📋 Key Information Summary
- Acute diarrhoea lasts <14 days; chronic diarrhoea persists ≥4 weeks and demands a structured diagnostic workup including FBC, CRP, faecal calprotectin, coeliac serology, and stool microscopy/culture.
- Bacterial food poisoning typically presents within 72 hours of ingestion with prominent vomiting and/or bloody stool; viral gastroenteritis (norovirus, rotavirus) is the most common cause of acute diarrhoea in Australia, usually self-limiting within 3–5 days.
- Oral rehydration solution (ORS) is first-line for mild–moderate dehydration in all age groups; IV normal saline or Hartmann's solution is reserved for severe dehydration or inability to tolerate oral intake.
- Campylobacter spp. is the most frequently notified enteric pathogen in Australia; antibiotic treatment (azithromycin 500 mg PO daily for 3 days) is recommended for severe or systemic infection, not routine cases.
- Inflammatory bowel disease (IBD) — Crohn's disease and ulcerative colitis — accounts for a significant burden of chronic diarrhoea in young Australians; faecal calprotectin >250 μg/g strongly suggests inflammatory aetiology and warrants urgent gastroenterology referral.
- Clostridioides difficile infection (CDI) should be suspected in any patient with diarrhoea and recent antibiotic exposure (within 12 weeks); first-line treatment is oral vancomycin 125 mg QDS for 10 days (PBS Authority Required).
- Chronic diarrhoea requires exclusion of coeliac disease (anti-tTG IgA), microscopic colitis (colonoscopic biopsies), bile acid malabsorption (SeHCAT or therapeutic trial of cholestyramine), and pancreatic insufficiency (faecal elastase-1).
- Antimotility agents (loperamide) are safe in non-invasive, non-bloody diarrhoea but contraindicated in suspected invasive bacterial infection, C. difficile, and children <2 years.
- Aboriginal and Torres Strait Islander peoples experience 3–5 times the rate of gastroenteritis hospitalisations compared with non-Indigenous Australians; access to clean water, sanitation, and timely primary care are critical determinants.
- Red-flag features requiring urgent assessment: signs of severe dehydration, bloody diarrhoea, fever >38.5°C with systemic toxicity, immunocompromised state, age >65 years with comorbidities, and diarrhoea lasting >7 days.
- IBD flare management involves corticosteroid induction (prednisolone 40 mg PO daily, weaned over 8 weeks), 5-ASA agents for maintenance, and biologic therapy (infliximab, vedolizumab) for moderate–severe disease, guided by a gastroenterologist.
- Notification requirements under state/territory public health legislation: Salmonella, Shigella, Campylobacter, C. difficile (in some jurisdictions), STEC, and Giardia are notifiable diseases in Australia.
Introduction & Australian Epidemiology
Diarrhoea — defined as the passage of three or more loose or watery stools per day, or an increase in stool weight above 200 g/day — is one of the most common presentations in Australian general practice and emergency departments. It is broadly classified as acute (<14 days), persistent (14–28 days), or chronic (≥4 weeks), with aetiologies ranging from self-limiting viral infections to life-threatening inflammatory and infectious conditions.
In Australia, gastroenteritis accounts for approximately 17.2 million cases annually, resulting in an estimated 15,000 hospital admissions per year. The annual economic burden exceeds 0 million in direct healthcare costs. Norovirus is the leading cause of acute gastroenteritis outbreaks in the community and healthcare facilities, while Campylobacter remains the most commonly notified enteric pathogen nationally (~33,000 notifications per year), followed by Salmonella species (~16,000 notifications/year).
Chronic diarrhoea affects approximately 5% of the Australian adult population at any given time. Inflammatory bowel disease (IBD) — encompassing Crohn's disease and ulcerative colitis — has an increasing incidence in Australia, with current prevalence estimated at 1 in 250 individuals (approximately 100,000 people). Australia has among the highest incidence rates of IBD globally, particularly in the paediatric population.
Clostridioides difficile infection (CDI) remains a significant healthcare-associated threat, with approximately 4,000–5,000 cases reported annually in Australian hospitals. The hypervirulent ribotype 027 has been increasingly identified, and recurrent CDI (occurring in 20–30% of cases) poses a substantial management challenge. Faecal microbiota transplantation (FMT) is now established as standard-of-care for multiply recurrent CDI, available through specialist centres across Australia.
This guideline provides a structured approach to the diagnosis and management of diarrhoea in Australian primary and secondary care, encompassing acute infectious causes, inflammatory bowel disease, C. difficile infection, and chronic diarrhoeal syndromes.
