C. albicans (A fungus, first isolated in 1844 from the sputum of a tuberculous patient) infections are undoubtedly a problem of growing clinical importance in general medicine and are frequently encountered in nutritional practice – or are they?
Of the 500 or so species representing 60 genera of yeasts, only a few are capable of causing human infections. These species must possess specific factors or mechanisms of pathogenesis that enable them to cause infection.
Frequently, the first mechanism is a species-specific ability of the organism to become established as a persistent member of the normal flora. C. albicans is known to colonise humans more frequently than other C. albicans spp., becoming established as a part of the flora of the oral cavity, GI tract, and female genitourinary tract. C. tropicalis and C. glabrata can be found as normal flora of the oral cavity, GI tract, and vagina but less frequently than C. albicans. C. krusei, C. guilliermondii, and C. parapsilosis are found more frequently as part of the skin flora. An opportunistic organism such as C. albicans is one of low virulence present in normal mucosa and/or skin flora generally maintained in a latent state not causing disease whilst in its normal balance.
C. albicans and C. albicans tropicalis are distinguished from less virulent yeasts by their secretion of acid proteases. C. albicans proteases cleave various human immunoglobulins including IgA2 and secretory immunoglobulins. These IgA-specific microbial proteases possess the ability to reduce the protective effects of secretory IgA antibodies. The fact that fungi such as C. albicans and C. tropicalis produce both IgA1-and IgA2-specific proteases has yet only recently been acknowledged in articles and discussions concerning the chronic C. albicans syndrome.
The last 20 years or so has seen a growing number of fungal infections coincident with a dramatic increase in the population of severely immunocompromised patients. These infections are due mainly to impairments in host defence mechanisms as a consequence of viral infections, especially the human immunodeficiency virus epidemic, haematological disorders such as different types of leukaemia, organ transplants, and more intensive and aggressive medical practices. Many clinical procedures and treatments, such as surgery, the use of catheters, injections, radiation, chemotherapy, antibiotics, and steroids, are risk factors for fungal infections. There have also been extensive changes to the nutritive of choice for many people and the food selections are also proposed to potentially contribute to increased infection. Of the various types of infective agents contributing to this expansion C. albicans is the most common fungal pathogen of humans and has become the fourth leading cause of nosocomial infections. , 
Nosocomial infections are those which are a result of treatment in a hospital or hospital-like setting, but secondary to the patient’s original condition. Infections are considered nosocomial if they first appear 48 hours or more after hospital admission or within 30 days after discharge. Nosocomial comes from the Greek word nosokomeion meaning hospital (nosos = disease, komeo = to take care of ).
At the most serious level, mortality rates from systemic candidiasis are high but frequency is low. However, the majority of patients, notably immunosuppressed individuals with human immunodeficiency virus (HIV) infection, experience some form of superficial mucosal candidiasis, most commonly thrush, and many suffer from recurrent infections.
There is an another group of individuals of both sexes with females being the more frequent who are ‘diagnosed’ as being the ‘victims’ of candidiasis. For which a wide range of bizarre symptoms and food/environmental sensitivities may be attributed either as a cause or effect.
The typical nutritional clinical practice is then advising a client/patient suspected of such a problem to adhere to an ‘anti C. albicans diet’.
C. albicans is found among the gut flora, that live in the human mouth and gastrointestinal tract. Under normal circumstances, C. albicans lives in 80% of the human population with no harmful effects, although overgrowth results in candidiasis. Candidiasis is often observed in immunocompromised individuals such as HIV positive patients. Candidiasis also may occur in the blood and in the genital tract. Candidiasis, also known as “thrush”, is a common condition that is usually easily cured in people who are not immunocompromised. To infect host tissue, the usual unicellular yeast-like form of C. albicans reacts to environmental cues and switches into an invasive, multicellular filamentous form.
This decision is often based on a questionnaire or symptom profile only – a method of diagnosis, known to be prone to misinterpretation. The client can then be subjected to months or even years of restrictive food intake in the aim of not feeding the fungi as well as being prescribed anti fungals in the pursuit of being ‘C. albicans free’.
