- August 9, 2013 at 11:00 pm #108866
I am new here although I have read some posts over the past couple of months for info.
I aquired my problem with candida because unfortunately I had to take antibiotics chronically over a 2 year period (not necessary anymore, but the damage is done).
I have been suffering with candida symptoms for probably at least a year now, but I was ignorant that a lot of these were in fact from candida. I only became truly aware of the problem a couple of months ago when I got a chronic vaginal yeast infection. At 1st I thought vaginal yeast was my only candida problem, and this was my big mistake. I went to my Gynecologist for an annual checkup and pap smear, and asked for topical and systemic yeast treatment. I assumed while he was doing the pap he would also do a culture. But he did not. So now I have the problem that I continue to struggle with all kinds of candida symptoms, but testing is coming out negative because treatment was already initiated. I was told only an antibody test is likely to come out positive after long term treatment (I have been using diflucan, ketoconazole, and nystatin orally; and topical terconazole cream, for about 2 months now). However, if there is a lab that offers antibody testing for any strain of candida aside from C. Albicans, I cannot locate it. I am almost certain I have a non-albicans strain, because before my doctor appointment all the over-the-counter topicals were failing miserably, until I used clotrimazole because I read it was effective against non-albicans candida. That one DID work to kind of “fend off” the worst symptoms until I saw my gynecologist. Then I was tested for C. Albicans antibodies and that was negative. Yet my symptoms do respond to candida treatment. This is why I am sure i have non-Albicans candida.
To break it down, based on symptoms and history I am both positive I have candida, and confident that it is not candida albicans
My central question in posting, is how do I get tested and prove this, so that I can get appropriate treatment? Does a test exist which will identify something such as C. Glabrata, in a person who has already been on a 2-month course of antifungals? I have negative vaginal cultures and nothing on vulvar biopsy except inflammation.
I am sure it is candida because MANY of my problems have cleared up aince I went on the candida diet and began to use both prescription and natural antifungals. Many problems I had no idea were candida related, such as chronic acne and debilitating neuropathy in my hands, are gone. The vaginal symptoms have calmed down a lot but are still present to a small degree and seem to be “waiting in the wings” to re-emerge when I stop topical treatment. I had a swollen throat and painful esophagus which are much improved but still can flare up if I do the wrong thing (like talk too much or eat something too irritating).
What I feel like is that I am in a battle and making progress, but unfortunately I don’t have a good doctor who will really believe I have resistant candida and treat me appropriately with the right oral meds. I don’t think diflican and ketoconazole do much for non-albicans candida, but I am not sure what to request instead (Lamisil? any other suggestions?), and I don’t feel like I am going to get any proper treatment until I am fully believed which requires a positive test – this is why testing is my primary question. The secondary question is, even if there is no good test at this point, in case I can impose my will on this idiot doctor I have, should I ask for a change of meds and if so to which meds? The doctor is one of the few in my area who believes “yeast syndrome” exists and is willing to treat for it, but he also believes in a lot of preudo – scientific voodoo and I think he is willing to hand out the RX’s not because he believes me, but because he is hoping to sell me some super-expensive quack treatment. He is pretty clueless: mainly I have to self – educate and inform him of what I need while he tries to sell me strange expensive magnets and such. I am in Southern nevada if anybody knows of a doctor here who REALLY understands candida.
lot of what has helped I do myself: Boric acid, essential oils, supplements, etc. – but I feel like the physician is the gatekeeper to some of what is necessary to truly knock this out.
Any advice is welcome.August 9, 2013 at 11:56 pm #108869
rasterParticipantTopics: 104Replies: 6821
Check out this link with the testing I recommend:
I would consider calling genova diagnostics and ask them your questions.
Unfortunately, I am unsure whether I would put much emphasis on which strain you may or may not have because they are all treated the same way, with probiotics and antifungals. You have been trying all of these prescription antifungals, but why not probiotics? Antifungals only kill candida, but guess what, you cannot kill all of the candida in the body! If you did kill all of the candida in the body, you would die because we actually need it be healthy and normal.
Another drawback is that these antifungal drugs do not address the root cause of the problem which is likely prior antibiotic use, lack of beneficial gut flora, deficiencies in minerals, a paralyzed immune system, and/or maybe heavy metal toxicity (mercury) from amalgams. What caused it to grow out of control?
Additionally, as I’ve stated to others, there is also a possibility that you have candida in your kidneys, and this specifically can affect your sexual organs (this is the belief my naturopath has). If you treated the kidneys, your vaginal woes may improve. There is no testing for this either as far as I know.
