Candida Community Group
To discuss, share research and information on candidiasis and its effects and treatment.
... If we can get our doctors to swallow the treatment...
Hi,
I'm self-diagnosed with Candidiasis, as a possible exacerbation factor in numerous confimed diagnoses that I suffer. I am absolutely appauled at the ignorant and arrogant attitudes of physicians concerning what this genera of fungi may be capable of, and tired of being treated like some ignorant hypochondriac after all of the research I've done into the pathogenic potential of Candida and other microbes.
Caregivers may wish to remember that there is enough misinformation out there for victims of pathogenic yeasts to end up confused, and that the misinformation being actively spread by doctors and even specialists isn't exactly helping - in fact, doctors doing so may put patients at risk of being victimized by "snake-oil salesmen" when patient complaints are rejected by doctors and patients feel they have nowhere to turn except some predator who is trying to charge them a hundred dollars for a "Colon Cleanser" made of the same psyllium seed husks you can get at any health food store for two dollars.
In my opinion, the world may have A LOT to learn about pathogenic yeasts, although occasionally while Googling the subject, I find forum threads that are absolute treasure-troves of good information on respectable sources compiled by patients who are emminently knowledgeable. To that end, I'd like to start a thread as a place to collect useful links and other information about Candida.
Two and a half years ago, I informed my doctor that in my opinion, Candida appears to be part of a disease over which doctors threatened to cut off my hands and feet, and furthermore that immunoreactivity to Candida may be playing a role in the exacerbation of my pulmonary disease symptoms. My doctor referred me to an infectious diseases specialist who completely ignored my complaints and wasted my visit on a 20-minute song and dance blaming me for all of my medical problems and dismissing the microbes that have turned up in my diagonses for as much as 20 or 30 years - this after acknowledging that I have chronic infections.
I have a piece of more recent research that supports the microbial etiology I attempted to provide my doctor with for this terrible circulatory disease (along with Candida, it includes anaerobic bacteria with very strong associations with thrombotic disease) and clarifies some of what Candida may be doing in the picture - namely, the anaerobic environment of a Candida biofilm may be playing host to and providing a safe refuge for anerobic bacteria in the patient. The research report in question goes on to state that thus far, this phenomenon of combination fungal/anaerobic bacterial biofilm seems to be partial to two anerobes in particular - the same two I named for my doctor two and a half years ago.
On my visit to my regular doctor last year, I was prescribed corticosteroid medications, and after expressing concerns about their well-known ability to promote Candida growth (which is acknowledged even by doctors), I was assured that Candida is "harmless" unless I have HIV. In my opinion, both the term "harmless commensal" and this "only if you have HIV" nonsense are two of the most ignorant things a physician could possibly say. My physician informed me they had just seen a four-hour presentation on Candida from Princeton - I managed to blurt out "Four hours? I'm pretty sure I've studied the organism for four months" (it's more like four years) before they evasively darted out the door. By the time I mentioned that Candida is a recogned allergen, they were gone.
Imagine my doctor mastering one of the hardest subjects I've ever encountered in biology in a matter of hours! Other people in medicine have studied yeasts for decades and we still have way too much to learn about them. Isn't it amazing how my doctor seems to think they know more about it than everyone else put together, how they seem to think they know so much they can just spit in the face of dozens or hundreds of clinical studies. It's not just my regular doctor - while I haven't been to that many doctors, every doctor that I have seen in ten years pulls this very same cynical know-it-all garbage on me.
Meanwhile, I have family that have spend decades researching pathogenic Candida - I'm tempted to offer my doctor their e-mail so my four-hour-expert doctor can write to this family member and tell them how they learned more in four hours than an expert has learned in 20 years. Maybe this family member could help me, but imagine how the conversation is going to go:
"Hey, I think I have one of those crazy Candida you devoted your life to studying, can you help me with it?"
"Sure. What is 'it" exactly? You probably don't know the strain, but do you know the species? What color it was? About how many were on the slide? Was there one species on the slide, or more than one? How did it behave in the culture dish, did it grow fast or slow? What medium did they use?"
"I don't know, I don't have any data"
"Why not?"
"Well, because one doctor after another turns into an arrogant instant expert on the subject and stubbornly refuses to take this seriously enough to gather the tiniest piece of data, in spite of the Infectious Diseases Society of America's recommendations".
