Reply To: TMI alert: Where is your candida overgrowth located?

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dvjorge
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The headquarter is in the Cecum. This is the most difficult part to treat of the complete infestation. Metabolites produced by candida colonies in the Cecum influence the immune system causing cell-mediated suppression. Candida albicans cells living in other mucous membranes begin to produce symptoms since there isn’t immune control. I believe I still have candida colonies in the Cecum. Very hard to treat orally and very difficult rectally. High enemas and retention antifungal enemas that reaches the Cecum are probably the only hope. Resolving the intestinal overgrowth fixes the rest of the problems most of the time.

Candida albicans and bacterial microbiota interactions in the cecum during recolonization following broad-spectrum antibiotic therapy.
Mason KL1, Erb Downward JR, Mason KD, Falkowski NR, Eaton KA, Kao JY, Young VB, Huffnagle GB.
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Abstract
Candida albicans is a normal member of the gastrointestinal (GI) tract microbiota of healthy humans, but during host immunosuppression or alterations in the bacterial microbiota, C. albicans can disseminate and cause life-threatening illness. The bacterial microbiome of the GI tract, including lactic acid bacteria (LAB), plays a vital role in preventing fungal invasion. However, little is known about the role of C. albicans in shaping the bacterial microbiota during antibiotic recovery. We investigated the fungal burdens in the GI tracts of germfree mice and mice with a disturbed microbiome to demonstrate the role of the microbiota in preventing C. albicans colonization. Histological analysis demonstrated that colonization with C. albicans during antibiotic treatment does not trigger overt inflammation in the murine cecum. Bacterial diversity is reduced long term following cefoperazone treatment, but the presence of C. albicans during antibiotic recovery promoted the recovery of bacterial diversity. Cefoperazone diminishes Bacteroidetes populations long term in the ceca of mice, but the presence of C. albicans during cefoperazone recovery promoted Bacteroidetes population recovery. However, the presence of C. albicans resulted in a long-term reduction in Lactobacillus spp. and promoted Enterococcus faecalis populations. Previous studies have focused on the ability of bacteria to alter C. albicans; this study addresses the ability of C. albicans to alter the bacterial microbiota during nonpathogenic colonization.

Cecal colonization and systemic spread of Candida albicans in mice treated with antibiotics and dexamethasone.
Bendel CM1, Wiesner SM, Garni RM, Cebelinski E, Wells CL.
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Abstract
Infections with Candida albicans have become a significant problem among very low birth weight infants in the neonatal intensive care unit. Risk factors are multiple and include administration of antibiotics and glucocorticoids, such as dexamethasone. Experiments were designed to study the combined effect of oral broad-spectrum antibiotics and parenteral dexamethasone on cecal colonization and extraintestinal dissemination of C. albicans in separate groups of mice that were orally inoculated with one of four C. albicans strains that were either wild-type INT1/INT1 or had one or more disruptions of the INT1 gene. Intestinal colonization was monitored by quantitative culture of the mouse cecum, and extraintestinal invasion was monitored by quantitative culture of the draining mesenteric lymph nodes and kidneys. At sacrifice, the average numbers of cecal C. albicans differed from 7.7 log(10)/g to 6.7 log(10)/g (p < 0.01) in mice orally inoculated with C. albicans containing two functional copies of INT1 and no functional copies of INT1, respectively. The incidence of extraintestinal dissemination to mesenteric lymph nodes and kidneys correspondingly varied from 57 to 13% (p < 0.01) and 83 to 4% (p < 0.01) in mice inoculated with these two C. albicans strains. Mice orally inoculated with C. albicans containing one functional copy of INT1 had intermediate levels of cecal colonization and extraintestinal dissemination. Thus, cecal colonization and extraintestinal dissemination of C. albicans was facilitated in antibiotic-treated mice given dexamethasone. In addition, the presence of two functional copies of the INT1 gene was associated with the greatest levels of cecal colonization and extraintestinal dissemination of C. albicans.