This common (for nutritionists) practice has had some dramatic results both in terms of improvement and worsening of health, – so should dietary management be a component of treating such an individual?
Clinical management of C.Albicans
Two key understandings are necessary to start.
Firstly; in patients who have no suppression of immune competence, when fed high sugar laden foods do not demonstrate an increase in the presence of C. albicans within the mucosal cavities. Therefore there must be a loss of immune stability in the mucosal tissues to allow for some increase in growth and potential virulent activity of this organism. Thus in clinical assessment and treatment the restoration and maintenance of immunological competence is essential to the long term resolution of C.Albicans problems.
Secondly; it is impossible to starve out C. albicans as this commensal/pathogen has evolved over a period of 12 million years and has some very special skills for remaining present inside our gastro intestinal tract and other mucosal tissues. Based on nucleotide polymorphism frequencies, estimations of the historical evolution of a recent common ancestor for the species is about 3-16 million years prior, with variation due to molecular clock calibration. As C. albicans genotypes have broad geographic associations, this suggests that the origins of DNA sequence variation coincided with early hominid evolution. That is to say the species has co-evolved with us, as have our microbiota.
This fits with an emerging view of a genetically complex organism that is able to survive under host immunity as an obligate commensal species. As a long time commensal, it has evolved a complex set of strategies to survive and profligate within the human mucosal tissues. As such it is able to confuse and avoid diminished immunological responses, setting itself up as a chronic immuno-irritant without being able to achieve an appropriate immunological response.
Why does sugar intake not affect C.albicans growth?
The vast majority of sugars are absorbed in the small intestine, and C. albicans is principally a large intestine occupant. So under normal conditions it does not have easy access to the sugary foods we consume, instead it relies on the breakdown of commensal bacteria, and gastro intestinal cell walls rich in polysaccharides and monosaccharide’s (carbohydrates) for a large part of its food source. Therefore if the therapeutic plan is to ‘starve’ out C. albicans, the only organism that will perish will be your client/patient.
So why do people consuming foods high in sugars note a difference to their function?
Well, not only C. albicans relies on carbohydrates for virulence activity, other organisms especially bacteria also use monosaccharide’s as fuel. So without an evidential base of presence, food exclusion based on assumption for the purpose of C. albicans eradication is not a clinically valid position.
Examples of monosaccharides include glucose (dextrose), fructose, galactose, and ribose
However, what is understood is that glucose acts as a morphogenic agent for C. albicans, triggering the yeast-to-hyphal transition; one of the vital determinants of virulence. Because glucose plays a central role as a carbon and energy source, glucose sensing and response is highly evolved and closely regulated in most organisms. The importance of glucose to yeast cells generally is illustrated by the large number of hexose (monosaccharide) transporters they possess: C. albicans appears to have over 20. Indeed it is somewhat surprising that C. albicans, an organism thought to prefer respiration and producing up to 38 ATPs per glucose molecule metabolized, also has evolved many of these hexose transporters.
Opinion is developing that this high number of receptors actually occurs to reflect the varied mucosal niches in which C. albicans thrives, and which most likely offer many different sugars as carbon sources. Fundamentally it is still the case that little is known but much is postulated about how C. albicans senses and responds to sugars.
What is known is given the nutrient opportunity combined with immunological suppression C. albicans can reversibly alter its mode of growth from a unicellular budding yeast to a filamentous form in the presence of inducing environmental signals. Hyphae are then able to adhere to and to invade host tissues more efficiently than the yeast form,  the yeast form is thought to disseminate easily via body fluids, and the hyphal form can extravasate into tissues or form mycelial biofilms, making it hard to eradicate. , 
Its actual “virulence” is due to its robust ability to access and thrive in various niches within its host, the effect of which is to provide an abundant source of microbes available to cause disease., To survive within the host; C. albicans must efficiently compete for nutrients with host cells and an extensive repertoire of resident microbes. These bacterial species and SIgA anti C. albicans antibodies combine with other agents to limit its expansion plans.
