Acute infectious diarrhoea

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Acute infectious diarrhoea is passage of frequent loose stool caused by viral, bacterial or protozoal infection, usually acquired through contaminated food or water, person-to-person spread, travel, animal contact or healthcare exposure. Vomiting may dominate early viral disease.

Most illness resolves with rehydration and hygiene. The important clinical tasks are recognising circulatory compromise, inflammatory or bloody disease, host vulnerability, outbreak implications and diagnoses in which antibiotic or antimotility treatment is harmful.

History defines probability: stool appearance, frequency and duration; pain, fever and vomiting; travel and food; sick contacts; antibiotics, admission and care work; sexual exposure; immunosuppression; and pregnancy. Examination focuses on volume status, perfusion and abdominal complications.

Testing and treatment are selective. Molecular stool panels detect organisms rapidly but may find colonisation or non-viable material, so results must be interpreted with symptoms and epidemiology. Public-health notification and exclusion rules are organism- and occupation-specific.

Key points

First decide whether the patient has shock, severe dehydration, sepsis or an acute surgical abdomen; organism naming comes later.
Use oral rehydration solution for most conscious patients, replacing sodium and glucose together rather than relying on plain water.
In adult shock give 500 mL crystalloid containing sodium 130 to 154 mmol/L over less than 15 minutes, then reassess before further boluses.
Request stool testing for blood, severe or prolonged illness, immunosuppression, travel, recent antibiotics, healthcare exposure or a possible outbreak.
Take blood cultures before antibiotics in systemic sepsis, enteric fever risk or suspected invasive infection.
Do not prescribe antibiotics routinely: most community gastroenteritis is self-limiting and treatment can prolong carriage or worsen STEC outcomes.
Avoid loperamide and other antimotility drugs in bloody diarrhoea, suspected STEC, C difficile, high fever or toxic colitis.
Use contact precautions, soap-and-water hand hygiene and safe food handling; alcohol gel alone is unreliable against some enteric pathogens and spores.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Person-to-person spread

Viruses and some bacteria pass through contaminated hands, surfaces and close-contact settings with a low infectious dose.

Foodborne exposure

Undercooked meat, eggs, seafood, unpasteurised products and cross-contamination transmit invasive organisms or preformed toxins. in susceptible exposed adults.

Water and travel

Unsafe drinking water, recreational water and sanitation failures expose travellers to bacteria, viruses and protozoa. in susceptible exposed adults.

Healthcare acquisition

Antibiotic disruption, environmental contamination and vulnerable hosts facilitate C difficile and institutional viral outbreaks. in susceptible exposed adults.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Enterotoxin secretion
Toxins activate epithelial ion transport, producing chloride and water secretion without major mucosal invasion. during active invasive disease.
2
Mucosal invasion
Campylobacter, Shigella and other organisms injure colonic epithelium, causing inflammation, fever, blood and tenesmus. during active invasive disease.
3
Adherence and malabsorption
Protozoa and selected bacteria disrupt brush-border function, reducing nutrient absorption and causing prolonged watery or greasy stool.
4
Systemic invasion
Enteric organisms cross mucosa into blood, particularly in enteric fever, immune compromise and invasive Salmonella infection.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Watery secretory illness

Large-volume watery stool, vomiting and cramping without blood commonly reflects viral or toxin-mediated disease and chiefly threatens dehydration.

Inflammatory dysenteryRed flag

Blood, mucus, fever, tenesmus and lower abdominal pain suggest colonic invasion or toxin injury and require stool testing.

Severe dehydrationRed flag

Thirst, dry mucosa, tachycardia, postural hypotension, reduced urine, confusion and cool peripheries mark progressive fluid loss.

Travel-associated disease

Destination, unsafe water, street food, freshwater, antibiotics and time since return distinguish enteric fever, protozoa and resistant bacteria.

Healthcare-associated diarrhoeaRed flag

Recent antibiotics, hospital stay, care facility or household healthcare exposure raises C difficile and outbreak-control priorities.

Outbreak patternRed flag

Similar illness among household, ward, care-home, nursery or food-event contacts suggests a common source and prompts early reporting.

