Foodborne illness (food poisoning)
Foodborne illness is acute gastrointestinal disease from a contaminated food, and the incubation period after the meal is the single fastest clue to the pathogen, splitting a short 1-6 hour vomiting-predominant preformed-toxin illness from an 8-16 hour toxin-mediated diarrhea and a longer than 16 hour invasive, often febrile or bloody, illness. Management rests on oral rehydration for nearly everyone, with antibiotics reserved for specific pathogens or severe disease and withheld in suspected enterohemorrhagic E coli because they raise the risk of hemolytic uremic syndrome.
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What this article covers
- Overview
Definition: foodborne illness is acute nausea, vomiting, diarrhea, or cramping from a preformed toxin, an in vivo-produced toxin, or an invasive pathogen ingested in contaminated food or water.
- Epidemiology
Nontyphoidal Salmonella: the most common bacterial cause of foodborne illness in the United States, from poultry, beef, eggs, milk, or reptile/amphibian contact.
- Risk factors
Improper food handling and storage: room-temperature holding allows S aureus and B cereus toxin formation; inadequate cooling before rewarming allows C perfringens spore germination.
- Pathophysiology
Preformed toxin ingestion (short incubation): S aureus and B cereus (cereulide) toxins form in the food before it is eaten and act directly on the gut and vomiting centers; both are heat-stable and survive cooking.
- Clinical features
Vomiting-predominant illness, onset 1 to 6 hours after the meal: abrupt severe vomiting with cramps, little or no fever, resolving within 24 hours; a preformed toxin (S aureus from mayonnaise, cream…
- Differential diagnosis
Enterohemorrhagic E coli hemorrhagic colitis: bloody diarrhea and severe cramps without fever, a pattern requiring recognition because antibiotics are harmful (hemolytic uremic syndrome is the feared complication).
- Diagnosis
This is primarily a clinical diagnosis from the food and timing history plus symptom pattern, not a laboratory diagnosis: the implicated food, the incubation band (1-6 h vomiting-predominant, 8-16 h…
- Management
Start oral rehydration first, in nearly every patient: oral rehydration solution in frequent small volumes, advancing to a regular diet once vomiting is controlled; sufficient alone for most non-invasive illness.
- Complications
Hemolytic uremic syndrome: microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney injury in under 10% of EHEC infections, about a week in as diarrhea improves; the leading harm from…
- Prognosis
Excellent for the great majority: toxin-mediated illness (S aureus, B cereus, C perfringens) is self-limited, resolving within 24 hours (S aureus, B cereus emetic) to 24-48 hours (C perfringens, B cereus diarrheal).
- Prevention
Cook to safe internal temperatures: ground beef and pork to at least 160 F (71 C), poultry to at least 165 F (74 C), seafood to at least 145 F (63 C), by thermometer.
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Related articles
- Salmonella infection
Salmonella infection splits into nontyphoidal disease, a usually self-limited foodborne gastroenteritis that can bacteremically seed bone and joints in sickle cell disease, and typhoidal disease (S. Typhi/Paratyphi), a prolonged travel-associated bacteremic enteric fever with stepwise fever, relative bradycardia, and rose spots. Nontyphoidal disease is diagnosed by stool culture and managed supportively, while enteric fever is diagnosed by blood culture and always treated with antibiotics.
- Shigella infection (shigellosis)
Shigella infection is a highly contagious bacillary dysentery caused by a very low inoculum of an invasive gram-negative rod, presenting with fever, crampy abdominal pain, tenesmus, and small-volume bloody or mucoid diarrhea. Diagnosis rests on stool culture or molecular testing, and unlike most enteric infections, antibiotics are indicated to shorten illness and limit person-to-person spread.
- Diarrhea
Diarrhea is three or more unformed stools daily, split by duration into acute (under 14 days, usually infectious), persistent (14 to 30 days, often parasitic), and chronic (over 30 days, usually noninfectious), and by mechanism into osmotic, secretory, inflammatory, malabsorptive, and motility diarrhea. Acute diarrhea is managed with rehydration and tested only when red-flag features are present, while chronic diarrhea is worked up by mechanism using stool studies, celiac serology, fecal calprotectin, and endoscopy.
- Clostridioides difficile infection
Clostridioides difficile infection is toxin-mediated colitis that follows disruption of normal colonic flora, most often by antibiotics, and ranges from watery diarrhea to fulminant colitis with shock, ileus, or megacolon. Diagnosis rests on unformed stool testing (NAAT and/or toxin EIA) in a patient with three or more unformed stools in 24 hours, and treatment is chosen by IDSA/SHEA severity grade, oral vancomycin or fidaxomicin for 10 days, escalating to high-dose vancomycin plus IV metronidazole for fulminant disease.
- Cholera
Cholera is a toxigenic Vibrio cholerae infection causing sudden, voluminous rice-water diarrhea from cyclic-AMP-driven intestinal secretion, diagnosed clinically and confirmed by stool culture, and treated primarily with volume-for-volume rehydration plus a single-dose antibiotic.
- Hemolytic uremic syndrome
Hemolytic uremic syndrome is a thrombotic microangiopathy defined by the triad of microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney injury, most often triggered in children by Shiga toxin-producing Escherichia coli O157:H7 after bloody diarrhea. Diagnosis rests on schistocytes with a negative Coombs test plus a normal ADAMTS13 level to exclude TTP, and typical STEC-HUS is managed supportively while antibiotics and antimotility agents are avoided, whereas complement-mediated atypical HUS requires eculizumab.
- Guillain-Barre syndrome
Guillain-Barre syndrome is an acute, post-infectious autoimmune polyradiculoneuropathy causing rapidly progressive ascending flaccid weakness and areflexia. Diagnosis is clinical, supported by albuminocytologic dissociation on CSF and demyelinating changes on electrodiagnostic studies; first-line treatment is IVIG or plasma exchange with close monitoring for respiratory failure.