It appears that the transition from harmless commensal to unrelenting pathogen is a fine line and one that is attributable to an extensive repertoire of virulence determinants selectively expressed under suitable predisposing conditions.
|Virulence attribute||Putative virulence roles||References|
|Adhesins||Adhesion and colonization||, ,,|
|Hyphae production||Adhesion, invasion, tissue damage||,.,|
|Extracellular hydrolytic enzymes & aspartyl proteinases||Nutrient acquisition, invasion, tissue damage, evasion of host response||,,,|
|Phenotypic switching||Adhesion, evasion of host response||,,,|
Immunology of C. albicans
Underlying acquired immunity to the fungus C. albicans is usually present in adult immunocompetent individuals and is presumed to prevent mucosal colonisation progressing to symptomatic infection. Exploration of immunological events leading to C. albicans resistance or susceptibility has indicated the central role of the innate and adaptive immune systems, the relative contribution of which may vary depending on the site of the primary infection. Nevertheless, acquired resistance to infection results from the development of TH1 responses. Cytokines produced by TH1 cells activate phagocytic cells to kill C. albicans.
In contrast, cytokines produced by TH2 cells inhibit TH1 development and deactivate phagocytic effector cells. Because reciprocal influences have been recognised between innate and adaptive TH cell immunity, it appears that an integrated immune response determines the life-long commensalism of the fungus at the mucosal level, as well as the transition to pathogen.
The “immunocompromised host” is a term used to describe a person with increased susceptibility to opportunistic pathogens due to a qualitative or quantitative defect of one or more components of the normal immune defence mechanism. Although the defect may be congenital, acquired defects predominate as an increasing by product of current diseases and/or modern approaches to their treatment, the choice of lifestyle and nutrient intake.
As a commensal, C. albicans may be endowed with the ability to elude the host’s immunological surveillance, thus allowing its persistence on mucosal surfaces. One important virulence factor of C. albicans is believed to be its ability to switch reversibly from a unicellular yeast form into various filamentous forms, all of which can be found in tissues. Although recent studies have clearly shown that the ability to switch from yeast to filamentous form is required for virulence.
Oral candidiasis occurs in immunocompromised patients and is often the result of Impaired salivary gland function., Secretion of saliva causes a diluting effect removing organisms from the mucosa. Key antimicrobial proteins in the saliva such as lactoferrin, sialoperoxidase, lysozyme, histidine-rich polypeptides, and specific anti C. albicans antibodies, interact with the oral mucosa and prevent overgrowth of C. albicans. IgA is the predominant antibody present at mucosal surfaces and is known to prevent the attachment of C. albicans to the mucosal epithelium.
The most important component of immunological understanding is that in order for there to be mucosal population growth there needs to be a relative T-cell depression, and a change in the hosts innate immune families of commensal bacteria The relative T-cell and innate immune depression reduces the host’s defence against opportunistic organisms, to restore health and function these aspects must also be included in the treatment plan. 
It has been reported that C. albicans infection of vaginal and oral mucous membrane is specifically inhibited by anti-C. Albicans SIgA. But, the mechanism still remains unclear.
Instead of vulvovaginal candidiasis being caused by defective or dysfunctional CD4 T helper 1-type cell-mediated immune reactivity, data suggests that symptomatic vulvovaginal candidiasis is associated with an aggressive response by Polymorphonuclear neutrophils, whereas protection appears to be innate and noninflammatory.
The role for innate immunity in both protection against, and promotion of, symptomatic vulvovaginal candidiasis is paradigm changing.
A negative correlation between specific IgA and quantity of C. albicans adherence exists in the mucosal tissues. The specific IgA was the important factor to keep the balance between opportunistic pathogen and host. The colonisation of C. albicans should elicit a local mucosal immune reaction through the production of SIgA and so limit C. albicans overgrowth., A failure to produce adequate SIgA will lead to opportunistic expansion with increased potential for down regulating health.
In the lamina propria there are B lymphocytes clones that secrete specific IgA against C. albicans. This Gut Associated Lymphoid Tissue (GALT) is an essential promoter of the key protein SIgA that maintains the normal ecological balance in the mucosal tissues. Plenty of specific IgA against C. albicans secreted to the surface of intestinal mucus membrane forms the antibody barrier.
