The diagnosis and effective treatment of candida overgrowth
The candida genus is a dimorphic fungus that can exist as a yeast or in mycelial form. There are many species of candida but the main species affecting humans is candida albicans. Other species rarely affect humans but include, tropicalis, parapilosis, and krusei.
This fungus is normally a saprophyte but can become a pathogen causing the following problems: Superficial Candidiasis, Mucocutaneous Candidiasis, Systemic Candidiasis, Candida Overgrowth.
This is a superficial infection that usually involves areas of the skin and mucous membranes such as the axilla, toes, and fingers (including the nail bed), the groin, mouth, and vagina. The diagnosis is made by clinical examination and a swab with direct microscopy identifying the yeast form. There is also an elevation of IgM and IgA to candida when performed by a sensitive test such as an ELISA procedure.
This is a serious condition and is mainly associated with a genetic defect of T cell function. The diagnosis is made by lymphocyte stimulation using PHA, Con A, Candida Albicans, Tetanus Toxoid, and Diphtheria. A specific defect against the stimulation by Candida Albicans is demonstrated (failure of the lymphocytes to respond to the simulation of Candida Albicans).
Systemic invasion by the candida yeast is a very serious condition and occurs in patients with profound immunodeficiency. This immunodeficiency is usually secondary to AIDS, chemotherapy for malignant disease and terminal leukemia. These patients can have lesions in the lungs, liver, kidney, and brain. The diagnosis is usually made by history, the demonstration of lesions and the appearance of circulating candida antigen.
Candida intestinal overgrowth was first described by Brabander and associates (1) in 1957 and has remained a controversial subject. They described symptoms of bloating, itching and skin rashes in their patients, symptoms that were further added to by Truss (2,3) and Crook. (4) The syndrome has been misnamed systemic candidiasis, and candida overload syndrome. It has been implicated in a variety of ailments from chronic fatigue to immune deficiency. The diagnosis of this syndrome has always been difficult to confirm. Questionnaires have been devised, and stool testing has met with limited success. (6) Serum antibody tests either measuring total antibody production or very sensitive procedures to detect the isotypes IgG, IgM and IgA, have also met with limited success when compared to clinical symptoms, (4,5) thus fueling the controversy about the very existence of the syndrome. What is needed is an objective and sensitive marker for candida overgrowth.
Candida Immune Complexes
An objective and highly specific and sensitive marker of candida overgrowth
In 1987, Dr. Alan Broughton developed a unique assay to measure candida specific IgG immune complexes. Candida immune complexes consist of antigen (candida albicans) bound to IgG antibodies specific to candida albicans and fragments of complement and are an indication that there is active removal of candida antigen. Candida Immune Complexes are also present in direct proportion to the candida antigen load and levels decrease quickly when the candida load is reduced. Candida Immune Complexes have been reported to be an objective, highly specific, and sensitive marker for candida overgrowth. (6,18)
In his studies, Dr. Stuart Lanson has reported that candida immune complexes performed by AAL Reference Laboratories, Inc. are an effective and objective marker for Candida Overgrowth. (6) His study found that 80% of patients with elevated candida immune complex levels respond to antifungal treatment with the candida immune complex level returning to normal when the patient reported improvement. The average length of treatment for patients with post treatment normal immune complexes was 154 days. The average symptom score from pre and post treatment questionnaires were as follows; pre treatment 6.6 and post treatment 1.8 which is a highly significant reduction (p=<0.001, Student t test). This demonstrates that 80% of patients who presented with candida overgrowth symptoms and had elevated candida immune complexes were cured after treatment with an antifungal regime.
The 20% of patients whose immune complexes remained positive after nine months of treatment showed no reduction in their symptom score. These patients were diagnosed with chronic unresponsive candida overgrowth.
Chronic Unresponsive Candida Overgrowth
These chronic unresponsive patients were further studied and reported in a recent paper by Drs. Lanson and Broughton. (7) Chronic unresponsive candida overgrowth patients were compared to patients known to have elevated candida immune complexes but not under treatment, and a group of apparently healthy volunteers who were selected as controls.
The following tests were performed on all three groups: Candida Immune Complexes, IgA and IgG antibodies to casein and gliadin and Total Phagocytic Index and Ingestion Index.
This study found that chronic unresponsive candida overgrowth patients had the following:
* Significantly higher candida immune complex levels than the other groups.
* Increased intestinal permeability as shown by the presence of antibodies to casein or gliadin (IgA antibodies suggesting current permeability and IgG suggesting past permeability). (8-12)
* A decrease of leucocyte phagocytosis both adhesion (Total Phagocytosis Index) and ingestment of particles (Ingestion Index).
This study also demonstrated that there is an inverse relationship between the candida immune complex level and the total phagocytosis index. But the ingestion index was independent of the candida immune complex level. This demonstrates that the presence of chronic candida overgrowth is associated with difficulty in the first phase of phagocytosis (adhesion of particles prior to ingestion).
Increased Intestinal Permeability
Increased permeability will allow the passage through the bowel of metabolites usually prevented by an intact bowel. These metabolites include the casomorphines and gliadomorphines from casein and gliadin respectively. These metabolites have been reported in the urine and serum of other conditions of increased intestinal permeability such as regional ileitis, (11) and may account for some of the symptoms associated with chronic unresponsive candida overgrowth. These patients develop intestinal permeability because of the progressive colonization of the gut wall by the candida that results in damage to the protein barrier in the lumen of the bowel. The appearance of symptoms related to delayed food allergy may also be related to increased intestinal permeability which allows foods across a normally intact membrane.