Diarrhoea Diagnostic Model
A systematic approach to the patient presenting with diarrhoea is essential to differentiate benign self-limiting illness from conditions requiring urgent intervention. The diagnostic model below integrates history, examination findings, and targeted investigations to guide clinical decision-making.
Step 1: Characterise the Diarrhoea
| Feature | Questions to Ask | Diagnostic Significance |
|---|---|---|
| Duration | <14 days vs ≥4 weeks | Acute: infectious most likely. Chronic: IBD, coeliac, functional (IBS-D), microscopic colitis |
| Stool consistency & volume | Watery vs mucoid vs greasy vs bloody | Watery: secretory/osmotic. Bloody: invasive organism or IBD. Greasy: malabsorption (coeliac, pancreatic) |
| Frequency | Number of stools per 24 hours | >6 stools/day with blood suggests severe colitis or dysentery |
| Nocturnal symptoms | Does diarrhoea wake the patient? | Nocturnal diarrhoea suggests organic disease (IBD, microscopic colitis, diabetic autonomic neuropathy), not IBS |
| Systemic symptoms | Fever, weight loss, arthralgia, rash | Fever + bloody stool: invasive bacteria or IBD flare. Weight loss: IBD, coeliac, malignancy |
| Dietary / travel / contacts | Recent food history, overseas travel, sick contacts | Travel: consider Salmonella, Shigella, Campylobacter, parasites. Raw shellfish: Vibrio, norovirus |
| Medications | Recent antibiotics, NSAIDs, metformin, PPIs, SSRIs | Antibiotics: C. difficile. Metformin: common cause of osmotic diarrhoea. PPIs: C. difficile risk factor |
Step 2: Clinical Assessment & Severity Grading
Step 3: Initial Investigations (Bedside & Laboratory)
Step 4: Diagnostic Decision Pathway
Bacterial Food Poisoning vs Viral Gastroenteritis
Distinguishing between bacterial food poisoning and viral gastroenteritis is a cornerstone of diarrhoea management. While most cases are self-limiting and require only supportive care, correct aetiological classification guides the need for antimicrobial therapy, infection control measures, and public health notification.
| Feature | Bacterial Food Poisoning | Viral Gastroenteritis |
|---|---|---|
| Incubation | 1–72 hours (toxin-mediated: 1–6 hrs; invasive: 12–72 hrs) | 12–48 hours (norovirus: 12–48 hrs; rotavirus: 1–3 days) |
| Onset | Often acute, may follow a recognised meal/event | Subacute; household/community spread common |
| Vomiting | Prominent in toxin-mediated (S. aureus, B. cereus); less prominent in invasive | Often prominent, especially norovirus. Projectile in rotavirus paediatric cases |
| Stool character | Invasive: bloody/mucoid. Toxin: watery. C. perfringens: watery, profuse | Watery, non-bloody. Green or yellow in rotavirus |
| Fever | Common in invasive infection (38.5–40°C). Absent in toxin-mediated | Low-grade (37.5–38.5°C) or absent |
| Duration | Toxin: 12–24 hrs. Invasive: 3–7 days. Campylobacter: up to 10 days | Typically 3–5 days; norovirus 1–3 days |
| Key organisms | Campylobacter, Salmonella, Shigella, STEC, S. aureus, B. cereus, C. perfringens | Norovirus, rotavirus, adenovirus 40/41, astrovirus |
| Treatment | Supportive ± antibiotics for severe/systemic illness. See drug cards below | Supportive care only. ORS + early refeeding. Antiemetics (ondansetron) if significant vomiting |
Common Bacterial Causes in Australia
Viral Gastroenteritis Management
Viral gastroenteritis is the most common cause of acute diarrhoea in all age groups in Australia. Norovirus is responsible for >90% of non-bacterial gastroenteritis outbreaks and the majority of gastroenteritis-related emergency presentations during winter months. Rotavirus, though now largely prevented by vaccination (Rotarix® or RotaTeq® on the National Immunisation Program for infants), still causes significant disease in unvaccinated or incompletely vaccinated children.