We could draw the conclusion that although C. albicans infection is common, it is possible to prevent and treat C. albicans infection by setting up a specific SIgA antibody barrier in the host.
The host is most vulnerable when there is a combination of loss of bacterial commensals and or a loss of adequate SIgA production. Post antibiotic therapy there is a significant increase in the likelihood of C. albicans expansion, therefore prevention as well as restitution is a significant clinical aim.
A study led by Dr Adam found that the incidence of post antibiotic induced Candidiasis could be significantly reduced by a prophylactic course of Saccharomyces boulardii taken both prior to and together with the antibiotic.
Saccharomyces boulardii also reduces the incidence of antibiotic associated diarrhoea. In vivo, Saccharomyces boulardii reduces the C. albicans population by 10-50 fold. This antagonistic effect is curative and preventive and is also reported successful for C. krusei and C. pseudotropicalis.
The use of Saccharomyces boulardii reduces the incidence of translocation to the mesenteric lymph nodes, liver and kidneys.
Providing resistance to adhesion of C. albicans to the mucosal surfaces is an important component of prevention and restoration of mucosal health. SIgA in human saliva and SIgA in the mucosal tissues are powerful and effective inhibitors.
Whole saliva prevents inhibition by 41% and secretory IgA by 55%. Loss of or reduced output of either will increase C. albicans adhesion and subsequent potential for translocation.
So what makes us feel bad?
C. albicans may be an allergen itself; and although the major antigenic component is thought to be proteases, there may be other as yet unidentified components. However the acid proteases released from the C. albicans species will actually break down secretory IgA so making the attachment of the species more likely.
This protease (C. albicans Acid Protease) appears to be a two edged sword, by lowering the anti inflammatory protective protein SIgA and also by triggering an IgE response in immune sensitive individuals.
The subsequent diminished mucosal barrier effectiveness can then lead to increased immunological burden and the development of many symptoms.
Is C. albicans a trigger in the onset of coeliac disease?
Coeliac disease is a T-cell-mediated autoimmune disease of the small intestine that is induced by ingestion of gluten proteins from wheat, barley, or rye. C. albicans may be a trigger in the onset of coeliac disease. The virulence factor of C. albicans albicans-hyphal wall protein 1 (HWP1), which it uses to adhere to the epithelium of the mucosal barriers, is the same as another amino acid known to initiate coeliac disease.
Furthermore, tissue transglutaminase and endomysium components could become covalently linked to the yeast. Subsequently, C. albicans might function as an adjuvant that stimulates antibody formation against HWP1 and gluten, and formation of autoreactive antibodies against tissue transglutaminase and endomysium. It is also known that pathogens increase food sensitivities through the down regulation of innate anti-inflammatory responses and the up regulation of co stimulatory adjuvants. 
Heavy Metals and C.albicans
Suggestions have been made and asserted that C. albicans assists the host by increasing in quantity to manage mercury or other heavy metal exposures. Yeasts in water ways have shown some capacity for modifying elemental mercury, but have not demonstrated any such capacity in humans. Even within the environmental set ups there has been no evidence that yeast is in any way beneficial to the host in terms of mercury exposure. The reason why there may be an overgrowth of C. albicans in patients with mercury exposure is that mercury and lead both inhibit an essential enzyme called myeloperoxidase. This enzyme induces a hypochlorite ion one of the bodies main mechanisms for maintaining normal C. albicans ecology.,,[64
Suggestions have been also been made that probiotics may absorb heavy metals and thus help their elimination through the faeces, arguably the largest detoxification component of the body, the endogenous enteric bacteria are an enormous reservoir, which can be constantly and safely replenished. This has far more credence, and may be a reason to partly explain the diminution of bacterial colonies in patients with heavy metal exposure. ,,
A 34 yr old female patient presents with a 2-3 year history of recurring vaginal thrush following a series of anti biotic treatments. She complains of vaginal irritation, discharge, non specific fatigue and malaise, food sensitivities, occasional bloating and collection of other mild non specific ailments. She has also noted some reduction in mental concentration and becomes more anxious than before.
