# Candida, Mayo clinic study, V. important !!!!



## Guest (Feb 26, 2000)

This to me is the most important piece of research to come out on this whole confusing Candida issue ever!! (And I never, ever exaggerate !!). Although this research applies to chronic sinusitus sufferers, i think the mechanism of illness described can be likly in the mucosal lining of the gut as well. However, i do not assert that all or even most IBS cases are due to the described mechanism, just some of us.Read below or go directly to the Mayo Clinic news release with link to the article at: www.mayo.edu/comm/mcr/news/news_773.html The Mayo Clinic "Proceedings" September, 1999 report "The Diagnosis and Incidence of allergic fungal sinusitis" (V.74, #9, article 877) describes research on 210 people suffering from chronic sinusitus of 3 months or longer.The researchers were surprised to discover that 96% of these cases cultured positive for fungi and yeasts in mucus samples, where non-sufferers rarely do. The reseachers looked at the mucus samples in the microscope, and found immune system agents called Eosinophils (a kind of white bllod cell) had been concentrated in the samples. The Mayo Clinic researchers conclude that in cases of fungal colonization, the immune response sends eosinophils to move to the site of infection, but in certain sensitive people, the Eosinophils irritate the sinus mucus cells, and cause the disease symtoms. Note that this condition isn't rare, as an estimated 37 million people complain of chronic sinus problems. They emphasize that this is not an allergic reaction problem per se, but an immune system dysfunction. And finally, 50% of the culture samples contained Candida!I am not a health specialist, but it seems to me that if mucosal cells in some individuals can be irritated by fungal or yeast colon-ization (couldn't resist that)including candida to produce symptoms (including the muscle spasms called sneezing) that this can happen in other mucosal cells of the body including the intestinal cells!hopefully, we can all quit arguing and start healing![This message has been edited by Chuck-w (edited 02-25-2000).][This message has been edited by Chuck-w (edited 02-26-2000).]


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## Guest (Feb 26, 2000)

Thanks for this information.


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## flux (Dec 13, 1998)

> quote: i think the mechanism of illness described can be likly in the mucosal lining of the gut as well. However, i do not assert that all or even most IBS cases are due to the described mechanism, just some of us.


So far the official count is zero.


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## jude_f (Feb 18, 2000)

I had an experience reasonably consistent with these findings. In 1998, when my IBS-C symptoms flared up after a period of remission.. I found myself falling into a deep abyss of health problems including the usual food sensitivity and IBS problems, but also constant allergies and colds that just wouldnt go away (chronic sinusitis and throw in some occasional nocturnal asthma, migraine with that as well). aka sick from head-to-toe.When I chanced upon DocDarren's Candida site.. My GI doc at UCLA would have none of this candida stuff.. I went to a naturopath doc (also an M.D.).. he put me on a strict anti-candida diet, herbal antifungals.. in a few weeks, my chronic sinusitis and related symptoms disappeared magically and havent reappeared in the last year and a half. I would say that my GI+sleep+spasms+related symptoms decreased 25% in that time frame. Furthermore, when I went back to a less stricter diet, my GI+related problems seemed to creep back up.My Conclusion:I likely had chronic sinusitis caused by fungal overgrowth in the respiratory and nasal passages as indicated in the article. Though the article did not say what the best cure for this kind of fungal infection was.However, my results did not support the Candida-GI hypothesis. Though I have to admit I did not try any strong antifungals like lamisil.


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## eric (Jul 8, 1999)