- Oral rehydration solution (WHO-ORS or Gastrolyte®) — small frequent sips
- Early refeeding with age-appropriate diet when tolerated (avoid prolonged fasting)
- Ondansetron 4 mg wafer PO (adults) / weight-based for children to reduce vomiting and facilitate ORS intake
- Loperamide 4 mg PO stat then 2 mg after each loose stool (max 16 mg/day) for adults with non-bloody, non-febrile diarrhoea — NOT for children <12 years
- No antibiotics indicated
- Unable to tolerate oral fluids for >4–6 hours
- Signs of moderate–severe dehydration (sunken eyes, poor turgor, tachycardia)
- Immunocompromised patient (HIV, transplant, chemotherapy)
- Age >65 with multiple comorbidities
- Bloody diarrhoea or high fever (>38.5°C)
- Duration >7 days without improvement
Inflammatory Bowel Disease (Crohn's Disease & Ulcerative Colitis)
Inflammatory bowel disease (IBD) is a chronic, relapsing inflammatory condition of the gastrointestinal tract with an increasing incidence in Australia. Approximately 100,000 Australians live with IBD, with peak onset between 15 and 35 years of age. Crohn's disease and ulcerative colitis have distinct pathological features, distributions, and management approaches, but both commonly present with chronic or recurrent diarrhoea.
| Feature | Crohn's Disease | Ulcerative Colitis |
|---|---|---|
| Distribution | Any part of GI tract (mouth → anus). Most commonly terminal ileum and colon (ileocolonic ~40%) | Colon and rectum only. Continuous inflammation starting at rectum, extending proximally |
| Pattern | Transmural, skip lesions, cobblestoning | Mucosal and submucosal only, continuous, diffuse erythema and friability |
| Diarrhoea character | Watery or semi-formed. Bloody stool less common unless colonic involvement. Steatorrhoea if small bowel disease | Bloody diarrhoea with mucus is hallmark. Urgency, tenesmus, nocturnal symptoms |
| Complications | Strictures, fistulae (perianal, enterocutaneous, entero-enteric), abscesses, malnutrition | Toxic megacolon, massive haemorrhage, colorectal cancer risk (↑ after 8–10 years of extensive colitis) |
| Extra-intestinal manifestations | Both: arthritis (peripheral and axial), erythema nodosum, pyoderma gangrenosum, uveitis/episcleritis, primary sclerosing cholangitis (more common in UC) | Same spectrum; PSC more associated with UC |
| Serology | ASCA positive (60–70%), pANCA negative | pANCA positive (60–70%), ASCA negative |
| Gold standard diagnosis | Ileocolonoscopy + biopsies showing non-caseating granulomas, transmural inflammation. MR enterography for small bowel assessment | Colonoscopy + biopsies showing continuous mucosal inflammation, crypt abscesses, goblet cell depletion |
IBD Severity Assessment
Pharmacological Management
IBD Monitoring Targets
Modern IBD management targets deep remission — clinical remission (symptom resolution) plus biochemical remission (normal CRP and faecal calprotectin <150 μg/g) plus endoscopic remission (mucosal healing on colonoscopy). Treatment decisions are increasingly guided by objective biomarkers rather than symptoms alone, given the discordance between symptom severity and mucosal inflammation.
- Faecal calprotectin: Monitor every 3–6 months. Target <150 μg/g. Rising levels prompt treatment adjustment even in asymptomatic patients.
- CRP: Monitor monthly during flares, every 3–6 months during remission.
- Drug levels: Trough infliximab levels 3–7 μg/mL during maintenance. Anti-drug antibody testing if loss of response.
- Colonoscopy: Surveillance colonoscopy for CRC screening in extensive UC/Crohn's colitis starting 8 years after diagnosis, every 1–3 years depending on risk factors.
C. difficile Infection & Chronic Diarrhoea
Clostridioides difficile Infection (CDI)
Clostridioides difficile infection is the leading cause of healthcare-associated diarrhoea in Australia, accounting for an estimated 15,000–20,000 bed-days per year. CDI occurs when disruption of normal colonic flora (most commonly by antibiotics) allows overgrowth of toxin-producing C. difficile strains. The organism produces toxins A (enterotoxin) and B (cytotoxin), which cause mucosal inflammation, fluid secretion, and pseudomembrane formation.