I’d consider pming dvjorge who has a variety of experience with these drugs you have mentioned and he may offer better advice than myself.
-rasterAugust 10, 2013 at 12:57 am #108876
Thanks raster 🙂
I am in fact using very high doses of quality probiotics as part of a comprehensive regimen, I just didn’t want my first post to be so involved that it was too long to be readable.
I have already contacted Genova and they said that their antibody test is for C. Albicans only. I have been told by an “expert” that my other tests (such as stool) could be expected to be false – negative due to initiation of treatment prior to testing. Have you or anybody else heard differently (that one can get a positive stool test this far into treatment)?
You mentioned treating the kidneys: how is that done?
I did notice in some of my prior searches on the board about C. Glabrata, that dvjorge’s name kept coming up. I think I will PM him if I can figure out how to do that, being brand new to this forum.August 10, 2013 at 3:14 am #108881
I think I have to write a little bit for you. First, it may not be a non-albican specie, even when is possible, but candida albicans itself. The fact that you don’t respond to Diflucan or any other systemic azole don’t say anything to me. The azoles are fungistatic, meaning they don’t kill at tolerable doses. Candida Albicans creates resistance to them quickly. For instance, some people need to rise the azole doses higher than standard doses to get results. Let say you were taking Ketoconazole 200 mg a day but you need to rise it to 400 mg a day. This has to be done monitoring the liver enzymes every 21 days. Don’t get alarmed, there are people who needs between 800 mg and 1200 mg a day, and keep it for a month without any liver disturbance. However, Ketoconazole affects the hormones and adrenal cortisol. Extremely high doses are risky. 400 mg is still considered a low dosage. This same analogy apply to any azole. You may need 300 mg of Diflucan or more. Most of the resistance to the Rx is acquired. There are two kinds of resistance, the intrinsic and the acquired. The intrinsic isn’t reversible but it must be treated with an effective drug against that species. However, the acquired is reversible using a drug combination. Ibuprofen has shown to revert the resistance created by candida species to the azoles. IMO, the combination is a lot more powerful than using Lamisil plus Diflucan or Lamisil plus Itraconazole. I will consider it seriously.
If you are thinking to treat the intestines, a thing I strongly suggest, you need a non systemic drug. Nystatin refrigerated powder make by Paddock Lab or Perrigo are the ideal. You should take around 3 000 000 of units a day starting with a lower dosage until reach this point. Let say 1 million of units 3 times a day. The diet must be restrictive as much as possible. 60 to 80 g of carbohydrates a day maximum.
If you follow the diet plus a treatment using 400 mg of Ketoconazole a day plus 400 mg of Ibuprofen plus 1 million of units of Nystatin powder 3 times a day plus an Apo-Lactoferrin capsule 250 mg 3 times a day, you probably respond to it quickly.
With this treatment you are preventing and overcoming acquired resistance, attacking the gut with a non-systemic drug, and supporting cell mediated immunity with lactoferrin that is also antifungal and has shown synergism with the azoles. It could be Transfer Factor too.
About the test, don’t lose your money and time. Genoma Lab has candida Immune Complexes in blood to detect CRC. It is an excellent test but what is affecting you is an intracellular candidiasis. Candida antibody don’t say anything regarding to this syndrome. The immune response that protect against CRC isn’t humoral but cell mediated.
Vaginal swab will be also negative since the yeast is inside the cells. The result is chronic inflammation, redness, and burning. The only possible test is a vulvar biopsy and microscopic analysis of it. It isn’t and standard test. Don’t worry, if your infection is caused by candida albicans, c. glabrata, or c. tropicalis, you should respond very well to my suggestions. The exception is c. krusei but it is rare in the vagina.
Now, you have tools. You look smart and dedicated to eradicate the infection. Research and speak with your Dr. As long as he will be able to monitor the liver, everything will be right.
Please, don’t send me PM since I am not answering them. I do it only to help.!
Jorge.August 10, 2013 at 3:26 am #108882
I forgot something. To support the liver you should take Sylimarin high doses ( more than 800 mg ), Vitamin E 800 mg a day. Lactoferrin is also a great anti-oxidant. Also, I suggest ALA if you don’t have amalgam fillings. ALA 600 mg a day. Clotrimazole plus an Ibuprofen cream that you can make yourself may work topically in the vagina.
