Infectious diarrhoea and foodborne illness

• Infectious diarrhoea ranges from a few unformed stools to life-threatening dehydration or dysentery; most acute cases are short, self-limited viral or unknown infections.
• The first questions are always the same: how dehydrated is the patient, are there red flags (blood, fever, age, immunocompromise, recent antibiotics), and what was eaten, drunk, swum in, or travelled through.
• Rehydration saves lives; reduced-osmolarity oral rehydration solution is first choice for mild to moderate dehydration, and intravenous isotonic fluid is needed for shock or severe dehydration.
• Antibiotics help in specific syndromes (dysentery, enteric fever, severe cholera, high-risk salmonellosis, symptomatic Shigella) but are unnecessary or harmful in most watery diarrhoea, and are avoided in EHEC because they may trigger haemolytic uraemic syndrome.
• A shared logic runs through the topic: identify the syndrome, support the patient, test selectively, treat the disease you can name, and report what public health needs to know.

By the end of this page you should be able to:

1. Classify infectious diarrhoea by duration and presentation (watery, dysenteric, toxin-mediated, persistent) and link each to its likely organisms.
2. Use the master organism table to match a source and incubation period to the clinical picture.
3. Order and interpret selective stool studies, including culture and multiplex nucleic acid testing, without over-investigating self-limited illness.
4. Choose rehydration, symptomatic treatment and antimicrobial therapy safely, recognising the main "traps" (antimotility drugs in fever or bloody diarrhoea, antibiotics in STEC).
5. Recognise the major extraintestinal complications and apply public-health reporting and prevention measures, including in low-resource settings.

Diarrhoea is an increase in stool frequency or a fall in stool consistency relative to that person's usual pattern, rather than any single count. Infectious diarrhoea is caused by a swallowed pathogen or its toxin. It is classified by duration: acute (under 2 to 3 weeks), persistent (2 to 4 weeks) and chronic (4 weeks or more), and by presentation: watery (small-bowel or secretory), dysenteric (frequent scant bloody stools with fever and tenesmus, indicating colonic invasion) and toxin-mediated (rapid vomiting or brief cramping illness after a suspect meal). The distinction between a toxic food poisoning and an invasive infection is clinically important, because it decides whether investigation and antibiotics are needed.

The burden of diarrhoeal disease falls hardest on children and older adults. Acute gastroenteritis is one of the commonest illnesses in every country, and infectious diarrhoea remains a leading cause of death in children aged 1 to 59 months. The causative mixture shifts with setting: in industrialised settings norovirus and nontyphoidal Salmonella lead the bacterial causes of hospitalisation and death; rotavirus dominated before vaccine introduction, and norovirus has taken the lead since. Campylobacter, Shigella, Yersinia and E. coli O157 together caused an estimated 291,000 illnesses in children under 5 in one US surveillance assessment. In low-resource settings, the dominant pathogens are E. coli (enterotoxigenic, enteropathogenic, enteroinvasive), Shigella, Salmonella (typhoidal and nontyphoidal), Campylobacter, V. cholerae, E. histolytica, Giardia, Blastocystis, Cyclospora, Cystoisospora and Cryptosporidium. Even in well-resourced settings, a considerable burden comes from endemic and outbreak-associated infection, and the low inoculum of organisms such as Shigella, E. histolytica, Giardia, norovirus, rotavirus and STEC means outbreaks spread easily in families, childcare, long-term care and recreational water venues. ^[1]

Most acute diarrhoea is infective, and most episodes are mild and self-resolving. The likely organism is driven by the patient, the food and the context:

