What is the pathophysiology of food poisoning?

Pathophysiology of Food Poisoning

Food poisoning results from multiple distinct pathophysiological mechanisms including preformed bacterial toxins causing direct cellular damage, bacterial invasion triggering inflammatory responses with fluid shifts into the gastrointestinal lumen, and histamine-mediated reactions causing vasodilation and systemic symptoms.

Primary Mechanisms

Preformed Toxin-Mediated Pathways

Bacterial toxins produced during food storage cause direct cellular injury without requiring bacterial invasion. 1

• Botulinum toxin blocks acetylcholine release by inhibiting synaptic vesicle fusion with plasma membranes through its light chain component, resulting in descending paralysis 2
• Cholera toxin consists of A and B subunits; the B subunit binds cell membranes, allowing internalization where the A subunit increases adenylate cyclase activity and cAMP levels, causing massive fluid and electrolyte efflux 2
• Staphylococcus aureus and Clostridium perfringens produce toxins causing rapid-onset gastrointestinal symptoms through direct mucosal irritation 3

Bacterial Invasion and Inflammatory Response

Invasive pathogens trigger systemic inflammatory cascades that fundamentally alter gastrointestinal physiology. 2

• Campylobacter jejuni (the most common bacterial trigger worldwide) causes gastroenteritis through mucosal invasion, with frequencies of 60-70% in certain regions like Bangladesh and China 2
• Bacterial invasion activates inflammatory cytokines (IL-1β, TNF) and stress-response mediators (cortisol), inducing catabolic processes 2
• Inflammation increases intestinal permeability through mucosal damage, allowing fluid shift into the gastrointestinal lumen 2

Histamine-Mediated Toxicity (Scombroid Poisoning)

Histamine accumulation in improperly stored fish causes vasodilation with paradoxical hypertension in some patients, along with distinctive oral burning and urticaria. 3

• Presents with peppery taste, oral burning, flushing, urticaria, and potentially bronchospasm 3
• Can cause cardiovascular instability requiring epinephrine in severe cases 3
• Symptoms typically occur within 2-6 hours of ingestion 3

Immune-Mediated Mechanisms

Non-IgE Mediated Pathways

Food protein-induced enterocolitis syndrome (FPIES) involves antigen-specific T cells and cytokines causing colonic and ileal inflammation without classic IgE involvement. 2

• Inflammation increases intestinal permeability with fluid shifts causing profuse vomiting 1-4 hours post-ingestion 2
• Can present with extreme lethargy, marked pallor, hypotension, and hypothermia 2
• Some patients paradoxically have IgE to trigger foods, suggesting overlapping mechanisms 2
• Successful ondansetron use implies neuroimmune mechanism involvement 2

Host-Dependent Metabolic Factors

Metabolic capacity deficiencies cause osmotic gastrointestinal effects independent of immune activation. 2

• Lactose and fructose intolerance result from inadequate enzymatic breakdown 2
• FODMAPs trigger osmotic effects, promote undesirable bacterial fermentation, and alter microbiota composition causing inflammation 2

Systemic Metabolic Consequences

Acute infection triggers massive lipolysis through inflammatory cytokines, adrenalin, glucocorticoids, and glucagon, with plasma triglycerides and free fatty acids increasing up to four-fold. 2

• Simultaneously, inflammation downregulates fatty acid oxidation enzymes, causing toxic FFA accumulation in organs 2
• This creates severe organ damage and energy deprivation by interfering with mitochondrial function 2
• Sickness-associated anorexia may represent adaptive response promoting catabolic, lipid-utilizing state with reduced inflammation 2

Clinical Timeframes and Presentations

Symptom onset varies dramatically by mechanism: preformed toxins cause symptoms within hours, while invasive pathogens may take days to weeks. 4

• Typical symptoms include nausea, vomiting, watery diarrhea, abdominal pain, cramps, and fever 4
• Duration ranges from hours to several days depending on pathogen 4
• Anthrax (though rare) causes massive edema and organ failure through three-component toxin system (protective antigen, edema factor, lethal factor) released after macrophage lysis 2

Common Pitfalls

• Distinguishing between viral gastroenteritis and FPIES requires meeting specific diagnostic criteria (major criterion plus ≥3 minor criteria) 2
• Scombroid poisoning can mimic allergic reactions but requires antihistamine treatment rather than allergen avoidance 3
• Geographic variation significantly affects pathogen likelihood: respiratory infections predominate in developed nations while gastroenteritis is more common in South Asia 2