How Fungal Blooming Shapes Complexity of C. difficile Infections

How Fungal Blooming Shapes Complexity of C. difficile Infections

United States: At ASM Microbe 2024 in Atlanta, microbiologist Jesus A Romo, PhD, presented findings suggesting a mutualistic relationship between fungal colonization and Clostridioides difficile, potentially impacting disease severity.

The role of bacteria in the gut has been extensively studied, yet fungal colonization also bears significant implications, according to Dr. Romo, an assistant professor at The University of Texas at San Antonio’s Department of Molecular Microbiology and Immunology. Among various behaviors, fungi can migrate beyond the gastrointestinal tract, causing systemic infections and disrupting bacterial communities’ stability, as per the reports published by

Notably, Nakaseomyces glabrata (formerly Candida glabrata) seems to influence C. difficile, although their exact interactions are still under investigation.

Antibiotic treatment diminishes gut microbiota, allowing C. difficile to flourish alongside other organisms like N. glabrata.

“After a decline in healthy microbiota, C. difficile can proliferate, release toxins, and harm the gut epithelium,” Dr. Romo noted. “Antibiotics also trigger fungal overgrowth in the gut due to their inefficacy against fungi.”

This shift creates an environment dominated by C. difficile and fungi, potentially setting the stage for severe C. difficile infections (CDI).

However, the exact dynamics remain ambiguous due to conflicting data. Some studies suggest fungi play a role in CDI, while others propose protective effects, such as Candida preventing C. difficile growth. Conversely, studies show negative impacts, especially during fecal microbiota transplants, where Candida albicans increase transplant rejection rates, highlighted.

“The role of these fungi in this environment remains unclear,” Dr. Romo emphasized, despite the observed activity.

N. glabrata, found in various environments including soil, water, and human guts, can cause opportunistic infections in immunocompromised individuals. Resistant to common antifungals like azoles, N. glabrata forms biofilms for survival.

Dr. Romo’s research focuses on N. glabrata’s role in CDI and its mechanisms. Studies indicate N. glabrata colonizes most of the gastrointestinal tract, much like C. difficile, suggesting similar responses to antibiotic treatment.

In a mouse model study, administering C. glabrata (pre-nomenclature change) alongside C. difficile resulted in earlier deaths compared to C. difficile alone, highlighting exacerbated disease outcomes, as per

“While C. glabrata alone does not cause illness in animals, its presence with C. difficile accelerates disease progression,” Dr. Romo explained. Further investigations reveal earlier toxin production in co-infected animals, underscoring the exacerbating role of both organisms in CDI.

Dr. Romo continues to explore the intricate interactions between C. difficile and N. glabrata, emphasizing their mutual exploitation within the gastrointestinal environment.

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