Just for the record, to the best of my knowledge, no one is accusing a commensal yeast of being a pathogen, but it's just one of numerous rookie mistakes I've caught my doctors making. To the best of my knowledge, what the research into Candida in HIV cases is REALLY trying to tell us is that an interaction between the virus and the fungus transforms Candida into something extremely virulent (the 'gray phenotype' of Candida), while the research on Candida biofilms that I mentioned describes how the combination of Candida and anaerobic bacteria can transform a harmless commensal yeast into something less virulent, but still pathogenic.
Here's another rookie doctor mistake - I say, "Doctor, I think I might have Candida issues" and they start lecturing me on how that Candida albicans is harmless. Who said Candida albicans? I didn't, I already know there are at least half a dozen recognized pathogenic species of Candida that we could be dealing with. This might be part of why the Infectious Diseases Society of America recommends speciation of problem Candida, and another part is that speciation matters to treatment. We have pathogenic species of Candida like Candida glabrata that as a species are supposed to be resistant to difluconazole and other azole antifungal agents, and a number of experts advise not even wasting time throwing diflucan at it.
(Also bear in mind that the max regimen I've seen suggested by clinical reports specified a year and a half worth of diflucan treatment for a Candida biofilm. Imagine going through that and THEN finding out you have a species that it was never going to work on anyway.)
Given the general level of ignorance displayed by the physician, I'm going to assume they said Candida albicans even when I didn't, because it's the only species of Candida they can actually name, in spite of their four hours worth of "expertise".
You've probably heard similar stories and complaints about ignorant, cynical physicians from other people who suspect they have Candida issues, so I'll try and move along to the information part here after a few more comments.
If you find yourself researching Candida, be careful - there is still a lot of misinformation out there coming from all directions, including well-meaning but misinformed patients. Try to keep a healthy level of skepticism (in contrast to doctors' unhealthy levels of skepticism) - don't be too quick to believe anything you read (including anything I write), but think it over and try to see if it fits together with other information to start form a coherent picture that might really help explain what Candida victims are going through.
Remember that fungi can be more complex in their biology than bacteria, which is going to make medical mycology difficult for anyone to master, and that even after hundreds or even thousands of research reports into the less virulent forms of pathogenic candida, there is still a huge gray area when it comes to associating Candida with symptoms or diagnoses. It doesn't seem to be until we caught Candida actually killing people that we were shaken out of the cozy delusion that it's "just a harmless girlie thing" and we may still have yet to do a proper job of studying less virulent pathogenic Candida.
Also keep in mind the diversity of Candida, as well as its abilities to transform from one form to another - just as the same antifungal may not work on all species or specimens, the same may be true of many "home remedies" for Candidiasis. Be careful to keep learning and not to become an "instant expert" like my doctors like to do.
I'm sure these sources aren't perfect, but this link is in my opinion a good overview what we are dealing with when it comes to Candida biofilms
http://www.holistichelp.net/candida-biofilms.html
And even if this is the only thread worth reading at this particular forum, I was impressed by the quality of some of the information here (nine pages worth)
http://lymebusters.proboards.com/thread/13762
So there is a place to start...
The Candida albicans Biofilm Matrix: Composition, Structure and Function.
https://www.ncbi.nlm.nih.gov/pubmed/28516088
4.4. Role of the C. albicans Biofilm Matrix in Mixed Fungal/Bacterial Biofilms
Polymicrobial biofilms are generating increased attention, and data is emerging on some unique properties that the C. albicans biofilm matrix plays when the fungus is co-cultured with different bacterial species. For example, it is presumably responsible for the generation of hypoxic microenvironments within the biofilm, allowing for the growth of anaerobic bacteria such as Clostridium perfringens and Bacteroides fragilis [33]. Most recently, the Jabra-Rizk group demonstrated that in mixed C. albicans/Staphylococcus aureus biofilms, the C. albicans biofilm matrix—particularly the secreted exopolymeric β-1,3 glucan—is responsible for conferring bacterial cells with a high degree of tolerance against antibacterial antibiotics [34]. The effect was mostly due to the C. albicans biofilm matrix preventing penetration of the antibiotic drugs [34]. In mixed biofilms, the same C. albicans matrix carbohydrate also increases ofloxacin tolerance in Escherichia coli [35].
This article is particularly helpful, and in one of the quoted passages it describes how the metabolic state of Candida biofilm can promote resistance to antimicrobial agents, whereas other articles have attempted to blame the biofilm itself for posing an obstacle to microbicidal agents.