Buy Ibuprofen liquid gel capsules, open one of it and mix a few drops with Clotrimazole cream. That will be an anti-inflammatory synergistic double antifungal cream. 🙂
Jorge.August 10, 2013 at 3:45 am #108884
Thanks! I was not aware of the value of ibuprofen taken internally or of the other supplementation you mentioned, and I will implement it all. I do have amalgam fillings, so does that make the ALA a definite no-no? I was aware of ibuprofen being a source of relief in a sitz bath, and so I have washed the sweet enteric coating off of ibuprofen tablets before, and dissolved them to use in a sitz bath along with tea tree oil. I wanted to use ibuprofen liquid gel caps which would have been easier, but every brand I could locate on the shelf contained sugar ingredients such as glycerine or sorbitol. Are you aware of a particular ibuprofen gel cap brand that is sugar free? If i can’t access one i will crush the pills: I have become quite the compounding pharmacist lately. I appreciate your help and your time.August 10, 2013 at 1:26 pm #108894
This is a fragment of one of my posts in another forum. It is well known by Science that candida species develop resistance to the azole drugs quickly. This is call acquired resistance and the cause of a high percent of treatment failure.
Acquired resistance can be reverted using antifungal combinations or a synergistic combination using different compounds. Science has studied the synergistic effect of many of this mixture against candida species.
One interesting result is the combination of one azole with Ibuprofen. It is demonstrated Ibuprofen reverses the acquired resistance rehabilitating the azole again.
I am absolutely sure many cases of failure may become success if we use this combination.
Clinical and therapeutic developments in fungal infection
Saturday, March 31, 2012, 15:18 – 15:30
Effective reversion of fluconazole resistance by ibuprofen in an animal model
S. Costa-de-Oliveira*, I. M Miranda, E. Ricardo, A. Silva-Dias, A. G Rodrigues, C. Pina-Vaz (Porto, PT)
Objectives: Ibuprofen was found to be an efficient reverter of in vitro fluconazole resistance due to overexpression of efflux pumps1,2; however its in vivo effect is still unproven.The aim of our study was to evaluate in an animal model the effect of ibuprofen associated to fluconazole in the treatment of an invasive infection by a resistant C. albicans isolate.
Methods: A C. albicans resistant (R) strain to fluconazole was obtained by subculturing with serial concentrations of fluconazole a susceptible strain (S) during 30 days. Minimal inhibitory concentrations (MIC) to fluconazole was determined in the presence of 100µg/ml of ibuprofen (IBU), an efflux pump blocker1,2.
Comparative transcriptome analysis between the S and the induced resistant strain (R) incubated with and without ibuprofen (RI) was performed using C. albicans DNA microarrays from Agilent Technologies.
The in vivo study was carried out according to the murine candidiasis model. Female BALB/c mice were infected with 5×105 cells in 0.1 ml of sterile saline via the lateral tail vein with the S strain (three groups) or the R strain (three groups). Antifungal therapy was administered intraperitoneally with FLC or IBU or FLC+IBU on both groups 3 hours after microbial challenge and repeated once a day for a total of four days. The kidney fungal burden was determined.
Results: Ibuprofen decreased azole MIC values, the R phenotype changing to S. Microarray analysis identified 836 and 1517 with differential expression in R and RI strains, respectively. The R strain showed overexpression of CDR11, ERG251, CDR4 and the transcription factor UPC2. In the RI and in the S strains those genes were down regulated.
FLC showed to be effective only in the treatment of the infection by the S strain, reducing dramatically the fungal burden. Interestingly, in mice infected with the R strain but treated with FLC + IBU, a significant decrease in the fungal burden was observed. In the absence of FLC, IBU did not display antifungal activity per se.
Conclusions: The in vivo synergic effect between fluconazole and ibuprofen demonstrated herein may represent a hopeful future approach for a better management of antifungal resistance conferred by efflux pump overexpression.
1. Pina-Vaz, C., et al. J Antimicrob Chemother 2005, 4: 678-85
Antifungal activity of ibuprofen alone and in combination with fluconazole against Candida species.
Pina-Vaz C, Sansonetty F, Rodrigues AG, Martinez-De-Oliveira J, Fonseca AF, Mårdh PA.
Department of Microbiology, Porto School of Medicine, University of Porto, Portugal. firstname.lastname@example.org
Ibuprofen, a non-steroidal anti-inflammatory drug, exhibited antimicrobial activity against Candida albicans and non-albicans strains. At 10 mg/ml, ibuprofen showed a rapid cidal activity against exponential growth phase C. albicans, accompanied by rapid and extensive leakage of intracellular K+, permeation to propidium iodide, lysis of spheroplasts and severe membrane ultrastructural alterations. These results indicate that the killing of Candida cells is due to direct damage to the cytoplasmic membrane. At 5 mg/ml, ibuprofen inhibited growth; however, it did not kill the yeasts and did not directly affect the cytoplasmic membrane. Evaluation of yeast metabolic vitality with the fluorescent probe FUN-1 showed that growth inhibition induced by the fungistatic drug concentration was due to metabolic alterations. The combination of ibuprofen with fluconazole resulted in synergic activity with eight of the 12 Candida strains studied, including four of the five fluconazole-resistant strains. The MICs of fluconazole for the fluconazole-resistant strains decreased 2-128-fold when the drug was associated with ibuprofen. When in combination with fluconazole, MICs for ibuprofen decreased by up to 64-fold for all the 12 strains studied. These results point to the practicability of using ibuprofen, alone or in combination with azoles, in the treatment of candidosis, particularly when applied topically, taking advantage of the drug’s antifungal and anti-inflammatory properties.