She has self diagnosed candidiasis, has sought anti fungal treatment from her GP and a mix of other CAM practitioners, has taken over the counter probiotics for 2 years and has used yogurt inter-vaginally, there have been periods of improved health and function but nothing has sustained. She has had no more antibiotics, follows a low carbohydrate diet and is bored and fed up with having to constantly watch her food choices.
A salivary immunoglobulin test reveals suppressed SIgA and the presence of IgG and IgA C.albicans antibodies, confirming mucosal immune suppression of the secretory protective Immunoglobulins and raised immune response to C.albicans.
For this patient the use of Saccharomyces Boulardii at 250mg to 500mg per day, the recommendation of > Bifidus probiotics and LGG Culturelle probiotics, and some broadening of her self imposed dietary restriction was the first point of intervention. This increased total SIgA production and improved innate immune capacity, the inclusion of a standardised oregano extract at a dose from 1-2 per day rising to 4 per day followed approximately 6 weeks after the initial treatment and was given 4 hours away from the other supplements.
At 2 months into the treatment her SIgA levels had returned to normal her mixed symptoms had begun to resolve and the treatment was maintained after a further 6 weeks the antibody test was repeated, her immune markers had greatly improved, her vaginal discharge had resolved and her physical and psychological symptoms had resolved. This treatment continued in line with an increasing introduction of food choice and two years later remains free of C.albicans. This treatment addresses the immune balance, the microbial balance and the food selection.
 Mandell GL, Bennett JE, Dolin R. Anti-fungal agents. Principles and practice of infectious diseases. 4th Ed. New York: Churchill Livingstone, 1994: 401–10
 R Ruchel. Cleavage of immunoglobulins by pathogenic yeasts of the genus C. albicansC. albicans. Microbiol Sci, October 1, 1986; 3(10): 316-9.
 Fotedar R, Al-Hedaithy SS Comparison of phospholipase and proteinase activity in C. albicansC. albicansC. albicansC. albicans and C. dubliniensis Mycoses. 2005 Jan;48(1):62-7.
 K Kett. C. albicansC. albicans species produce IgA proteases–an important biological property. Tidsskr Nor Laegeforen, June 30, 1989; 109(19-21): 2037
 Edmond, M. B., S. E. Wallace, D. K. McClish, M. A. Pfaller, R. N. Jones, and R. P. Wenzel. 1999. Nosocomial bloodstream infections in United States hospitals: a three-year analysis. Clin. Infect. Dis. 29:239-244
 Pfaller, M. A., R. N. Jones, S. A. Messer, M. B. Edmond, and R. P. Wenzel. 1998. National surveillance of nosocomial blood stream infection due to C. albicans albicans: frequency of occurrence and antifungal susceptibility in the SCOPE Program. Diagn. Microbiol. Infect. Dis. 31:327-332
 Sobel, J. D. 1988. Pathogenesis and epidemiology of vulvovaginal candidiasis. Ann. N. Y. Acad. Sci. 544:547-557
 Sobel, J. D. 1992. Pathogenesis and treatment of recurrent vulvovaginal candidiasis. Clin. Infect. Dis. 14(Suppl. 1):S148-S153
 Weig M, Werner E, Frosch M, Kasper H. Limited effect of refined carbohydrate dietary supplementation on colonization of the gastrointestinal tract of healthy subjects by C. albicans albicans.
Am J Clin Nutr. 1999 Jun;69(6):1170-3.
 Fungal Genet Biol. 2005 May; 42(5):444-51. The human commensal yeast, C. albicansC. albicansC. albicansC. albicans, has an ancient origin. Lott TJ, Fundyga RE, Kuykendall RJ, Arnold J.
 Hudson, D. A., Q. L. Sciascia, R. J. Sanders, G. E. Norris, P. J. Edwards, P. A. Sullivan, and P. C. Farley. 2004 . Identification of the dialysable serum inducer of germ-tube formation in C. albicans albicans. Microbiology 150:3041-3049.
