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Small Bowel Bacterial Overgrowth: Presentation, Diagnosis, and Treatment Virmeet V Small Bowel Bacterial Overgrowth: Presentation, Diagnosis, and Treatment Virmeet V. Singh, MD and Phillip P. Toskes, MD Address A comprehensive understanding of SBBO requires a Department of Medicine, Division of Gastroenterology, Hepatology sound knowledge of several key aspects of the gastrointesti- and Nutrition, University of Florida, PO Box 100214, Gainesville, FL nal tract, including motility, physiology of nutrient absorp- 32610-0214, USA. E-mail: [email protected] tion, and indigenous flora. In this review, emphasis is placed on pitfalls in the diagnosis of SBBO and recent Current Gastroenterology Reports 2003, 5:365–372 Current Science Inc. ISSN 1522-8037 trends in the management of this clinical condition. Copyright © 2003 by Current Science Inc. Small bowel bacterial overgrowth (SBBO) syndrome is Pathophysiology Understanding the pathophysiology of SBBO involves associated with excessive numbers of bacteria in the an intimate knowledge of small bowel homeostasis, proximal small intestine. The pathology of this condition mechanisms of malabsorption, and predisposing factors involves competition between the bacteria and the human for the disorder. host for ingested nutrients. This competition leads to intraluminal bacterial catabolism of nutrients, often with Homeostasis production of toxic metabolites and injury to the entero- In the healthy human host, control of the growth of enteric cyte. A complex array of clinical symptoms ensues, result- bacterial populations is multifactorial. The most important ing in chronic diarrhea, steatorrhea, macrocytic anemia, control mechanisms are the ability of gastric acid to inhibit weight loss, and less commonly, protein-losing enteropa- or kill swallowed microorganisms and the cleansing effects thy. Therapy is targeted at correction of underlying small of normal intestinal motility [1]. Other important mecha- bowel abnormalities that predispose to SBBO and appro- nisms include immunoglobulins in the intestinal secre- priate antibiotic therapy. The symptoms and signs of tions and an intact ileocecal valve. Achlorhydria resulting SBBO can be reversed with this approach. from gastric mucosal atrophy, gastric resection, vagotomy, or highly effective antacid or antisecretory therapies permit viable swallowed bacteria to pass into the small intestine Introduction [6–9]. When overgrowth of bacteria occurs in the small bowel In the small bowel, the cleansing action of antegrade proximal to the distal ileum, symptoms of vitamin malab- peristalsis, especially the migratory motor complex sorption, malnutrition, and weight loss may occur. This (MMC), is responsible for sweeping bacteria into the colon clinical entity is known as blind loop, stagnant loop syn- [10]. Thus, conditions that result in dysmotility of the drome, or small bowel bacterial overgrowth (SBBO) syn- small bowel are frequently complicated by bacterial over- drome. In this syndrome the enteric flora of the proximal growth, which may not necessarily be symptomatic [1,6,7]. small intestine resemble those of the healthy colon [1]. Stagnation of intraluminal flow and incomplete The high concentration of bacteria interferes with normal competence of the ileocecal sphincter account for the small bowel nutrient absorption, and patients develop ordinarily higher bacterial counts in the distal ileum. In malnutrition and such gastroenterologic symptoms as the colon, bacterial interaction, competition for nutri- diarrhea, steatorrhea, and macrocytic anemia, which can ents, and the anaerobic environment attributable to bac- significantly impair quality of life. Patients at risk are those terial metabolism are significant factors that control with dysmotility syndromes, anatomic alterations of the microbial populations. gastrointestinal tract secondary to surgery, certain medical Antibiotic therapy is known to alter microflora of the conditions, or advanced age. SBBO may also be an under- intestinal tract by the eradication or suppression of appreciated cause of malnutrition in the elderly [2–4]. selected populations of bacteria while permitting resistant Treatment options are aimed at returning the small intes- microbes to flourish. These effects depend on the composi- tine to its normal bacterial environment, which includes tion of the native enteric flora and the spectrum of activity, treatment of predisposing conditions associated with bac- dose, route of administration, duration of treatment, and terial overgrowth and antibiotic therapy [5••]. pharmacokinetics of the antibiotic [11]. 