Ibuprofen may possess a marked therapeutic potential, particularly due to its ability to revert resistance to fluconazole. The serum
concentration of ibuprofen needed to achieve an anti-inflammatory
effect27 is lower than the concentration needed to obtain an antifungal effect.9
This concentration is thus sufficient to induce the
blockade of efflux pumps and to revert resistance to azoles. The
anti-inflammatory and analgesic properties of ibuprofen might also
represent an additional advantage. Additionally, our study opens
new perspectives for treatment of candidosis by rehabilitating an
important drug like fluconazole.
Potent synergic effect between ibuprofen and azoles on Candida resulting from blockade of efflux pumps as determined by FUN-1 staining and flow cytometry
Cidália Pina-Vaz1,2,*, Acácio Gonçalves Rodrigues1,2, Sofia Costa-de-Oliveira1, Elisabete Ricardo1 and Per-Anders Mårdh3
+ Author Affiliations
1Department of Microbiology, Porto Faculty of Medicine, Alameda Prof. Hernani Monteiro, 4200 Porto, Portugal; 2IPATIMUP—Institute of Pathology and Molecular Immunology of Porto University, Porto, Portugal; 3Department of Obstetrics and Gynecology, University Hospital, Lund, Sweden
*Corresponding author. Tel: +351-91-9358514; Fax: +351-229962096; E-mail: email@example.com
Received April 29, 2005.
Revision received May 24, 2005.
Revision received June 15, 2005.
Accepted June 23, 2005.
Objectives: Resistance to antifungals often relates to efflux pumps exporting drugs; several modulators may block them, reverting resistance. Verapamil, β-oestradiol and progesterone, known efflux pump inhibitors of human neoplastic cells, and ibuprofen were tested as potential modulators of resistance of Candida spp.
Methods: Forty-two clinical isolates of Candida (38 fluconazole-resistant), two ATCC type strains and two C. albicans strains with known mechanisms of fluconazole resistance were incubated with subinhibitory concentrations of the modulators. After exposure, MICs of fluconazole, itraconazole and voriconazole were re-determined. Simultaneously, yeasts exposed to modulators were stained with FUN-1 and analysed by flow cytometry. 3H-labelled itraconazole was also used to study efflux in the presence and absence of modulators.
Results: Fluconazole MICs decreased in most strains after exposure to modulators, including control strains with documented efflux overexpression. No significant MIC variation was noticed for: all C. krusei strains tested, for the resistant strain by target change, for susceptible strains, and for a very few other clinical isolates. Reverted resistant phenotypes showed cross-resistance to itraconazole and to voriconazole, which was also reverted by the modulators. For these strains, an increase in FUN-1 staining and increased accumulation of 3H-labelled itraconazole were noticed after incubation with modulators.
Conclusions: Resistance related to overexpression of efflux pumps was common among clinical isolates and could be reverted by the assayed modulators, particularly ibuprofen. The mechanism of resistance in all tested C. krusei and in a few other strains seems, however, to be of a different nature. Ibuprofen is a promising compound in association with azoles, deserving future clinical trials. FUN-1 proved to be a good marker of efflux in Candida.August 10, 2013 at 1:30 pm #108895
Synergistic antifungal effect of lactoferrin with azole antifungals against Candida albicans and a proposal for a new treatment method for invasive candidiasis.
Kobayashi T, Kakeya H, Miyazaki T, Izumikawa K, Yanagihara K, Ohno H, Yamamoto Y, Tashiro T, Kohno S.
Department of Molecular Microbiology and Immunology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki 852-8501, Japan.