FYI:Anti-HIV Drug, Antifungal BeingDeveloped From Traditional MedicinesWASHINGTON, Feb 25 (Reuters Health) - Traditionalmedicines derived from natural sources such as plants arebeing used as the starting point for the development of newdrugs, according to a series of presentations here last weekendat the annual meeting of the American Association for theAdvancement of Science. "Nature is the ultimate molecular architect, because nature hasbeen working for eons to produce drugs of just wonderfulstructure and wonderful complexity," said Dr. Gordon M.Cragg of the National Cancer Institute in Bethesda, Maryland."Drug discovery development is going to be a combination ofthe natural resources with these new technologies such ascombinatorial chemistry to expedite the discovery of noveldrugs." Two of the presenters, Dr. Mahabir P. Gupta of the Universityof Panama, and Dr. Kurt Hostettmann of the University ofLausanne, Switzerland, described promising drugs derivedfrom traditional medicines in Latin America and Africa. Dr. Gupta told the audience of a program he coordinatesconsisting of university laboratories and pharmaceuticalcompanies from 19 Latin American countries, plus Spain andPortugal, that are screening extracts for activity andcharacterizing the bioactive molecules. Latin America contains60% of all known plants, he pointed out, and has a rich historyof use of traditional medicines. An extract from a tree in Argentina is showing "remarkableanti-HIV activity," he said, and his group is currently isolatingthe active molecules. Agreements with industry are necessary,he said, because pharmaceutical companies have the ability toscreen thousands of extracts using high-throughput methods, andcan provide equipment and training for scientists within thecountry. Using a similar approach, Dr. Hostettmann said, his grouprecently found a compound from the root bark of an Africantree with strong antifungal activity against 200 different fungi,particularly Candida albicans. "We expect to develop this as adrug in oral form in treating mycosis associated with AIDS," hesaid. The research group has obtained a US patent on the compoundand is developing the drug with a pharmaceutical company inthe US, with the hope that the compound will be on the marketin a few years. The presenters noted that many issues exist over disappearingbiodiversity and the need for developing countries to benefitfrom drugs developed through the knowledge of theirtraditional healers. Resentment over real or perceived lack ofbenefits may cause countries to close their borders to drugdevelopment, Dr. Hostettmann noted. He also warned that drug developers have to collect theinformation from healers quickly, because "traditionalknowledge of healers is disappearing."


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## Guest (Feb 26, 2000)

Chuck: My gut is sneezing!


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## HipJan (Apr 9, 1999)

Thank you, thank you, thank you, chuck and eric! No further comment, except great. And, I will also say that that article you posted, eric, was both encouraging and humorous..."He also warned that drug developers have to collect the information from healers quickly, because "traditional knowledge of healers is disappearing." We have some "healers" here in the U.S. But perhaps the pharm. co's don't want anyone to know they exist? Yup, I've been taking stuff like root bark, etc., myself, for a while now.







------------------Cultivate gratitude. Believe in possibilities.[This message has been edited by HipJan (edited 02-26-2000).]


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## moldie (Sep 25, 1999)

Thanks for posting these fascinating articles Chuck and eric. Put, 'My gut is sneezing!' That's a good one!!!


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## Guest (Feb 26, 2000)

TO that fine fellow Flux....."so far.......".


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## Guest (Feb 27, 2000)

Thank you for that info!I've suffered sinusitis for years & all the doctors claim allergies but none of the allergy shots or meds have helped. So allergy are probably not my problem at all. It's great to hear this. I will inform the docs about this research!Birdie


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## vikee (Feb 5, 2000)

Birdie,Thanks for your post. Injections have not helped my sinusitis either. They did control other symptoms. I will show the article to my doc.vikee


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## jude_f (Feb 18, 2000)

I tried allergy shots too.. they didnt help much.. last year i stopped my allergy shots.. and faxed the anti-candida treatment that worked to my allergist. but, i am sure he is still pretty clueless.


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## SteveE (Jan 7, 1999)

I find that article interesting as well, but you should be very cautious against making leaps of logic regarding your own treatment. Note that the real problem in that study was with the immune system (not the candida). We all have some level of yeast/fungi colonization. It is simply part of the natural balance in our guts. So I strongly urge IBSers not to jump on candida diet bandwagons over this.Even if there were some kind of immune system regulation diet that we could follow it wouldn't make sense to do so because it is a huge leap in logic to assume that we have an immune problem.Follow a normal healthy diet with lots of fiber, water, exercise and relaxation so that you feel as well as possible in these all-too-short lives of ours until science has taken it's proper course.Flux is right guys and gals...the count so far IS zero.


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## Guest (Feb 28, 2000)

Wow, Yes I too have sinus problems. Does and one ever have and extremely runny nose before or after BMs? Now that I think about it when my doctor and I settled in to figure out what was wrong with me that is a question me asked (Do you have an sinus problems?) Yes, I'm blowing my nose constintly. Thanks for the info it's so interesting and thank you chuck for the work.