366 Small Intestine Table 1. Clinical conditions associated with are normally secreted to form mixed micelles with partially bacterial overgrowth digested dietary lipids. These conjugated bile salts are not readily reabsorbed until they reach the ileum. When bacte- Gastric ria overgrow in the proximal small bowel, they deconju- Hypochlorhydria or achlorhydria: atrophic gastropathy, gate bile salts to form free bile acids, which are readily gastrectomy, vagotomy Sustained hypochlorhydria induced by absorbed by the jejunum. This process may impair forma- proton-pump inhibitors tion of the bile–salt–lipid micelle complex, so that dietary Surgery fat is malabsorbed. In addition, the free bile acids formed Resection of diseased ileocecal valve in SBBO may be toxic to the mucosa and contribute Afferent loop of Billroth II partial gastrectomy directly to the patchy mucosal lesion of SBBO [15]. Malab- Surgical blind loop (end-to-side anastomosis) sorption of fat-soluble vitamins (vitamins A, D, E, and K) Anatomic Intestinal obstruction (stricture, inflammation, neoplasm, may occur as a consequence of general fat malabsorption, radiation enteropathy) but this is seldom of any clinical significance. Duodenal-jejunal diverticulosis Carbohydrate malabsorption may also be a conse- Gastrocolic or jejunocolic fistula quence of SBBO. This may result from a combination of Dysmotility intraluminal carbohydrate degradation by bacteria and Scleroderma damage to the brush border disaccharidase functions of Idiopathic intestinal pseudoobstruction the small bowel mucosa. Furthermore, malabsorbed carbo- Absent or disordered migrating motor complex Diabetic autonomic neuropathy hydrates can be catabolized by small bowel and colonic Miscellaneous medical conditions bacteria to form short-chain organic acids that increase Crohn’s disease osmolarity of the intestinal fluid and contribute to diar- Chronic pancreatitis rhea. Protein malabsorption results from a combination of Cirrhosis impaired absorption of amino acids, intraluminal utiliza- Immunodeficiency syndromes tion of protein by bacteria, and protein-losing enteropathy End-stage renal disease caused by mucosal damage and leakage of protein into the lumen [1,16–18]. Cobalamin (vitamin B12) deficiency that cannot be There is some evidence to support a contributing role corrected by intrinsic factor but improves after antibiotic of the immune system in the regulation of the intestinal administration is a classic manifestation of SBBO. At the flora. Patients with SBBO may have altered levels of resident pH of the proximal small bowel, gastric intrinsic intraluminal secretory IgA or increased mucosal IgA immu- factor normally binds tightly to cobalamin, facilitating its nocytes [12,13]. However, bacterial overgrowth in the eld- absorption in the distal ileum. However, in SBBO, various erly seems not to be related to immunosenescence [14]. anaerobic and facultative gram-negative aerobes competi- Other modulating factors that are less well described tively utilize dietary cobalamin. Intrinsic factor inhibits include the bacterial production of bacteriocins, toxic cobalamin utilization by aerobic bacteria but has no effect metabolites, transfer of antibiotic resistance, and the role on the ability of gram-negative anaerobic flora to take up of the mucosa in elaborating growth factors. Little evidence dietary cobalamin [19]. Although enteric bacteria also syn- is available to indicate a significant role for dietary compo- thesize some cobalamin, they retain this vitamin, and thus sition or manipulation on regulation of the microbial pop- it remains unavailable to the host for absorption. Paradox- ulation of the normal bowel [1]. ically, cobalamin deficiency then ensues in patients with SBBO although they harbor large quantities of the vitamin Mechanisms of malabsorption within bacteria in their small bowel. In general, malabsorption in SBBO can be attributed to the Two additional factors may contribute to the pathogen- intraluminal effects of proliferating bacteria combined esis of diarrhea and other features of SBBO. First, such bac- with the damage to small bowel enterocytes. A characteris- terial metabolites as free bile acids, hydroxylated fatty tic microscopic small bowel mucosal lesion is usually seen, acids, and other organic acids stimulate secretion of water consisting of villous blunting, loss of structural integrity of and electrolytes into the bowel lumen. This effect may con- epithelial cells, and inflammatory infiltrate of the lamina tribute to the secretory diarrhea in SBBO. Second, experi- propria. Various functional consequences of this damage mental bacterial overgrowth in rats may induce further have been detected, including diminished disaccharidase dysmotility of the bowel, which may encourage further activity; decreased transport of monosaccharides, amino bacterial overgrowth [20]. acids, and fatty acids; and protein-losing enteropathy [1]. Fat malabsorption (steatorrhea) in SBBO is a conse-
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