• Food source tells much. Undercooked poultry and eggs suggest Salmonella and Campylobacter; beef and minced meat suggest STEC; pork or wild game and undercooked pork products suggest Yersinia and Trichinella; shellfish suggest Vibrio species and norovirus; unpasteurised milk or soft cheese suggests Salmonella, Campylobacter, Yersinia, S. aureus and Listeria; fruits, vegetables and sprouts suggest STEC, Salmonella, Cyclospora and Cryptosporidium. ^[1]
• Setting. Childcare outbreaks raise rotavirus, Cryptosporidium, Giardia and Shigella; long-term care and hospitals raise norovirus and C. difficile; swimming raises Cryptosporidium; farm and petting-zoo contact raises STEC, Cryptosporidium and Campylobacter; contact with young poultry or reptiles raises nontyphoidal Salmonella. ^[1]
• Host. Nontyphoidal Salmonella is more invasive in infants under 3 months, adults over 50 with atherosclerosis, immunocompromise and haemoglobinopathy. Yersinia and Salmonella are more dangerous with iron overload or liver disease. Immunocompromise (especially advanced HIV) opens the door to Cryptosporidium, Cyclospora, Cystoisospora, microsporidia, Mycobacterium avium complex and cytomegalovirus. ^[1]
• Recent antibiotics or hospitalisation within about 8 to 12 weeks redirect attention to C. difficile and resistant Salmonella. ^[1]
• Recent international travel redirects the differential to the region: E. coli (ETEC, EPEC, EAEC), Shigella, typhoidal and nontyphoidal Salmonella, Campylobacter, V. cholerae, E. histolytica, Giardia and the coccidian parasites; enteric fever presents with fever, headache and abdominal pain, with diarrhoea often absent. ^{[1] [3]}

The table below is the working reference for the rest of the page. Incubation periods and incubation windows come from the CDC confirming-an-etology tables and food-safety pages; stronger or weaker statements are flagged in the text.

These illnesses are not tissue infections but intoxications with pre-formed toxins, so they are brief and often begin within hours; testing stool or leftover food for toxin confirms the diagnosis. Staphylococcus aureus causes nausea, vomiting, cramps and sometimes diarrhoea 30 minutes to 8 hours after eating food handled after cooking. Bacillus cereus has two syndromes: an emetic syndrome (1 to 6 hours, vomiting, often fried rice) and a diarrhoeal syndrome (6 to 24 hours, cramps and diarrhoea). Clostridium perfringens causes diarrhoea and cramps 6 to 24 hours after meat or poultry held at unsafe temperatures, with vomiting and fever uncommon. ^{[4] [5]}

Typhoid and paratyphoid fever are systemic bacteremic illnesses, not simple diarrhoea. Typhoid incubates for 6 to 30 days and paratyphoid for 1 to 10 days. Illness begins gradually with rising fever (39 to 40 °C), headache, malaise, anorexia, abdominal pain and constipation or diarrhoea; hepatosplenomegaly and a transient rose-spot rash may appear. About 9.2 million cases of typhoid and 3.8 million of paratyphoid occur each year worldwide, causing about 133,000 deaths; serious complications such as intestinal haemorrhage, perforation and encephalopathy occur in 10 to 15% of hospitalised patients, usually after 2 to 3 weeks. Untreated mortality historically exceeded 10%; with prompt care it is under 1%. Relapse occurs in up to 10% and 1 to 4% become chronic carriers. Blood culture is the preferred diagnostic test. Empiric treatment follows the travel history: azithromycin for uncomplicated cases in travellers from most countries and ceftriaxone or azithromycin as appropriate, azithromycin for those returning from Iraq or Pakistan or without international travel, and a carbapenem for complicated XDR disease; treatment is then narrowed to the isolate's susceptibilities. ^[3]

Yersinia enterocolitica causes fever and diarrhoea, then right-lower-quadrant pain from mesenteric adenitis that can mimic appendicitis, especially in school-aged children; it is linked to pork, chitterlings and unpasteurised dairy, and is more dangerous in people with iron overload or chronic liver disease. Campylobacter is the commonest bacterial cause of bloody diarrhoea in many industrialised settings and is followed, in susceptible people, by Guillain-Barre syndrome and reactive arthritis. Shigella triggers dysentery with fever and tenesmus, seizures in young children, and HUS after S. dysenteriae type 1; non-O157 and other STEC can also cause bloody diarrhoea with little fever. Post-infectious complications across these infections include reactive arthritis (Salmonella, Shigella, Campylobacter, Yersinia, rarely Giardia and Cyclospora), Guillain-Barre syndrome (Campylobacter), haemolytic uraemic syndrome (STEC, mainly types carrying Shiga toxin 2, and Shigella dysenteriae type 1), glomerulonephritis, IgA nephropathy, and post-infectious irritable bowel syndrome (Campylobacter, Salmonella, Shigella, STEC, Giardia). Shigella also causes the Ekiri syndrome, a lethal toxic encephalopathy with seizures, and Listeria is an important cause of meningitis, especially in infants under 3 months and pregnant or immunocompromised people. ^[1]

