Candida is not the cause of antibiotic-associated diarrhea
Candida toxins do not affect the development of antibiotic-associated diarrhea and there is insufficient evidence that excessive growth of Candida alone can cause antibiotic-associated diarrhea in adults.
The role of candida in the etiology of antibiotic-associated diarrhea (AAD) has long been controversial. Since mushrooms of this type are physiologically normal flora of the gastrointestinal tract, the presence of a small number of fungal cells in the stool is generally considered normal. However, an increase in their number is generally considered to be a possible cause of the development of diarrhea in patients taking antibacterial drugs. But data from several clinical studies has shown that this is not true. To date, there is not enough evidence to suggest that fungi of the genus Candida are capable of causing ADA in adults.
German scientists conducted a study to determine the presence of fungi of the genus Candida in the stool and to calculate the number of fungal cells. The study included 395 patients with or without symptoms of diarrhea, whether or not they are taking antibiotics.
The frequency of excretion of Candida fungi in the stool and the number of fungal cells in patients with antibiotic-associated diarrhea have not been shown to differ from these indicators in patients with symptoms of diarrhea who also took antibiotics. Excessive growth of fungi in patients with diarrhea who did not take antibacterial drugs was less common than in patients with AAD, however, the frequency of excretion of candida was the same in both groups. In addition, it has been suggested that a decrease in the number of bacteria in the stool caused by taking antibiotics and an increase in the liquid volume of the stool during diarrhea leads to an increase in the number of fungal cells of the genus Candida. As a hypothesis, it was noted that fungal toxins and toxin-like substances (aspartyl proteinase - Saps and phospholipases) may be responsible for the development of AMA. However, it was found that their content did not differ between the groups of patients studied. In addition, the production of phospholipases by strains of candida isolated from the stool of patients with AAA did not differ from that of the control group. In this regard, we can conclude that the main virulence factors of fungi of the genus Candida - Saps and phospholipases - are not associated with the development of antibiotic-associated diarrhea in adults.
Another study found that excessive growth of candida isolated from the stool of patients with AAD is associated with a decrease in the number of factors that inhibit their growth, especially short-chain fatty acids and secondary bile acids, as well as nutrients for the normal flora of the gastrointestinal tract.
The theory that candida is responsible for the development of AMA was also based on individual clinical trials of antimycotics and several reports of rapid elimination of symptoms from the gastrointestinal tract when prescribing antifungal therapy. However, the design of many of these studies did not involve the presence of a control group and included a small number of patients.
Thus, we can conclude that antibiotic therapy and diarrhea themselves contribute to an increase in the number of Candida fungi in the stool. In turn, an increase in fungal growth is more the result of the administration of antibiotics or diarrhea itself due to a violation of the endogenous intestinal flora and a decrease in the fatty acid content short chain, that directly cause the AAD. Candida Saps and phospholipase toxins have been shown not to affect the development of ADA, and there is insufficient evidence that the excessive growth of Candida fungi alone can cause antibiotic-associated diarrhea in adults.