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## eric (Jul 8, 1999)

FYI:CandidiasisEpidemiology and MicrobiologyCandida infection in AIDS is almost exclusively mucosal; systemic invasion is a rare and lateevent. Oropharyngeal candidiasis occurs in approximately three-quarters of all HIV-infectedpatients. In a third of these individuals the infection tends to be recurrent and progressively moresevere as immunodeficiency advances. Esophageal involvement is reported in 20% to 40% ofall AIDS patients; again, predominantly in patients with advanced disease and severe depletionof CD4+ cells. It is important to recognize, as with other opportunistic infections since theadvent of HAART, the incidence of new Candida infections has decreased by as much as 60%to 80%[1]. Key Point: Candida infections are the most common fungal infections in AIDS; they are almost always confined to mucosal surfaces.Vulvo-vaginal candidiasis occurs in approximately 30% to 40% of HIV-infected women.Although HIV infection is often cited as a risk factor for vulvo-vaginal infection, it is unclearwhether vaginal candidiasis is in fact more common in women with HIV infection when otherimportant risk factors for vaginal infection, such as sexual activity, and racial and ethnicbackground, are considered. However, it is apparent that concomitant HIV infection influencesthe severity and persistence of vulvo-vaginal Candida infection.Candida albicans is the primary causative agent of mucosal candidiasis in HIV-positivepatients. It is associated with virtually all initial episodes and approximately 75 to 90% ofrecurrent infections. Recently, a related strain, C dubliniensis, has been implicated in manycases of HIV-associated infection[2]. This becomes relevant since it appears that this strain ismore likely to acquire resistance to azole antifungals, especially fluconazole[3]. Recurrentdisease is caused by the same strain of Candida in approximately half of cases; the remaining50% of cases are caused by new strains of C albicans or new species[4]. Other species, notablyTorulopsis glabrata and Candida parapsilosis, tend to cause infection in patients with veryadvanced disease with extensive prior exposure to antifungal agents (especially the azoles).Most patients are colonized readily with Candida which appears as part of the mouth flora ingreater than 80% of HIV-positive patients[5]. The actual defects in local immunity that predisposefor progression from colonization to disease are not well characterized. It is logical to assumethat some deficiency in T cell immunity is important, as disease is clearly more common andmore severe as the CD4+ cell count falls. Additional defects in local oral clearance mechanisms(eg, epithelial barriers, salivary flow, lysozyme and lactoferrin release) have been described inHIV-positive patients and may be relevant to candidiasis[6]. In addition, nonspecific factors suchas dental hygiene, smoking and the use of antibacterials for prophylaxis are all recognized riskfactors for oral candidiasis and may increase the risk for specific patients.Clinical FeaturesMost patients are symptomatic and may complain of some oral discomfort. Clinicalmanifestations include pseudomembranous, erythematous (or atrophic), hypertrophic and angularcheilitis. The characteristic appearance of pseudomembranous candidiasis (also known as thrush) is a creamy white exudative plaque (cottage-cheese-like) on the palate, tonsils, or buccal mucosa that can be removed with a tongue depressor, with bleeding. Figure 1. Pseudomembraneous candidiasis Erythematous candidiasis appears as flat, red atrophic plaques also on the mucosal surfaces. Figure 2. Atrophic (erythematous) candidiasis The hypertrophic form often involves the lower surface of the tongue or the palate and buccal mucosa and is characterized by a non-scrapable raised plaque (very similar to oral hairy leukoplakia). Figure 3. Hypertrophic candidiasis Angular cheilitis is associated with red, fissured, crusting lesions (which may ulcerate) at the corner of the mouth. These lesions often cause pain, burning or difficulty opening the mouth.Fungal cultures are rarely required for diagnosis; indeed, cultures can cause confusion, sincemany patients are colonized with Candida. However, a scraping of a lesion will showcharacteristic spherical budding yeasts and pseudohyphae when examined using potassiumhydroxide (KOH) wet mount or gram stain. Figure 4. Candida albicans (microscopy) Most patients with vaginal candidiasis present with vaginal itching, burning or pain and vaginaldischarge. Examination of the vaginal cavity reveals thrush, identical to that seen in theoropharynx.Patients with esophageal candidiasis develop pseudomembranes, erosions and ulcers on theesophagus. These individuals typically experience dysphagia. The combination of oralcandidiasis and esophageal symptoms is both specific and sensitive in predicting esophagealinvolvement. Patients who present in this manner can be treated empirically with antifungaltherapy. Endoscopy is usually reserved to evaluate for the presence of other diagnoses such asherpetic or cytomegalovirus esophagitis, idiopathic ulceration, or resistant candidiasis in thosepatients who fail to respond[7]. Key Point: Patients with symptoms attributable to Candida esophagitis can usually be treated with empiric antifungal therapy.TreatmentA number of options, both local and systemic, are available for the treatment of oral candidiasis.