Although parasites more often cause persistent than acute diarrhoea, three helminth infections have a clear gastrointestinal presentation and serious acute complications.

Hydatid presentation and treatment are stage-specific: WHO image-based staging classifies cysts as active, transitional or inactive; liver cysts are 70 to 85% of lesions and lung cysts about 20%, with other sites under 10%. Active cysts may be treated with albendazole, PAIR (puncture, aspiration, injection, reaspiration) or surgery; inactive cysts are usually watched. Surgery is now reserved for complicated, large or refractory cysts, because removal of the pericyst lowers recurrence. Rupture can cause anaphylaxis and peritoneal seeding, and about 30% of liver cysts develop complications such as suppuration, adjacent-organ compression or rupture. ^{[8] [9]}

For T. solium, intestinal taeniasis is treated with a single dose of praziquantel (5 to 10 mg per kg), with albendazole as an alternative; neurocysticercosis needs imaging and stage-appropriate cysticidal therapy plus corticosteroids and anticonvulsants. For trichinellosis, treatment begun within the first few days (and ideally within 3 days) may prevent muscle invasion; treatment started later may not eliminate established symptoms. ^{[6] [7] [9]}

In straightforward acute watery diarrhoea in a healthy person, no tests are needed: the illness is self-limited and testing does not change management. Testing becomes useful when there are red flags: blood or mucus in the stool, fever, severe or dehydration-prone disease, hospital or antibiotic exposure, travel or immunocompromise, outbreak potential, or symptoms lasting more than a few days. When indicated, the following are the high-yield tests:

• Selective culture and reporting. Routine stool culture in most laboratories recovers Salmonella, Shigella, Campylobacter and E. coli O157 or Shiga toxin-producing E. coli; tell the laboratory when yersiniosis, Vibrio or special pathogens are suspected, because culture conditions and media differ. ^[1]
• Multiplex PCR panels simultaneously detect viral, bacterial and parasitic targets (including ETEC, EPEC and EAEC), but they detect nucleic acid, not necessarily viable organisms; a positive result must be interpreted in the clinical context, and a positive culture may still be needed for public-health typing and susceptibility. ^[1]
• Shiga toxin testing is required to detect non-O157 STEC, and Sorbitol-MacConkey agar (or a chromogenic alternative) screens for O157:H7. Frequent monitoring of haemoglobin, platelets, urea and creatinine is recommended once STEC is diagnosed, because HUS can develop days later. A peripheral smear for fragmented red cells is essential if HUS is suspected. ^[1]
• Blood cultures are needed in infants under 3 months, in sepsis or suspected enteric fever, in systemic manifestations, immunocompromise, haemolytic anaemia and enteric-fever-endemic travel. Bone marrow culture is the most sensitive test for enteric fever after antibiotics. ^{[1] [3]}
• Enteric fever diagnosis. Culture blood (and consider bone marrow, stool, duodenal fluid or urine); serologic tests should not be used. Typhoid and paratyphoid are nationally notifiable in the USA. ^[3]
• Parasites. Ova and parasite examination, including a permanent stained smear (and species-specific E. histolytica immunoassay or PCR), is reserved for persistent diarrhoea 14 days or more, travel, immunocompromise or outbreak settings. Cryptosporidium, Cyclospora and Cystoisospora testing must be requested specifically. ^[1]
• C. difficile. Test only people over 2 years with antibiotic or healthcare association; a single diarrhoeal stool sample is adequate, and multiple specimens do not increase yield. Testing within 8 to 12 weeks of antibiotics is recommended in travellers with persistent diarrhoea. ^[1]
• Other. Stool frequency and character, electrolytes, renal function, full blood count and, where malabsorption is suspected, stool fat, faecal elastase and coeliac serology. Endoscopy is reserved for persistent, unexplained diarrhoea or for clinically evident colitis.