 Fan, J., V. Chaturvedi, and S. H. Shen. 2002 . Identification and phylogenetic analysis of a glucose transporter gene family from the human pathogenic yeast C. albicans albicans. J. Mol. Evol. 55:336-346.
 Dumitru, R., J. M. Hornby, and K. W. Nickerson. 2004 . Defined anaerobic growth medium for studying C. albicans albicans basic biology and resistance to eight antifungal drugs. Antimicrob. Agents Chemother. 48:2350-2354.
 Brown,V. Sexton,JA. Johnston,M. A Glucose Sensor in C. albicans Albicans. Eukaryot Cell. 2006 October; 5(10): 1726–1737.
 Cutler J E. Putative virulence factors of C. albicans albicans. Annu Rev Microbiol. 1991;45:187–219.
 Edwards, J E., Jr . C. albicans species. In: Mandell G L, Douglas R G Jr, Bennett J E. , editors. Principles and practice of infectious diseases. 3rd ed. New York, N.Y: Churchill Livingstone; 1990. pp. 1943–1958.
 Bendel, C. M., D. J. Hess, R. M. Garni, M. Henry-Stanley, and C. L. Wells. 2003 . Comparative virulence of C. albicans albicans yeast and filamentous forms in orally and intravenously inoculated mice. Crit. Care Med. 31:501-507.
 Sudbery, P., N. Gow, and J. Berman. 2004 . The distinct morphogenic states of C. albicans albicans. Trends Microbiol. 12:317-324.
 Andrutis, K. A., P. J. Riggle, C. A. Kumamoto, and S. Tzipori. 2000 . Intestinal lesions associated with disseminated candidiasis in an experimental animal model. J. Clin. Microbiol. 38:2317-2323
 Kullberg, B. J., and A. M. Oude Lashof. 2002 . Epidemiology of opportunistic invasive mycoses. Eur. J. Med. Res. 7:183-191.
 Backhed, F., R. E. Ley, J. L. Sonnenburg, D. A. Peterson, and J. I. Gordon. 2005 . Host-bacterial mutualism in the human intestine. Science 307:1915-1920.
 Sweet, S. P. 1997. Selection and pathogenicity of C. albicans albicans in HIV infection. Oral Dis. 3:S88-S95.
 Calderone, R., and N. A. R. Gow. 2002. Host recognition by C. albicans species, p. 67-86. In R. A. Calderone (ed.), C. albicans and candidiasis. ASM Press, Washington, D.C.
 Calderone, R. A., and P. C. Braun. 1991. Adherence and receptor relationships of C. albicans albicans. Microbiol. Rev. 55:1-20
 Chaffin, W. L., J. L. Lopez-Ribot, M. Casanova, D. Gozalbo, and J. P. Martinez. 1998. Cell wall and secreted proteins of C. albicans albicans: identification, function, and expression. Microbiol. Mol. Biol. Rev. 62:130-180
 Staab, J. F., and P. Sundstrom. 2003. URA3 as a selectable marker for disruption and virulence assessment of C. albicans albicans genes. Trends Microbiol. 11:69-73.
 Brown, A. J., and N. A. Gow. 1999. Regulatory networks controlling C. albicans albicans morphogenesis. Trends Microbiol. 7:333-338
 Brown, A. J. P. 2002. Expression of growth-form specific factors during morphogenesis in C. albicans albicans, p. 87-93. In R. A. Calderone (ed.), C. albicans and candidiasis. ASM Press, Washington, D.C.
 Brown, A. J. P. 2002. Morphogenetic signaling pathways in C. albicans albicans, p. 95-106. In R. A. Calderone (ed.), C. albicans and candidiasis. ASM Press, Washington, D.C.
 Liu, H. 2001. Transcriptional control of dimorphism in C. albicans albicans. Curr. Opin. Microbiol. 4:728-735
 Hube, B. 1996. C. albicans albicans secreted aspartyl proteinases. Curr. Top. Med. Mycolo. 7:55-69
 Hube, B. 2000. Extracellular proteinases of human pathogenic fungi, p. 126-137. In J. F. Ernst and A. Schmidt (ed.), Contributions to microbiology. Dimorphism in human pathogenic and apathogenic yeasts. S. Karger AG, Basel, Switzerland
 Hube, B., and J. Naglik. 2001. C. albicans albicans proteinases: resolving the mystery of a gene family. Microbiology 147:1997-2005.
