This approach to diagnosis is limited by the inability to differentiate disease-promoting microbes from potentially beneficial microbes and the inability to sample microbes in different regions of the small intestine. This has been extrapolated for the diagnosis of SIBO in other conditions. SIBO is currently defined as ≥ 10 5 CFU/mL (colony-forming units per ml) on aspirate culture, based on the initial description in Billroth II anatomy patients with stagnant loop syndrome 15, 16, 17. SIBO is implicated in driving GI symptoms such as diarrhea, abdominal pain, and bloating the gold standard test for SIBO is a duodenal aspirate culture to measure microbial density in the duodenum 12, 13, 14. The bolus transport in the duodenum, however, may be decreased or associated with retrograde bolus transfer events in diabetic gastroparesis 11. The ileum primarily serves as a reservoir 9 and exhibits significant differences in motor function when compared with the upper small intestine, which acts as a conduit 10 with little stasis and lower bacterial counts. There are additional small studies that have characterized the small intestinal microbial composition using ileostomy effluent samples that allow for easier collection 7, 8, but are not necessarily reflective of normal small intestinal microbiota. Recent studies comparing small bowel mucosal microbiota (obtained via either Watson capsule biopsy or enteroscopy with biopsy) in IBS patients and healthy volunteers in Sweden and in Taiwan found either no changes or IBS-associated increases in Prevotella spp., respectively 5, 6. This is relevant, as a quantitative increase in the small intestinal bacteria, characterized as small intestinal bacterial overgrowth (SIBO), has been implicated in symptoms associated with FGIDs, though mechanisms underlying this effect remain poorly defined.įew studies have attempted to characterize the small intestinal microbiota, primarily owing to the difficulty in accessing the small intestine and lower microbial density that makes it difficult to obtain sufficient bacterial DNA 4. The small intestinal microbiome, however, remains relatively unexplored in most GI disorders including FGIDs. The majority of microbiome studies focus on stool, which is broadly reflective of the GI microbiome, and the colonic mucosa, where microbes may play a role in triggering inflammation 3. Its role in modulating important physiological processes such as GI motility and secretion, maintenance of epithelial barrier integrity, and its role in communication between the gut and the central nervous system may underlie its contribution to symptoms associated with FGIDs such as irritable bowel syndrome (IBS) 1, 2. The human gut microbiome has emerged as an important factor in the pathogenesis of functional gastrointestinal (GI) disorders (FGIDs). Our findings demonstrate that characterizing small intestinal microbiomes in patients with gastrointestinal symptoms may allow a more targeted antibacterial or a diet-based approach to treatment. In a pilot interventional study we found that switching from a high fiber diet to a low fiber, high simple sugar diet triggered FGID-related symptoms and decreased small intestinal microbial diversity while increasing small intestinal permeability.
Small intestinal microbial composition, on the other hand, is significantly altered in symptomatic patients and does not correspond with aspirate culture results.
Here we show that SIBO based on duodenal aspirate culture reflects an overgrowth of anaerobes, does not correspond with patient symptoms, and may be a result of dietary preferences. Small intestinal bacterial overgrowth (SIBO) has been implicated in symptoms associated with functional gastrointestinal disorders (FGIDs), though mechanisms remain poorly defined and treatment involves non-specific antibiotics.