We have a very similar situation with bacterial biofilms, where some researchers seem to be laboring under the misconception that biofilm itself presents an obstacle to antibiotics, even after other researchers have shown effective doses of antibiotics getting past the biofilm in a matter of minutes. Perhaps the best picture emerging is very similar to what is stated here for Candida, with the microbe developing temporary resistance to antimicrobials by entering a dormant-like state in which it is not very actively engaged in the activities of actively growing and dividing cells, which are often the targets of conventional antimicrobial agents. For example, biofilm bacteria because they are not actively dividing may thereby be automatically resistant to penicillins, which target actively dividing bacteria.
Candida Biofilm - Candida albicans Biofilms and Human Disease
Clarissa J. Nobile, Alexander D. Johnson
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4930275
...Although we know little about the formation and roles of persister cells in C. albicans biofilms, we do know that the drug resistance of persister cells is independent of cell membrane composition and efflux pump expression; rather, it is the result of the metabolically dormant state of the cells (88, 100)...
...Although C. albicans is the fungal pathogen most frequently isolated from human infections, other Candida species have been found together with C. albicans in polymicrobial biofilms from patients (27). These species include C. dubliniensis, C. tropicalis, C. parapsilosis, C. guillermondii, C. krusei, and C. glabrata (80, 90, 118, 151). We know virtually nothing about the interactions among these Candida species in polymicrobial biofilms...
...Another study examined dual-species biofilms C. albicans forms with one of five prevalent members of the human gut microbiota: Bacteroides fragilis, Clostridium perfringens, Escherichia coli, Klebsiella pneumoniae, or Enterococcus faecalis (60). In this study, biofilms formed by C. albicans provided a hypoxic microenvironment that could support the growth of the two strictly anaerobic bacteria, B. fragilis and C. perfringens—even though the biofilms were grown under oxygen-rich conditions. Thus, a C. albicans biofilm can act as a safe haven for anaerobic pathogens in oxygen-rich environments. Moreover, when cultured together with C. albicans in ambient oxygen, these anaerobes could induce the latter to form mini-biofilms, which, in turn, could protect the bacteria and allow them to proliferate under otherwise toxic conditions. Interactions occurring between different species in polymicrobial biofilms and their relevance to human health are clearly of great interest and importance...
Anaerobic bacteria grow within Candida albicans biofilms and induce biofilm formation in suspension cultures.
https://www.ncbi.nlm.nih.gov/pubmed/25308076
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4252622
Abstract The human microbiome contains diverse microorganisms, which share and compete for the same environmental niches. A major microbial growth form in the human body is the biofilm state, where tightly packed bacterial, archaeal, and fungal cells must cooperate and/or compete for resources in order to survive. We examined mixed biofilms composed of the major fungal species of the gut microbiome, Candida albicans, and each of five prevalent bacterial gastrointestinal inhabitants: Bacteroides fragilis, Clostridium perfringens, Escherichia coli, Klebsiella pneumoniae, and Enterococcus faecalis. We observed that biofilms formed by C. albicans provide a hypoxic microenvironment that supports the growth of two anaerobic bacteria, even when cultured in ambient oxic conditions that are normally toxic to the bacteria. We also found that coculture with bacteria in biofilms induces massive gene expression changes in C. albicans, including upregulation of WOR1, which encodes a transcription regulator that controls a phenotypic switch in C. albicans, from the "white" cell type to the "opaque" cell type. Finally, we observed that in suspension cultures, C. perfringens induces aggregation of C. albicans into "mini-biofilms," which allow C. perfringens cells to survive in a normally toxic environment. This work indicates that bacteria and C. albicans interactions modulate the local chemistry of their environment in multiple ways to create niches favorable to their growth and survival.
Comment in
Biofilms: five-star accommodations for the aerobically challenged. [Curr Biol. 2014]
PMID: 25308076 PMCID: PMC4252622 DOI: 10.1016/j.cub.2014.08.057 [PubMed - indexed for MEDLINE] Free PMC Article
Mazaheri-Tehrani (2012). In vitro interactions between viruses and Candida biofilm
Conference Paper: The Italian Society of Virology, At Orvieto, Italy
Available online from ResearchGate
https://www.researchgate.net/publication/260513748_In_vitro_interactions_between_viruses_and_Candida_biofilm
Mazaheri-Tehrani (2014). Human pathogenic viruses are retained in and released by Candida albicans biofilm in vitro
Virus Res. 2014 Jan 22;179:153-60.
PMID: 24184317
Ascione et al (2017). Herpes simplex virus-1 entrapped in Candida albicans biofilm displays decreased sensitivity to antivirals and UVA1 laser treatment
Ann Clin Microbiol Antimicrob. 2017; 16: 72.
PMID: 29137671 PMCID: PMC5686830
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