 Hube, B., and J. R. Naglik. 2002. Extracellular hydrolases, p. 107-122. In R. A. Calderone (ed.), C. albicans and candidiasis. ASM Press, Washington, D.C.
 Soll, D. R. 1992. High-frequency switching in C. albicans albicans. Clin. Microbiol. Rev. 5:183-203
 Soll, D. R. 2002. Phenotypic switching, p. 123-142. In R. A. Calderone (ed.), C. albicans and candidiasis. ASM Press, Washington, D.C.
 Soll, D. R., B. Morrow, T. Srikantha, K. Vargas, and P. Wertz. 1994. Developmental and molecular biology of switching in C. albicans albicans. Oral Surg. Oral Med. Oral Pathol. 78:194-201
 Soll, D. R., B. Morrow, and T. Srikantha. 1993. High-frequency phenotypic switching in C. albicans albicans. Trends Genet. 9:61-65
 Kobayashi, S. D., Cutler, J. E. (1998) C. albicans albicans hyphal formation and virulence: is there a clearly defined role? Trends Microbiol 6,2-4
 Gale, C. A., Bendel, C. M., McClellan, M., Hauser, M., Becker, J. M., Berman, J., Hostetter, M. K. (1998) Linkage of adhesion, filamentous growth, and virulence in C. albicans albicans to a single gene, INT1 Science 279,1355-1358
 Epstein JB. Antifungal therapy in oropharyngeal mycotic infections. Oral Surg Oral Med Oral Pathol 1990;69:32–41
 Peterson DE. Oral candidiasis. Clin Geriatr Med 1992;8:513–27
 Vudhichamnong, K., D. M. Walker, and H. C. Ryley. 1982. The effect of secretory immunoglobulin A on the in-vitro adherence of the yeast C. albicans albicans to human oral epithelial cells. Arch. Oral Biol. 27:617-621
 Romani L.J Innate and adaptive immunity in C. albicansC. albicansC. albicansC. albicans infections and saprophytism Leukoc Biol. 2000 Aug;68(2):175-9
 Shu Q, Gill H. Immune protection mediated by the probiotic Lactobacillus rhamnosus HN001 (DR20) against Escherichia coli O157: H7 infection in mice. FEMS Immunol Med Microbiol 2002; 34: 59
 Nakasaki H, Mitomi T, Tajima T, Ohnishi N, Fujii K. Gut bacterial translocation during parenteral nutrition in experimental rats and its countermeasure. Am J Surg 1998; 175: 38-43
 Fidel PL Jr. Immunity in vaginal candidiasis. Curr Opin Infect Dis. 2005 Apr; 18(2):107-11.
 Wozniak KL, Wormley FL Jr, Fidel PL Jr. C. albicansC. albicans-specific antibodies during experimental vaginal candidiasis in mice. Infect Immun 2002; 70: 5790-5799
 Belazi M, Fleva A, Drakoulakos D, Panayiotidou D. Salivary IgA and serum IgA and IgG antibodies to C. albicansC. albicansC. albicans in HIV-infected subjects. Int J STD AIDS 2002; 13: 373-377
 Bai X, Xiao G, Tian X. The relationship between post burn gene expression of modulators in gut associated lymph tissue and the change in IgA plasma cells. Zhonghua Shaoshang Zazhi 2000; 16: 108-110
 Koga-Ito CY, Unterkircher CS, Watanabe H, Martins CA, Vidotto V, Jorge AO. Caries risk tests and salivary levels of immunoglobulins to Streptococcus mutans and C. albicansC. albicansC. albicans in mouth breathing syndrome patients. Caries Res 2003; 37: 38-43
 Adam. J et al. Controlled double blind clinical trials of saccharomyces Boulardii, Multi centre study involving 25 physicians and 388 cases. Medicine et Chirugie Digestives 1976; 5:401-05
 Surawicz CM, Elmer GW, Speelman P, McFarland LV, Chinn J, van Belle G. Prevention of antibiotic-associated diarrhoea by Saccharomyces boulardii: a
Prospective study. Gastroenterology. 1989 Apr; 96(4):981-8.