The combination of lactoferrin with fluconazole has been reported to synergistically enhance the antifungal activity of fluconazole against Candida spp. and inhibit the hyphal formation in fluconazole-resistant strains of Candida albicans. In this study, we investigated the association between the therapeutic effects of this combination and the pharmacological characteristics of fluconazole and itraconazole and the variation in these effects with differences among the strains in terms of the susceptibility and resistance mechanisms. Lactoferrin enhanced the growth-inhibitory activity of fluconazole against two different ergosterol mutants but not againt pump mutants or an azole-susceptible strain; but increased the activity of itraconazole against all the strains tested in this study. Exogenous iron cancelled the synergistic effect, which suggests that the iron-chelating function of lactoferrin may contribute to the synergism. Besides, radiolabeled fluconazole assays revealed that lactoferrin did not affect the intracellular concentrations of fluconazole, thereby indicating that these synergistic effects were not due to the alteration of the intracellular uptake of the drug. The development of new clinical treatments and therapeutic method against resistant Candida will depend on our understanding of the resistance mechanisms and methods to overcome them by the application of suitable drug combinations with synergistic effects. The results of this study might contribute to the improvement of our understand of the mechanisms underlying the resistance of Candida strains.
Bovine lactoferrin supplementation supports immune and antioxidant status in healthy human males.
Mulder AM, Connellan PA, Oliver CJ, Morris CA, Stevenson LM.
Center for Phytochemistry and Pharmacology, Southern Cross University, Lismore, NSW 2480, Australia.
Dietary supplements of bovine lactoferrin are purported in consumer literature to enhance and support the immune system response through their antioxidant, antibacterial, and antiviral properties. Our aim was to investigate more fully the potential immune modulating properties and antioxidant activity of an oral supplementation of bovine lactoferrin in humans. Using an intraindividual repeated measure design, 8 healthy males aged 30 to 55 years, self-administered daily for 21 days, one capsule of placebo for 7 days, followed by 100 mg of lactoferrin for 7 days, followed by 200 mg of lactoferrin for 7 days. Peripheral blood lymphocyte subset counts, T-cell activation, natural killer (NK) cell cytotoxicity, serum cytokine levels (tumor necrosis factor [TNF]-alpha, interferon [IFN]-gamma, interleukin [IL]-2, IL-4, IL-6, and IL-10), and serum hydrophilic, lipophilic, and total antioxidant capacity were repeatedly measured before and after each progressive supplementation. Statistically significant increases were found between presupplementation levels and levels after 200 mg of supplementation in total T-cell activation (as measure by CD3(+)) (P < .001), helper T-cell activation (as measure by CD4(+)) (P < .001), cytotoxic T-cell activation (as measured by CD8(+)) (P < .001), and hydrophilic antioxidant capacity (P < .05). No significant changes were seen in the other parameters measured. These results support the proposal that oral supplements of bovine lactoferrin may be a useful adjunct toward modulation of immune activity, in particular T-cell activation and antioxidant status.
Synergistic fungistatic effects of lactoferrin in combination with antifungal drugs against clinical Candida isolates.
Kuipers ME, de Vries HG, Eikelboom MC, Meijer DK, Swart PJ.
Section of Pharmacokinetics and Drug Delivery, Groningen University Institute for Drug Studies, University Centre for Pharmacy, 9713 AV Groningen, The Netherlands. firstname.lastname@example.org
Because of the rising incidence of failures in the treatment of oropharyngeal candidosis in the case of severely immunosuppressed patients (mostly human immunodeficiency virus [HIV]-infected patients), there is need for the development of new, more effective agents and/or compounds that support the activity of the common antifungal agents. Since lactoferrin is one of the nonspecific host defense factors present in saliva that exhibit antifungal activity, we studied the antifungal effects of human, bovine, and iron-depleted lactoferrin in combination with fluconazole, amphotericin B, and 5-fluorocytosine in vitro against clinical isolates of Candida species. Distinct antifungal activities of lactoferrin were observed against clinical isolates of Candida. The MICs generally were determined to be in the range of 0.5 to 100 mg. ml(-1). Interestingly, in the combination experiments we observed pronounced cooperative activity against the growth of Candida by using lactoferrin and the three antifungals tested. Only in a limited concentration range was minor antagonism detected. The use of lactoferrin and fluconazole appeared to be the most successful combination. Significant reductions in the minimal effective concentrations of fluconazole were found when it was combined with a relatively low lactoferrin concentration (1 mg/ml). Such combinations still resulted in complete growth inhibition, while synergy of up to 50% against several Candida species was observed. It is concluded that the combined use of lactoferrin and antifungals against severe infections with Candida is an attractive therapeutic option. Since fluconazole-resistant Candida species have frequently been reported, especially in HIV-infected patients, the addition of lactoferrin to the existing fluconazole therapy could postpone the occurrence of species resistance against fluconazole. Clinical studies to further elucidate the potential utility of this combination therapy have been initiated.
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