Dietary or supplemental fermentable fiber intake reduces the presence of Clostridium XI in mouse intestinal microbiota: The importance of higher fecal bacterial load and density.

objectivesClostridium difficile infection is a public health concern. C. difficile was found in healthy human intestine as a member of Clostridium XI. Because soluble fermentable fiber ingestion affects intestinal microbiota, we used fiber-containing diets to determine the intestinal microbial condition that could reduce the presence of Clostridium XI.

methodsNewly weaned male mice were assigned to three published diets: Control AIN-93G purified diet with only poorly fermented cellulose; Control plus 5% purified fermentable fiber inulin; Chow with wheat, soybean and corn that provide a mixture of unpurified dietary fibers. Methods were developed to quantify 24-hour fecal microbial load and microbial DNA density. The relative abundance of bacterial genera and the bacterial diversity were determined through 16S rRNA sequence-based fecal microbiota analysis.

resultsMice adjusted food intake to maintain the same energy intake and body weight under these three moderate-fat (7% w:w) diets. Chow-feeding led to higher food intake but also higher 24-h fecal output. Chow-feeding and 1-8 wk ingestion of inulin-supplemented diet increased daily fecal microbial load and density along with lowering the prevalence of Clostridium XI to undetectable. Clostridium XI remained undetectable until 4 weeks after the termination of inulin-supplemented diet. Fermentable fiber intake did not consistently increase probiotic genera such as Bifidobacterium or Lactobacillus. Chow feeding, but not inulin supplementation, increased the bacterial diversity.

conclusionsIncrease fecal microbial load/density upon fermentable fiber ingestion is associated with a lower and eventually undetectable presence of Clostridium XI. Higher bacterial diversity or abundance of particular genera is not apparently essential. Future studies are needed to see whether this observation can be translated into the reduction of C. difficile at the species level in at-risk populations.