Colonization Resistance

Varying levels of bacteria throughout the GI tract have inherent benefit to the function of each portion of the GI tract. Thus, selective discouragement of colonization is necessary. For example, the low number of bacteria in the small bowel allows the function of nutrient breakdown and absorption. Intrinsically, the small bowel limits the levels of bacteria through antegrade peristalsis, and bactericidal action of the gastric acid and biliary enzymes of the liver. The ileocecal valve at the terminal end of the small bowel functions as a gate deterring the entrance of colonic bacteria into the small bowel. Presence of higher concentrations of colonic bacteria causes mucosal inflammation and villous atrophy ultimately interfering in its function.

Bacterial overgrowth syndrome is due to anatomical and physiologic alterations of the small bowel causing proliferation of bacteria in the upper GI tract. Conditions causing hypochlorhydria (decreased secretion of hydrochloric acid) such as gastritis, drug therapy, and dysmotility contribute to bacterial overgrowth. Surgical or anatomical malformations resulting in ineffective peristalsis or absence of the ileocecal valve also contribute to this syndrome. Impaired micelle formation causes fat malabsorption and steatorrhea. Higher levels of free bile acids in the proximal portion of the small bowel bind with vitamin B12 thus preventing absorption in the terminal end. Additionally, amino acid and carbohydrate malabsorption occurs leading to increased fecal nitrogen, lower serum proteins, and ultimately protein calorie malnutrition.

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