Red flags requiring action

Shock, altered mental state, weak pulse, prolonged capillary refill or minimal urine output indicates severe intravascular depletion or sepsis.
Peritonism, marked distension, ileus or systemic toxicity can indicate perforation, toxic megacolon or surgical abdominal disease.
Bloody diarrhoea with falling platelets, anaemia or rising creatinine suggests STEC-associated haemolytic uraemic syndrome.
Recent antibiotics, healthcare exposure or care-home residence increases Clostridioides difficile and outbreak risk.
Severe illness in pregnancy, older age, immunosuppression or major comorbidity needs a lower admission and testing threshold.
Multiple linked cases, food-handler illness, healthcare work or recent institutional exposure requires urgent infection-control and public-health action.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Stool PCR or culture panelFirst step
Why
Identify bacterial and selected viral pathogens in severe, bloody, persistent, imported or outbreak-associated diarrhoea.
Interpretation and limitations
Select the local panel using exposure details; positive molecular detection requires clinical interpretation and some isolates need culture for susceptibility or public health.
02
C difficile toxin pathway
Why
Assess clinically significant new diarrhoea after antibiotic or healthcare exposure.
Interpretation and limitations
Test only unformed stool from a symptomatic patient using the local multistep algorithm; carriage can produce organism detection without toxin disease.
03
Full blood count, urea, electrolytes and creatinine
Why
Quantify haemoconcentration, electrolyte loss, renal injury, thrombocytopenia and possible haemolytic uraemic syndrome.
Interpretation and limitations
Rising creatinine, falling platelets and anaemia after bloody diarrhoea require blood-film and haemolysis assessment with urgent specialist review.
04
Blood cultures
Why
Detect bacteraemia in sepsis, suspected enteric fever, invasive Salmonella disease or severe immunosuppression.
Interpretation and limitations
Collect before antimicrobials when this does not delay treatment; later stool cultures may remain positive when bloodstream yield falls.
05
CRP, venous gas and lactate
Why
Assess inflammatory burden, acid–base disturbance, perfusion and response in severe illness.
Interpretation and limitations
Raised lactate may reflect hypovolaemia or sepsis and triggers prompt resuscitation; a normal CRP does not exclude early invasive infection.
06
Abdominal imaging
Why
Investigate peritonism, obstruction, toxic megacolon, perforation or an alternative acute abdomen.
Interpretation and limitations
Imaging is not routine uncomplicated gastroenteritis; urgent CT or plain radiography is selected with surgical or gastroenterology input.
07
Exposure-directed parasite testing
Why
Identify Giardia, Entamoeba and other parasites in prolonged diarrhoea, travel or water exposure.
Interpretation and limitations
Several specimens or targeted antigen/PCR may be required because shedding varies; communicate travel and immune status to the laboratory.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Inflammatory bowel disease

Ulcerative colitis or Crohn disease causes bloody diarrhoea, urgency and systemic inflammation and can be triggered or mimicked by infection.

Ischaemic colitis

Abrupt abdominal pain followed by blood in an older or vasculopathic patient requires urgent vascular and surgical assessment.

Drug-induced diarrhoea

Metformin, laxatives, magnesium, antibiotics and many other medicines cause loose stool without primary enteric infection. on focused clinical assessment.

Overflow diarrhoea

Liquid stool passes around faecal impaction in frail adults and is identified by rectal and abdominal assessment.

Endocrine or malabsorptive disease

Thyrotoxicosis, coeliac disease and pancreatic insufficiency usually cause a more chronic pattern than acute infectious illness.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01TRIAGEGrade severity before aetiologyFirst stepAn adult presents with acute diarrhoea or vomiting.

1Check airway, breathing, circulation, mental state, capillary refill, postural symptoms and urine output and examine for peritonism or distension.
2Identify pregnancy, frailty, immune compromise, renal or cardiac disease and medicines that increase dehydration or acute kidney injury risk.
3Isolate suspected infectious diarrhoea and take a concise exposure history including travel, antibiotics, healthcare and linked cases.
4Admit urgently for shock, severe dehydration, sepsis, inability to retain fluid, significant bleeding or abdominal complication.

02REHYDRATEReplace fluid and electrolytesThere is volume depletion without an immediate surgical complication.

1Give frequent oral rehydration solution to a conscious patient who can drink; continue light food as tolerated and replace ongoing losses.
2For shock, give 500 mL sodium-containing crystalloid over less than 15 minutes and reassess pulse, pressure, perfusion, lungs and urine.
3Use smaller cautious boluses with frequent review in heart failure, renal impairment, older frailty or pregnancy-related risk.
4Measure and correct potassium, sodium, glucose and acid–base abnormalities and review nephrotoxic or volume-sensitive medicines.

03TESTTarget microbiology and public healthStool is bloody, illness is severe or prolonged, the host is vulnerable, or travel, antibiotic or outbreak exposure is present.

1Send unformed stool with symptom duration and exposure details for the appropriate culture, PCR, toxin or parasite pathway.
2Take blood cultures before antibiotics for systemic sepsis or possible typhoid or invasive bacterial disease.
3Notify the infection-control team and local health-protection service early for linked cases, high-consequence organism suspicion or occupational risk.
4Use results to narrow precautions and treatment; do not prescribe merely because a multiplex panel detects a possible coloniser.

04TREATReserve antimicrobials for defined benefitA specific treatable pathogen, invasive syndrome or high-risk host is identified.