Reduced-osmolarity ORS (glucose 75 mmol per litre, sodium 75, chloride 65, potassium 20, citrate 10, total osmolarity 245 mOsm per kg water) is first-line for mild to moderate dehydration from any cause, including cholera. Give it in small, frequent amounts, and use intravenous isotonic fluid (lactated Ringer's or normal saline) for severe dehydration, shock, altered mental state, ileus or failure of oral rehydration. Switch back to ORS as soon as the patient can drink. Continue breastfeeding or resume an age-appropriate diet during or immediately after rehydration, and add zinc (10 to 20 mg daily for 10 to 14 days) for children aged 6 months to 5 years, particularly in zinc-deficient or resource-challenged settings. ^{[1] [2]}

In cholera, rehydration is the foundation of treatment for most patients, with intravenous fluid reserved for severe dehydration or shock Antibiotics are adjuncts for severe disease, high stool output, HIV, severe acute malnutrition or pregnancy; they reduce fluid requirements and shorten illness. Zinc supplementation reduces severity and duration in children in resource-limited areas. ^[2]

Antiemetics such as ondansetron may be used in children over 4 years and adolescents to facilitate oral rehydration. Antimotility drugs (loperamide) may be used in immunocompetent adults with acute watery diarrhoea, but they are not given to children under 18 years and must be avoided in any age when toxic megacolon could result, including inflammatory diarrhoea or diarrhoea with fever, and in suspected or proven C. difficile. Antimotility drugs do not treat the cause and can worsen invasive infection. ^[1]

Most acute watery diarrhoea in healthy people does not need antibiotics. Empiric antibiotics for bloody diarrhoea while awaiting results are reserved for infants under 3 months, ill adults with fever documented in a medical setting plus bacillary dysentery, and people with recent international travel and body temperature 38.5 °C or above or sepsis, with local susceptibility guiding the drug (fluoroquinolone or azithromycin in adults; third-generation cephalosporin or azithromycin in younger or neurologically involved patients). Immunocompromised people with severe bloody diarrhoea should also be considered for empiric therapy. ^[1]

Antibiotics are retained for:

• Dysentery and severe Shigella, which shorten fever and diarrhoea by about 2 days (with increasing resistance, ciprofloxacin and azithromycin are the commonly recommended oral agents, with third-generation cephalosporins such as ceftriaxone as alternatives). ^{[5] [1]}
• Campylobacter (azithromycin) in severe, bloody or high-risk disease, because it reduces symptoms and limits post-infectious complications.
• Enteric fever (typhoid and paratyphoid), after blood cultures, with susceptibility-guided therapy. ^[3]
• Severe cholera (single-dose doxycycline or azithromycin, subject to local susceptibility). ^[2]
• High-risk nontyphoidal salmonellosis (infants, older adults, immunocompromise, bacteraemia, haemoglobinopathy, aneurysm or osteomyelitis risk). ^[1]
• Giardia (nitroimidazole or nitazoxanide) and amoebiasis (nitroimidazole followed by a luminal agent such as paromomycin), and Cyclospora (trimethoprim-sulfamethoxazole).

Antibiotics are deliberately avoided for:

• STEC, especially O157:H7 and any strain carrying Shiga toxin 2 or an unknown toxin genotype, because antibacterial therapy may increase the risk of HUS. Monitoring (haemoglobin, platelets, renal function) matters more. ^[1]
• Most uncomplicated watery diarrhoea, where antibiotics do not help the patient and add resistance and C. difficile risk.
• Persistent watery diarrhoea of 14 days or more, which should be evaluated rather than treated empirically. ^[1]

