Candida spp. have commonly been identified as part of the healthy human mycobiome. Host defense interruption, or immunocompromise, is required for them to act as pathogens.
Candida albicans is the most prevalent among the Candida spp.
Fungi, including Candida, are ubiquitous in our environment and are part of natural foods and industrial processes, including antibiotic production, bread, cheese, alcoholic beverages, decomposing natural debris, fruits, and soil nutrients.
Candida is present in the gut of up to 70% of healthy adults, but certain factors, including diabetes, antibiotics, antacid, and steroid inhaleruse, promote overgrowth.
Candida growth in the GI tract is positively correlated with carbohydrate consumption.
Candida pathogenesis depends on virulence factor expression, like germ tube formation, adhesions, phenotypic switching, biofilm formation, and hydrolytic enzyme production. Most Candida disease processes are primarily due to biofilm formation.
During overgrowth, Candida produces pseudohyphae that push their way into the intestinal lining, destroying cells and brush borders, and may eventually send toxic metabolic by-products through the intestinal wall into the blood.
High-level Candida colonization is frequently observed in ulcer and IBD patients. This may in part reflect common treatments for these conditions. In addition, the presence of Candida delays healing and exacerbates disease.
Most patients are asymptomatic, and Candida is considered a commensal organism. Depending on the host’s immune status and comorbidities, symptoms will vary.
Candida overgrowth in the GI tract has been shown to cause diarrheal illness.
Other GI symptoms sometimes seen include thrush, bloating, gas, intestinal cramps, rectal itching, and altered bowel habits.
Some generalized symptoms of patients with yeast infections include chronic fatigue, mood disorders, and malaise.
Candida albicans/dubliniensis
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