1Continue rehydration and source precautions regardless of whether an antimicrobial is indicated.
2Avoid antibiotics and antimotility drugs when STEC is suspected until appropriate microbiology and clinical review.
3Use organism- and susceptibility-specific therapy for enteric fever, severe shigellosis, selected Campylobacter, cholera, protozoal disease or severe immunocompromise.
4Review at 24 to 48 hours and stop empirical treatment when evidence does not support benefit or a harmful diagnosis becomes likely.

Key medicines and prescribing safety4 treatments · regimens, roles and cautions

Replaces water, sodium and glucose through coupled intestinal absorption in mild to moderate dehydration.

Oral rehydration solution

Give frequent small volumes prepared exactly to the product instructions, increasing intake to replace each loose stool and continuing as tolerated.

Do not over-dilute or concentrate sachets; vomiting is managed with slower repeated sips, while shock or impaired consciousness requires intravenous treatment.

Restores circulating volume during severe hypovolaemia or septic shock.

Intravenous crystalloid for shock

Give 500 mL crystalloid containing sodium 130 to 154 mmol/L over less than 15 minutes in an adult, then reassess before repeating.

Use smaller boluses and close lung, perfusion and urine monitoring in cardiac or renal impairment; ongoing haemorrhage needs blood-product strategy.

Relieves fever and pain without reducing intestinal motility.

Paracetamol

Give 500 mg to 1 g orally up to four times daily, maximum 4 g in 24 hours for a suitable adult who can retain medication.

Lower the maximum in low body weight, frailty, liver disease or heavy alcohol use; avoid unnecessary NSAIDs during dehydration and renal injury.

Treats infections with demonstrated benefit rather than routine self-limiting gastroenteritis.

Pathogen-directed antimicrobial

Use the exact national or local organism-specific adult regimen only after syndrome, travel, susceptibility, pregnancy, allergy and renal function are assessed.

Antibiotics can prolong Salmonella carriage, precipitate C difficile and may increase STEC toxin-related harm; obtain specialist advice for severe imported disease.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Hypovolaemic kidney injury

Water and sodium loss reduce renal perfusion, causing oliguria, rising creatinine and dangerous medicine accumulation. without timely definitive management.

Electrolyte disturbance

Potassium, sodium and bicarbonate losses produce weakness, arrhythmia, seizures or acid–base derangement. without timely definitive management.

Toxic megacolon

Severe colonic inflammation causes dilatation, systemic toxicity, ileus, perforation and emergency colectomy risk. without timely definitive management.

Haemolytic uraemic syndrome

Shiga toxin damages endothelium, leading to microangiopathic haemolysis, thrombocytopenia and acute kidney injury. without timely definitive management.

Reactive sequelae

Campylobacter, Salmonella and Shigella can trigger reactive arthritis, while Campylobacter rarely precedes Guillain–Barré syndrome. without timely definitive management.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Record fluid intake, stool and vomit losses, urine output, weight and postural or haemodynamic response.
Recheck sodium, potassium, bicarbonate and creatinine after significant intravenous replacement or continuing high losses.
Monitor stool blood, abdominal tenderness, distension and bowel sounds for evolving colitis or perforation.
In suspected STEC repeat full blood count, platelets, creatinine, blood film, LDH and haptoglobin according to clinical risk.
Review culture or PCR results promptly and notify public health when the organism or setting requires it.
Reassess temporarily withheld ACE inhibitor, ARB, diuretic, metformin or nephrotoxic medicines when hydration and kidney function recover.
Give safety-net advice for reduced urine, dizziness, inability to drink, persistent fever, increasing pain, blood or symptoms beyond expected duration.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Plain water is incomplete

Large gastrointestinal losses remove sodium as well as water; correctly constituted oral rehydration solution improves absorption and electrolyte replacement.

A panel is not a diagnosis

Molecular assays may detect carriage or residual nucleic acid, so symptoms and epidemiology determine whether a result explains illness.

Antibiotics are conditional

More treatment is not automatically safer: benefit differs markedly between Campylobacter, Shigella, non-typhoidal Salmonella, STEC and parasites.

Handwashing remains central

Soap and water physically remove organisms and spores that alcohol hand rub may not reliably inactivate.

Outbreak clues alter duty

Occupation, institutional residence and linked cases change notification, exclusion and clearance requirements even in mild disease.

Renal injury can be delayed

Haemolytic uraemic syndrome may emerge after gastrointestinal symptoms begin to improve, so warning blood trends need follow-up.

11Common pitfallsFrequent interpretation and management errors.

01
Do not give repeated fluid boluses without reassessing perfusion and pulmonary signs.
02
Do not use loperamide in bloody diarrhoea, suspected STEC, C difficile or toxic colitis.
03
Do not prescribe empirical antibiotics for every traveller with loose stool.
04
Do not test formed stool for C difficile or interpret organism detection without symptoms.
05
Do not overlook linked cases, food handling, healthcare work or institutional exposure.
06
Do not discharge a high-risk patient without urine-output and deterioration safety-netting.