Removal of particularly gliadin and casein from the diet will produce temporary relief of some of the symptoms. After three months gliadin and casein should be reintroduced and the Intestinal Permeability Evaluation #2330 repeated one month after the reintroduction of casein and gliadin. If the IgA antibodies have disappeared then the intestinal permeability has been cured. But if they still have IgA antibodies then the patient should return to the casein and gliadin free diet. At this point gluten sensitivity should be excluded by testing for endomysial and reticulin antibodies (test #369 & 370). If the endomysial and reticulin antibodies are positive, the patient must stay on the gliadin free diet for the rest of their life. If these antibodies are negative then the patient has a bowel with active intestinal permeability which may take months to heal.
Leucocyte Phagocytic Function
Similar defects in phagocytosis to those described in Drs. Lanson and Broughton’s study (7) have been seen in other intestinal diseases such as ulcerative colitis and Crohn’s disease. (3-15) These defects in phagocytosis prevent the normal destruction of the yeast (16) by the leucocytes, and despite frequent changes in antifungal therapy the patients only have transient improvement at best. Therefore it is important to understand why these patients have a failure of phagocytosis. As discussed by Drs. Lanson and Broughton, (7) the recurrent oxidative bursts produced by polymorphonuclear cells during repeated attempts to phagocytose the yeasts generates free radicals which progressively damage the polymorphonuclear cells.
Treatment with antioxidants, such as vitamin E, (d alpha tocopherol), vitamin C, and beta carotene may help to restore the phagocytosis activity. The amino acid taurine may also be helpful because it is not only a free radical scavenger in the white cells, but also may act as a detoxifer of xenobiotics in the liver.
The patient who presents with symptoms of candida overgrowth should have the candida immune complexes (#323) performed. If this test is normal then the patient does not have candida albicans overgrowth but a different problem such as overgrowth due to some other species of candida (unusual but occurs in approximately 1% of patients), or a problem unrelated to candida.
If the test for candida immune complexes is positive, the patient should be treated with an antifungal regime and diet modification for at least three months and then have the candida immune complexes (#323) repeated. If the candida immune complex level has fallen and their symptoms have improved, the patient has been cured (80% of patients with increased candida immune complexes responded to antifungal treatment).
If the candida immune complexes are still increased and their symptoms are still present, the patient has Chronic Unresponsive Candida Overgrowth and should be evaluated accordingly. The Intestinal Permeability Evaluation #2330 should be performed as well as assessing for additional factors such as chemical exposure, chronic fatigue, and viral diseases.
If the candida immune complexes are normal and the patient still has symptoms, the candida overgrowth has been eliminated, but some other problem is causing the persistent symptoms such as intestinal permeability, chronic fatigue or chemical exposure.
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2. Truss CO, Tissue injury induced by candida albicans J Orthomol Psy. 1978;7:1-19.
3. Truss CO, The role of candida albicans in human disease J Orthomol Psy. 1981;10:228-238.
4. Crook WG, The yeast connection and the woman P.O. Box 3246 Jackson TN Professional Books Inc. 1995.
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6. Lanson S.Z. Immune Complexes to Candida Mannan: An objective marker of candida overgrowth. J Advance Med 1997; 10:179-186.
7. Broughton A., Lanson S.Z., Increased intestinal permeability and reduced leucocyte phagocytosis in patients with chronic unresponsive candida overgrowth J Advance Med 1997; 10:187-194.
8. Aitola PT, Soppi ET, Edenholm H, et al. Studies on IgA and IgG to gliadin in patients with ulcerative colitis. Scand J Gastroent 1994; 29:646-650.
9. Lerner A, Ross TM, Park B, et al, Serum antibodies to cows milk proteins in pediatric inflammatory bowel disease. Acta Pediatric Scand 1989; 78:384-389.
10. Lerner A, Ross TM, Park B, et al, Serum antibodies to cows milk proteins in pediatric inflammatory bowel disease v ulcerative colitis Acta Pediatric Scand 1989; 78:81-86.
11. Shetty NP, Raj IS, Macaden RS, Non specific reactions in enzyme linked immunosorbent assays for serum antibody to entamoeba histolytica and Giardia lamblia in non endemic areas J Clin Pathol 1990; 43:950-952.
12. Knoflach P, Park BH, Cunningham R, et al, Serum antibodies to cows’ milk proteins in ulcerative colitis and Crohn’s disease. Gastroenterology 1982;92:479-485.
13. Nelson OH, Elmgreen J, Activation of neutrophil chemotaxis by leukotriene B4 and 5 hydroxyeicosatetetraenoic acid in chronic inflammatory bowel disease. Scand J Clin Lab Invest 1987; 47:605-611
14. Hermanowicz A, Hermel A, Novak A, et al. Function of phagocytes in experimentally induced colitis in rabbits 11, The Shwartzman phenomenon in the colon. Int Arch Allergy Appl Immunol 1986; 80:245-252
15. Wandall J. Function of exudative neutrophilic granulocytes in patients with Crohn’s disease or ulcerative colitis. Scand J Gastroenterol 1985; 20:1151-1156.
16. Bennett J.E, In: Principles of Internal Medicine (12th ed Wilson et al. McGraw Hill New York) 1991 pp 743-751.
17. Resseger C. Chronic Fatigue and Candida Overgrowth, Antibody Assay Laboratories Candida Symposium, Tucson 1995.
Alan Broughton, MD, Medical Director
AAL Reference Laboratories
1715 E. Wilshire #715
Santa Ana, California 92705 USA
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