V. cholerae is a classic secretory infection: cholera toxin raises intracellular cyclic AMP, driving massive chloride secretion. The result is sudden large-volume watery "rice-water" diarrhoea with little or no fever, vomiting and rapid dehydration. Severe (cholera gravis) disease occurs in about 10% and, untreated, can cause 50% mortality within hours; with timely rehydration mortality falls to under 1%. Antibiotics are useful adjuncts but rehydration comes first. Ciprofloxacin resistance is increasing, with reduced susceptibility reported in many regions, while azithromycin and tetracyclines often remain active; susceptibility testing should guide choices. The single-dose oral cholera vaccine (CVD 103-HgR) is licensed in the USA and recommended by ACIP for travellers aged 2 to 64 years going to areas with active transmission. ^[2]

See the enteric fever section above. In practice, start broad-spectrum empiric therapy after cultures in anyone with suspected sepsis, then narrow; if fever does not settle within 5 days, reconsider the antibiotic, look for a persistent focus such as an abscess or deep-seated infection, and remember that relapse and chronic carriage occur. ^[3]

Norovirus produces vomiting and watery diarrhoea for 12 to 48 hours, with low-grade fever in the first 24 hours in about 40% of infections; rotavirus is short-lived but severe in unvaccinated infants. Illness is managed with rehydration and feeding; antibiotics have no role. Rotavirus vaccination has dramatically reduced severe disease, and outbreaks in older adults in long-term care carry significant mortality. Norovirus is the dominant foodborne outbreak agent. ^[1]

• Haemolytic uraemic syndrome (HUS): associated with STEC (mainly Shiga toxin 2-producing strains, usually O157:H7) and S. dysenteriae type 1; about 10% of STEC-infected patients who develop HUS do not have bloody diarrhoea. Thrombocytopenia, microangiopathic haemolysis and acute kidney injury define it; management is supportive, with meticulous hydration during the diarrhoeal phase reducing renal injury. ^[1]
• Reactive arthritis: after Salmonella, Shigella, Campylobacter, Yersinia, rarely Giardia and Cyclospora. ^[1]
• Guillain-Barre syndrome: after Campylobacter (the single most important antecedent infection in many series, though most Campylobacter infections do not lead to it). ^[1]
• Post-infectious irritable bowel syndrome: after Campylobacter, Salmonella, Shigella, STEC and Giardia; a common reason for chronic symptoms after a resolved infection. ^[1]
• Neurologic disease: seizures in shigellosis; Listeria meningitis in neonates, pregnant and immunocompromised people; cysticercosis presenting with seizures, hydrocephalus or chronic meningitis. ^{[5] [1] [7]}
• Intestinal perforation, haemorrhage and deep-seated infection: in enteric fever (perforation, haemorrhage, encephalopathy) and invasive Salmonella or Yersinia in older adults and those with vascular disease or iron overload. ^{[1] [3]}
• Malnutrition and growth faltering in children with persistent diarrhoea, especially where hygiene is poor and feeding interrupted.

Children. Children under 5 carry the highest risk of severe dehydration and death; rotavirus (before vaccination), norovirus and bacterial pathogens all matter. Rehydration with reduced-osmolarity ORS, continued feeding, zinc supplementation (10 to 20 mg daily for 10 to 14 days) and, where relevant, rotavirus vaccination are the anchors. Antimotility agents are avoided. Persistent diarrhoea of 14 days or more in a child demands active management to prevent malnutrition. ^{[1] [2]}

Pregnancy. Listeria (unpasteurised dairy, soft cheeses), Salmonella and, in some settings, parasites are of particular concern; severe Campylobacter or Shigella requires treatment with pregnancy-compatible agents, guided by local formulary and susceptibility. Hydration and nutrition are the priorities.