(Table 1). Initially, most patients respond well clinically to most forms of antifungal therapy,although mycologic responses are less common. However, nystatin appears to be less effectivethan other treatments[8]. Many noncomparative studies have clearly established the effectivenessof treatment of oropharyngeal candidiasis in patients with AIDS. Clinical responses with theresolution of symptoms and signs occur in 90% to 100% of patients generally within 7 days ofinitiating treatment. Mycologic responses are not usually as high and Candida can still becultured from the oral cavity in many patients.Table 1: Therapeutic Options for Oral or Esophageal Candidiasis Agent Formulation Dosage1 Nystatin Oral suspension Pastille 400-600,000 units (4-6 mL) 4 times daily 1-2 pastilles 4 times daily Clotrimazole Troche 10 mg (1 troche) 5 times daily Ketoconazole Tablet 200 mg daily 400-600 mg daily2 Fluconazole Tablet Oral suspension 50-100 mg daily 200-400 mg daily2 Itraconazole Capsule Oral suspension 200 mg daily 100 mg (10 mL) twice daily Amphotericin B IV infusion Oral suspension Pastilles (available in Europe, but not in the US) 0.3-0.5 mg/kg per day 100 mg (1mL) 3-4 times daily 1 Dosage is the usual dose for the typical patient. The average duration of therapy is 7-14 days. Individual patients may require higher doses or more prolonged treatment. 2 Esophageal diseaseSeveral studies have also been conducted comparing topical and systemic therapy. The clinicalresponse rates are generally similar with all therapeutic regimens, although signs and symptomsof disease tend to respond more rapidly with systemic therapy. Patients treated with topicalagents are less likely to have mycologic clearance at the end of the treatment[9]. Similarly, moststudies comparing systemic treatments demonstrate results to be similar in clinical effectiveness.Response rates of 75% to 100% are generally reported. The relapse rates with systemictherapies also appear to be equivalent. From a practical standpoint, in patients with advanceddisease, fluconazole and itraconazole may be preferable to ketoconazole. The absorption ofketoconazole is dependent on gastric acidity, and achlorhydria can be a problem in patients withadvanced AIDS. Ketoconazole can be given with Coca-Colaï¿½, which is effective in providingacidic conditions in the stomach and enhancing the absorption of ketoconazole. Itraconazoleshould be taken with food. The oral suspension of itraconazole is associated with morefavorable clinical responses. Key Point: Both topical and systemic antifungal therapy are usually successful in mucosal candidiasis, although symptoms tend to respond more rapidly to systemic agents.Initial episodes of vulvo-vaginal candidiasis are managed readily with topical therapy and alarge number of agents are available[10]. In general, short courses of topical clotrimazole,miconazole or butoconazole (either creams or suppositories) are very effective and systemictherapy is rarely needed for uncomplicated cases. Fluconazole, given as a single dose of 150 mg,is a popular alternative.Treatment of esophageal candidiasis requires systemic antifungal therapy. A multicenter,double-blind, randomized study comparing fluconazole 100 mg daily and ketoconazole 200 mgdaily, demonstrated a clear-cut superiority of fluconazole in treatment of this disease[11].Eighty-one percent of patients randomized to fluconazole experienced resolution of symptoms,compared with 66% of patients assigned to ketoconazole therapy. Endoscopic responses werealso significantly more frequent in the fluconazole-treated patients. More recent trials comparingfluconazole and itraconazole have found these agents to be equivalent in activity for the treatmentof Candida esophagitis[12]. Oral azole treatment may be ineffective in advanced disease. In thiscircumstance, systemic amphotericin B, 20-30 mg/day for 7-14 days may be necessary.Relapses of any form of mucosal candidiasis are common and at least one-third of patientsdevelop recurrent mucosal candidiasis. One approach to clinical management is to treat eachepisode as it occurs. However, in many patients, recurrent symptomatic disease may besufficiently severe to warrant consideration of chronic suppression. Fluconazole, 100-200mg/day, has proven very successful for the suppression recurrent oropharyngeal disease andprevention of esophagitis[13]. A dose of 100 mg/weekly can prevent