| Risk Factor | Details |
|---|---|
| Antibiotic exposure | Any antibiotic within 12 weeks. Highest risk: clindamycin, fluoroquinolones, broad-spectrum cephalosporins, carbapenems |
| Proton pump inhibitors | Omeprazole, esomeprazole, pantoprazole — associated with increased CDI risk (consider deprescribing in hospital) |
| Age ≥65 years | Significantly increased risk of severe/fulminant CDI and mortality |
| Immunosuppression | Chemotherapy, solid organ transplant, IBD patients on immunomodulators/biologics, HIV |
| Hospitalisation | Prolonged inpatient stay, ICU admission, nasogastric feeding, GI surgery |
| Previous CDI | 20–30% recurrence rate after first episode; higher after each subsequent episode |
CDI Severity Classification & Treatment
CDI Treatment Algorithm
Recurrent CDI & Faecal Microbiota Transplantation (FMT)
Recurrent CDI (defined as recurrence of diarrhoea within 8 weeks of completing treatment for a prior episode) occurs in 20–30% of patients after first-line treatment and increases with each subsequent recurrence. Management involves:
- First recurrence: Vancomycin 125 mg PO QDS for 10 days, then taper and pulse regimen (125 mg PO BD × 7 days → 125 mg PO OD × 7 days → 125 mg PO every 2–3 days for 2–8 weeks). OR fidaxomicin 200 mg PO BD for 10 days.
- Second or subsequent recurrence: Faecal microbiota transplantation (FMT) is recommended by Australian and international guidelines. Delivered via colonoscopy, enema, or oral capsules. Success rates 80–90%. Available at major Australian tertiary centres (e.g., St Vincent's Melbourne, Royal Adelaide, Mater Brisbane).
- Alternative: Vancozyme (fecal microbiota, live-jslm) oral capsules — recently TGA-approved for recurrent CDI. Check current availability and PBS status with hospital pharmacy.
Chronic Diarrhoea — Differential Diagnosis & Workup
Chronic diarrhoea (≥4 weeks) requires a structured, stepwise evaluation to identify the underlying cause and direct treatment. The following table outlines the major aetiologies, distinguishing features, and diagnostic approach.
| Aetiology | Key Features | Investigation | Treatment |
|---|---|---|---|
| Coeliac disease | Chronic diarrhoea, bloating, weight loss, iron deficiency, dermatitis herpetiformis. Affects ~1 in 70 Australians | Anti-tTG IgA + total IgA. Positive → gastroscopy with duodenal biopsies (≥4 biopsies). HLA-DQ2/DQ8 to exclude | Strict lifelong gluten-free diet. Dietitian referral essential |
| Microscopic colitis | Watery, non-bloody diarrhoea in older adults (peak 60–70 years). F:M ratio 5:1. Normal macroscopic colonoscopy. Associated with PPIs, NSAIDs, SSRIs | Colonoscopy with random biopsies (must take biopsies even if mucosa appears normal). Collagenous vs lymphocytic subtype | Budesonide 9 mg PO OD for 6–8 weeks (induction), then 3–6 mg OD maintenance. First-line. ⚠️ PBS Authority Required |
| Bile acid malabsorption (BAM) | Watery diarrhoea, often worse after fatty meals. Post-cholecystectomy, post-ileal resection, or idiopathic. Under-recognised cause in Australia | SeHCAT scan (limited availability in AU) or therapeutic trial of cholestyramine. Elevated serum C4 or 7α-hydroxy-4-cholesten-3-one | Cholestyramine (Questran Lite®) 4 g PO OD–BD before meals. Titrate to response. ✔ PBS General Benefit |
| Pancreatic exocrine insufficiency | Steatorrhoea (bulky, pale, foul-smelling stools), weight loss, fat-soluble vitamin deficiency. Post-pancreatitis, pancreatic cancer, cystic fibrosis | Faecal elastase-1 (<200 μg/g). 72-hour faecal fat (>7 g/day abnormal). CT abdomen if structural cause suspected | Pancreatic enzyme replacement therapy (PERT): Creon® 25,000 units PO with meals. Titrate based on symptoms. ⚠️ PBS Authority Required |
| Medication-induced | Metformin (very common), magnesium-containing antacids, NSAIDs, colchicine, SSRIs/SNRIs, PPIs, acarbose, ARBs | Temporal relationship with medication initiation/change. Diagnosis of exclusion | Review and adjust medications. Trial cessation if safe and alternative available |
| IBS-D (functional) | Recurrent abdominal pain associated with defecation (Rome IV criteria). Onset ≥6 months ago. No nocturnal symptoms, no weight loss, no blood. Often young adults | Diagnosis of exclusion. FBC, CRP, coeliac serology, faecal calprotectin normal. Consider FIT if age >45 | Low FODMAP diet (dietitian-guided), loperamide PRN, eluxadoline (Viberzi® — specialist), rifaximin 550 mg TDS for 14 days (specialist use) |
Special Populations
Aboriginal and Torres Strait Islander Health Considerations
📚 References
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