targets to treat biofilm infections. > > PMID: 17130296 [PubMed - indexed for MEDLINE] > PMCID: PMC1797745 > > > -------------------------------------------------------------------- ------------ > > 11: Antimicrob Agents Chemother. 2006 Oct;50(10):3488-91. > > > > Protein O-mannosyltransferase isoforms regulate biofilm formation in Candida albicans. > > Peltroche-Llacsahuanga H, Goyard S, d'Enfert C, Prill SK, Ernst JF. > > Institut für Medizinische Mikrobiologie, RWTH Aachen, Germany. > > Five isoforms of protein mannosyltransferase (Pmt) O-mannosylate secretory proteins in Candida albicans. pmt mutants were differentially defective for biofilm formation on plastic in static and flow-through systems, and a Pmt inhibitor blocked early stages of biofilm formation. Conceptually, Pmt inhibition may prevent surface anchoring and biofilm-dependent resistance of fungal pathogens. > > Publication Types: > a.. Research Support, Non-U.S. Gov't > > PMID: 17005840 [PubMed - indexed for MEDLINE] > PMCID: PMC1610076 > Quote Link to comment Share on other sites More sharing options...
Guest guest Posted October 13, 2008 Report Share Posted October 13, 2008 Hi Sharon --- Please excuse me if prob. due to too many emails I'm not sure what situation you are talking about, just thought I'd put in my 2 cents. cause the absolute best antimicrobial I have found --- and I'm sure I'm not the only one --- is Oil of Oregano, that comes from wild oregano. The brand I'm partial to is North American Herbs. It ain't cheap but just a couple drops a day is usually all thats needed so it lasts long. I heard of mangosteen and wasn't too sure what it really was so found a link from chet day's site on a ralph moss report which leads to my next comment: I do steer away from fruit-y antimicrobials since they contain sugar which is usually bacteria food --- unless its raw honey which also -- can -- kill 'em dead. Having said that --- doesn't mms kill the nasties? too much not good stuff around. good luck to you. - Marilyn - At 09:29 AM 10/13/2008 -0000, Sharon wrote: >I have been taking mangosteen which is an antimicrobial. I buy it at >Costco for $17 a bottle and it last me about a month. I take two >tablespoons a day. > >I have been feeling okay as of late and have returned to work but it >is a long path to recovery for what I have. > >Sharon > > >> >> >The immune system can use this killer to only >> attack those germs, bacteria and viruses that are harmful to the >body, and >> does not affect the friendly bacteria in the body nor any of the >healthy >> cells. < >> >> Marilyn and , >> >> I have done a little research regarding the yeast issue due to a >family member having a serious case of it. I pasted below a series of >abstracts discussing candida and biofilm. What I gathered from these >abstracts is that yeast grows a layer of biofilm rather quickly. When >you release it from biofilm, if you don't get it out of the gut in a >hurry, more biofilm grows. I helped my family member overcome his >yeast by dosing the MMS regularly throughout the day, sometimes every >two hours. It was sort of a " shock and awe " approach in the hopes >that we could release the yeast, kill it, and move it out before new >biofilm formed. It worked. It also worked for strep, and in the >process, his chronically loose BMs improved. I don't think any >beneficial bacteria were harmed, though he was also taking probiotics. >> >> -- >> HUGE SNIP Quote Link to comment Share on other sites More sharing options...
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