vaginal candidiasis[14]. Themajor risk of this treatment approach is the possibility of developing azole-resistant disease[15]. Key Point: Fluconazole-resistant candidiasis is a feature of very advanced HIV infection, occurring in patients with extensive prior exposure to fluconazole.Prior to the use of HAART, approximately 5% to 7% of patients with advanced HIV diseasedeveloped candidiasis that was refractory to standard fluconazole therapy. The prevalenceappears to be much less common since the introduction of HAART, although no formal data areavailable. The major risk factors for the development of resistance include advanced HIVdisease (CD4+ counts less than 50 cells/mm3 and often less than 10 cells/mm3) and extensiveprior exposure to fluconazole[16,17]. Isolates are more likely to be species other than C. albicansand tend also to be resistant in vitro, with MICs >/= 64 mcg/mL to fluconazole, in manycircumstances. Isolates with a more intermediate susceptibility have also been described[18]. Theclinical expression of disease is identical to that observed in patients with sensitive infection,but the disease tends to be more progressive and symptomatic due to the lack of effectivetherapy. Thus, esophagitis is common.Therapy for resistant Candida infection is unsatisfactory (Table 2). Improving immune function(eg, with more potent antiretroviral therapy, if available) is often most beneficial[19]. Higherdoses of fluconazole (up to 800 mg) may be effective in patients with infection caused byorganisms with intermediate susceptibility; a reasonable initial strategy may be to increase thedosage of fluconazole in patients with apparent clinical failure to standard dosages[20]. Thisincreased dosage is usually not effective for truly resistant strains, unless there is a question ofdrug interactions or patient adherence leading to reduced serum levels. The cyclodextrin oralsuspension formulation of itraconazole has been reported to be effective in approximately 60%of cases; however, the benefit is short-lived if some form of chronic maintenance therapy is notprescribed[21]. Amphotericin oral suspension is also effective in approximately 40% of patients;however, many patients require parenteral amphotericin B for symptomatic control[22].Table 2: Therapeutic options for candidiasis unresponsive to fluconazole Agent Comment Higher doses of fluconazole (800 mg) May be effective for patients with Candida infections caused by organisms whose susceptibility in vitro is "intermediate" rather than resistant Itraconazole oral suspension Effective in approximately 50% of cases; need maintenance therapy; breakthroughs occur Amphotericin B oral suspension Optimal dosage unclear; need more than current labeling information Amphotericin B parenterally 0.3 mg/kg for about 7-10 days is usually effective; but relapses off therapy are common Flucytosine No formal studies but may have a role as maintenance alone or combined with fluconazole or intermittent amphotericin Maximal antiretroviral therapy Anecdotal experience suggests many patients improve dramatically with the introduction of more effective antiretrovirals Case History (continued) Symptoms and signs resolved after treatment with clotrimazole troches, and  the patient remained well for nine months. She then experienced another episode of oropharyngeal candidiasis that again responded well to topical antifungal therapy. Her CD4+ count at that time had declined to 94 cells/mm3. Three months later, the patient presents to the emergency room complaining of an eight day history of fever including a five day history of frontal headache gradually increasing in intensity. Examination reveals several small papulo-pustular lesions on her trunk and arms that the patient had not previously noticed. Her temperature is 39ï¿½C. There is no neck stiffness. Neurological examination is nonfocal, although she appears to be somewhat lethargic. A lumbar puncture reveals 18 white cells (all lymphocytes), protein 51, glucose 18. CSF cryptococcal antigen is 1:2048. The opening pressure is 55 cms/H20. Culture was subsequently positive for C neoformans. Her CD4+ count is 37 cells/mm3.FYIostgrad Med J 1992 Jun;68(800):453-4 The role of faecal Candida albicans in the pathogenesis of food-intolerant irritable bowel syndrome. Middleton SJ, Coley A, Hunter JO Department of Gastroenterology, Addenbrooke's Hospital, Cambridge, UK. Candida albicans was sought in stool samples from 38 patients with irritable bowel syndrome and 20 healthy controls. In only three patients with irritable bowel syndrome was C. albicans discovered and these patients had either recently received antibiotics or the stool sample had been delayed more than 24 hours in transit. C. albicans was isolated from none of the control stool samples. We conclude that C. albicans is not involved in the aetiology of the irritable bowel syndrome.


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