Immunocompromised hosts. The differential widens to include Cryptosporidium, Cyclospora, Cystoisospora, microsporidia, Mycobacterium avium complex and cytomegalovirus (CMV); severity and recurrence are commoner. Antimicrobial-associated diarrhoea (C. difficile) is frequent, and norovirus can become chronic after transplantation. Broaden testing and manage the underlying immune defect. ^[1]

Low-resource settings. Diarrhoeal disease is endemic where water and sanitation are poor; children under 3 have on average three episodes a year. The greatest gains come from simple, reproducible steps: recognise dehydration by skin pinch and ability to drink, use ORS prepared as one packet in 1 litre of safe water, continue feeding, give zinc for 10 to 14 days, promote exclusive breastfeeding and rotavirus vaccination, and maintain handwashing, safe water and sanitation. Aggressive intravenous rehydration is needed once shock is present. Cholera outbreaks require rapid volume replacement. ^{[2] [1]}

• Hand hygiene after toilet use, nappy changing, before food preparation and eating, after handling refuse or animals and their environment, especially in petting zoos and childcare. ^[1]
• Food safety: separate raw and cooked foods, cook meat and eggs properly, keep foods hot or cold, avoid high-risk foods (undercooked meat and seafood, unpasteurised milk and soft cheese, raw sprouts), and educate food handlers, who are implicated in most restaurant-associated outbreaks. ^[1]
• Water and sanitation: safe water, latrines and chlorine disinfection (Cryptosporidium is chlorine-tolerant, so boiling or filtration matters). ^[1]
• Vaccines: rotavirus for all infants without contraindication; two typhoid vaccines in the USA (Vi polysaccharide for those aged 2 years and over, live attenuated Ty21a for those aged 6 years and over) as an adjunct for travellers to endemic areas, people with intimate exposure to a chronic carrier, and laboratory personnel; live oral cholera vaccine (CVD 103-HgR) for adults aged 18 to 64 years travelling to cholera-affected areas. Typhoid fever can still occur in vaccinated travellers because protection is 50 to 80%. ^{[1] [2] [3]}
• Reporting: nationally notifiable diseases causing diarrhoea (including Salmonella, STEC O157, Shigella and Listeria) must be reported to state, territorial or local health departments, with submission of isolates so that outbreaks are detected and controlled. Enteric fever is also notifiable. Use hospital and public-health laboratories' culture capacity alongside multiplex panels. ^{[1] [3]}
• Post-exposure control: people with diarrhoea should avoid swimming, food preparation or service and sexual contact while symptomatic, and should adhere to meticulous hand hygiene. Asymptomatic contacts in most settings do not need treatment but should follow infection-control advice. ^[1]
• Probiotics may reduce symptom severity and duration in immunocompetent adults and children (weak recommendation). ^[1]

• Most acute diarrhoea is infective and short-lived; the first priorities are dehydration, red flags and cause.
• About 80% of acute diarrhoeas are infective, and many specific pathogens (Shigella, E. histolytica, Giardia, norovirus, rotavirus, STEC) spread by low inoculum.
• Reduced-osmolarity ORS is first-line for mild to moderate dehydration; intravenous isotonic fluid for severe or shock; zinc 10 to 20 mg daily for 10 to 14 days in children 6 months to 5 years in deficient or resource-challenged settings.
• Antibiotics are reserved for dysentery, enteric fever, severe cholera, high-risk salmonellosis and symptomatic Shigella; avoid them in STEC and in most uncomplicated watery diarrhoea.
• Antimotility drugs are unsafe in children under 18 years, in inflammatory or febrile diarrhoea, in C. difficile and generally in bloody diarrhoea.
• STEC is diagnosed with culture and Shiga-toxin testing; monitor blood counts and renal function to catch HUS, which complicates 5 to 10% of cases, mostly children.
• Rehydration during the STEC diarrhoeal phase reduces oligoanuric renal failure in those who later develop HUS.
• Typhoid and paratyphoid carry about 10 to 15% complication rates in hospitalised patients; cure rates are high but relapse and chronic carriage occur.
• Post-infectious complications include reactive arthritis, Guillain-Barre syndrome, HUS and post-infectious IBS; these should be anticipated rather than treated as new disease.
• Prevention rests on handwashing, safe water and food, antisepsis, vaccination for rotavirus and (for travellers) typhoid and cholera, and prompt notification and outbreak investigation.

Approach to diarrhoea; gastroenteritis workup; enteric fever; Clostridioides difficile infection; malabsorption and chronic diarrhoea; inflammatory bowel disease.