 Ducluzeau R, Bensaada M. Effet compare de l’administration unique ou en continu de saccharomyces Boulardii sur L’establishment de diverses souches de C. albicans dans le tractus digestif de souris gnotoxeniques. Ann Microbiol 1982; 133: 491-501
 Berg R. Bernasconi P, Fowler D. Inhibition of C. albicansC. albicans translocation from the gastrointestinal tract of mice by oral administration of saccharomyces Boulardii. J infect Dis 1993; 168:1314-18.
 Elguezabal N, Maza JL, Ponton J.Oral Dis. Inhibition of adherence of C. albicans and C. albicansC. albicans dubliniensis to a resin composite restorative dental material by salivary secretory IgA and monoclonal
antibodies. 2004 Mar; 10(2):81-6.
 Ruchel R Cleavage of immunoglobulins by pathogenic yeasts of the genus C. albicansC. albicans Microbiol Sci. 1986 Oct; 3(10):316-9.
 Akiyama K, Yasueda H, Mita H, Yanagihara Y, Kaneko F, Maeda Y, Hayakawa T,
Hesegawa M, Shida T, Yamamoto T, et al.Arerugi. [The allergic reaction to acid protease released by C. albicans] 1993 Oct; 42(10):1628-32. [Article in Japanese]
 Nieuwenhuizen WF, Pieters RH, Knippels LM, Jansen MC, Koppelman SJ Is C. albicansC. albicans Albicans a trigger in the onset of coeliac disease? Lancet. 2003 Jun 21;361(9375):2152-4.
 Shi HN, Liu HY, Nagler-Anderson C. Enteric infection acts as an adjuvant for the response to a model food antigen.J Immunol. 2000 Dec 1;165(11):6174-82.
 Perlingeiro RC, Queiroz ML Polymorphonuclear phagocytosis and killing in workers exposed to inorganic mercury. Int J Immunopharmacol. 1994 Dec;16(12):1011-7.
 Aratani Y, Kura F, Watanabe H, Akagawa H, Takano Y, Suzuki K, Dinauer MC, Maeda
N, Koyama H. In vivo role of myeloperoxidase for the host defense Jpn J Infect Dis. 2004 Oct;57(5):S15.
 Aratani Y, Kura F, Watanabe H, Akagawa H, Takano Y, Suzuki K, Dinauer MC, Maeda N, Koyama H. Relative contributions of myeloperoxidase and NADPH-oxidase to the early host defense against
pulmonary infections with C. albicansC. albicans Albicans and Aspergillus fumigatus. Med Mycol. 2002 Dec;40(6):557-63.
 Aratani Y, Kura F, Watanabe H, Akagawa H, Takano Y, Suzuki K, Dinauer MC, Maeda N, Koyama H.J Critical role of myeloperoxidase and nicotinamide adenine dinucleotide phosphate-oxidase in high-burden systemic infection of mice with C. albicansC. albicans Albicans. Infect Dis. 2002 Jun 15;185(12):1833-7. Epub 2002 May 16.
 Summers AO, Wireman J, Vimy MJ, Lorscheider FL, Marshall B, Levy SB, et al. Mercury released from dental “silver” fillings provokes an increase in mercury- and antibiotic-resistant bacteria in oral and intestinal floras of primates. Antimicrob Agents Chemother. 1993;37:825–34.
 Lorscheider FL, Vimy MJ, Summers AO, Zwiers H. The dental amalgam mercury controversy—inorganic mercury and the CNS; genetic linkage of mercury and antibiotic resistances in intestinal bacteria. Toxicology. 1995;97:19–22.
 Brudnak MA. Probiotics as an adjuvant to detoxification protocols. Med Hypotheses. 2002;58:382–5.