What is the pathophysiology of Small Intestine Bacterial Overgrowth (SIBO)?

Pathophysiology of Small Intestinal Bacterial Overgrowth (SIBO)

Core Pathophysiological Mechanism

SIBO develops when protective mechanisms that normally maintain low bacterial counts in the small intestine fail, allowing excessive bacterial proliferation—typically defined as >10⁵ colony-forming units/mL of coliform bacteria in the proximal jejunum. 1

The pathophysiology centers on disruption of multiple endogenous defense systems that work synergistically to prevent bacterial colonization of the small bowel. 2, 3

Primary Defense Mechanisms That Fail in SIBO

Impaired Migrating Motor Complex (MMC)

• The MMC normally clears intestinal debris and prevents bacterial stasis through coordinated propulsive contractions. 2, 3
• When the MMC is disrupted, gut stasis occurs with failed forward propulsion, creating stagnant loops where anaerobic bacteria proliferate in accumulated intestinal contents. 2
• Neuropathies (enteric or autonomic) alter intestinal coordination, causing non-propulsive contractions that lead to bacterial accumulation. 2
• This mechanism is particularly prominent in diabetic patients with autonomic neuropathy and in pseudo-obstruction syndromes. 2

Loss of Gastric Acid Barrier

• Gastric acid normally prevents bacterial colonization of the stomach and proximal small intestine. 3, 1
• Proton pump inhibitors reduce this acid barrier, allowing bacterial overgrowth to develop. 2, 3
• This represents a distinct pathological state where gastric bacterial overgrowth can occur without meeting criteria for SIBO. 3

Ileocecal Valve Incompetence

• An intact ileocecal valve prevents reflux of colonic bacteria backward into the small intestine. 2, 3
• Surgical resection or functional incompetence allows colonic bacteria to migrate proximally, establishing overgrowth. 2, 4

Impaired Bacteriostatic Secretions

• Pancreatic and biliary secretions provide bacteriostatic properties in the small intestine. 2, 3
• Pancreatic insufficiency reduces these protective secretions, with SIBO complicating up to 92% of chronic pancreatitis cases with exocrine insufficiency. 2, 4

Defective Local Immunity

• Altered intestinal immunoglobulin secretion compromises bacterial population control. 2, 3
• Impaired local intestinal immunity allows bacterial proliferation despite other intact defense mechanisms. 2

Specific Etiological Categories

Motility Disorders

• Medications affecting motility (vincristine, anticolinérgicos, clozapina) induce SIBO by disrupting the MMC. 2
• Chronic intestinal pseudo-obstruction represents severe dismotility where SIBO becomes practically inevitable. 2
• In severe chronic dismotility, SIBO can cause cachexia even without evident diarrhea. 2

Anatomic Alterations

• Prior abdominal surgery, particularly procedures altering normal intestinal anatomy, creates conditions for bacterial stasis. 2, 4
• Surgical changes that disrupt normal flow patterns or create blind loops promote bacterial accumulation. 4

Multifactorial Nature

• In most patients, SIBO etiology is multifactorial with more than one mechanism involved simultaneously. 2, 4
• The combination of dilated gut segments and reduced propulsion creates ideal conditions for bacterial colonization. 2

Microbiome Alterations in SIBO

Quantitative vs. Qualitative Changes

• SIBO represents true quantitative bacterial overgrowth in the small intestine (>10⁵ CFU/mL). 1, 5
• This differs from colonic dysbiosis, which manifests as qualitative changes in bacterial composition rather than simple overgrowth. 3
• Studies show depletion of beneficial anaerobes (Bacteroides, Bifidobacterium, Lactobacillus, Eubacterium) in affected patients. 3

Metabolic Consequences

• Bacterial overgrowth disrupts normal bacterial balance, leading to altered metabolism of nutrients and substrates. 6
• This metabolic disruption contributes to malabsorption of micro- and macronutrients in severe cases. 1

Clinical Manifestations Arising from Pathophysiology

• Bacterial fermentation of intestinal contents produces bloating, flatulence, and abdominal distention. 1, 5
• Bacterial deconjugation of bile acids impairs fat absorption, contributing to diarrhea and malabsorption. 1
• Bacterial consumption of vitamin B12 and production of folate create characteristic nutritional deficiency patterns. 1
• Mucosal inflammation from bacterial products and metabolites causes abdominal pain. 5

Important Pathophysiological Distinctions

A critical pitfall is confusing SIBO with other forms of bacterial alterations: gastric bacterial overgrowth from PPI use does not equal SIBO, and colonic dysbiosis represents altered composition rather than small intestinal overgrowth. 3 Breath test abnormalities often reflect rapid transit with colonic fermentation rather than true small intestinal bacterial proliferation. 3

The pathophysiology explains why treatment must address underlying causes (motility disorders, anatomic issues, acid suppression) rather than simply administering antibiotics. 7, 1, 5 SIBO is not contagious and develops from overgrowth of bacteria already present in the gastrointestinal tract, requiring underlying predisposing factors rather than person-to-person transmission. 4