Infective Diarrhoea: Organisms, Travel and Public Health

Introduction

Acute diarrhoea and vomiting from infection is common, usually self-limiting, and managed with rehydration alone in the great majority of cases - the general approach to assessment, dehydration and supportive management is covered in the gastroenterology notes on infectious gastroenteritis. This article takes an organism-led view: which pathogen a given history points towards, when that distinction actually changes management, and the public health duties that a positive stool culture or a notifiable diagnosis creates - all high-yield UKMLA territory that a purely symptom-based approach can miss.

A simple mechanistic split is worth holding in mind throughout: non-inflammatory (secretory) diarrhoea is watery, caused by a toxin acting on the small bowel without invading it, and is typically less unwell-making; inflammatory (invasive) diarrhoea is bloody, caused by an organism directly damaging the colonic mucosa, and is more often associated with fever, tenesmus and systemic upset.

Bacterial causes by exposure and clinical clue

The history - what was eaten, where, and how soon symptoms began - does most of the diagnostic work before any test result comes back.

Protozoal and parasitic causes

These typically cause more prolonged illness than a straightforward bacterial infection and should be actively considered when diarrhoea persists beyond 2 weeks, particularly with a travel history.

Giardia lamblia

Acquired from contaminated water, including in the UK from streams and lakes, as well as abroad. Causes prolonged, greasy, foul-smelling, non-bloody diarrhoea with bloating and flatulence, reflecting malabsorption rather than mucosal invasion - there is no fever and no blood in the stool. Diagnosed on stool microscopy for cysts and trophozoites (often needing repeat samples) or stool antigen testing, and treated with metronidazole.

Entamoeba histolytica (amoebiasis)

Causes amoebic dysentery - bloody diarrhoea with abdominal pain, which can mimic ulcerative colitis clinically and endoscopically. Its most important complication is an amoebic liver abscess, presenting with fever and right upper quadrant pain, often without concurrent diarrhoea, weeks to months after the original exposure. Diagnosis is by stool microscopy or antigen testing, and serology or aspirate analysis for suspected liver abscess; treatment is metronidazole followed by a luminal agent (such as paromomycin) to clear intestinal cysts and prevent relapse.

Cryptosporidium

Acquired from contaminated water, including swimming pools, and from contact with farm animals. Causes watery diarrhoea that is usually self-limiting in an immunocompetent host but can be severe, prolonged and life-threatening in advanced HIV or other significant immunosuppression - a recognised AIDS-defining illness when chronic. Diagnosed with a modified Ziehl-Neelsen stain or antigen testing on stool.

Travellers' diarrhoea

Affects a substantial proportion of travellers to resource-limited settings, most often within the first 2 weeks of a trip. Enterotoxigenic E. coli (ETEC) is the single commonest cause worldwide, with Campylobacter, Salmonella, Shigella and norovirus all contributing, and Giardia or amoebiasis worth considering if symptoms persist beyond 2 weeks.

• Prevention - safe food and water precautions ("boil it, cook it, peel it, or forget it"), though adherence in practice is poor and prevention is only partially effective
• Self-treatment - oral rehydration is the mainstay; loperamide can be used for watery, non-bloody diarrhoea without fever to control symptoms, but should be avoided if there is blood, mucus or fever, where it risks worsening an invasive infection
• Standby antibiotics - a short course, typically azithromycin, may be advised for travellers to high-risk areas or with certain medical conditions, to self-treat moderate-to-severe diarrhoea; fluoroquinolones are used less now given rising resistance, particularly in Campylobacter acquired in South and Southeast Asia

Investigations

• Stool culture (and PCR panel where available) - for anyone with bloody diarrhoea, systemic illness, recent hospitalisation or antibiotic use, or occupational risk (food handlers, healthcare workers)
• Stool microscopy for ova, cysts and parasites - for persistent diarrhoea or a relevant travel or exposure history, ideally three samples
• Clostridioides difficile toxin testing - for diarrhoea developing after recent antibiotic use or in hospital, covered in its own article
• Blood cultures - if there are features of bacteraemia or sepsis, particularly relevant to invasive Salmonella
• U&Es and FBC - to assess dehydration and, in suspected STEC infection, to monitor for the platelet fall and rising creatinine of evolving haemolytic uraemic syndrome
• Group and travel-specific tests - thick and thin films for malaria, and blood cultures for enteric fever, in anyone unwell after travel to an endemic area, since these can present with diarrhoea and must not be missed

When antibiotics actually help

Most bacterial gastroenteritis is self-limiting and antibiotics make no difference to its course, so the default is supportive care alone. There are, however, specific situations where antibiotics change the outcome, and knowing them - rather than treating every positive stool culture - is the point being tested.

Public health and infection control

Infective diarrhoea is not only a clinical problem: several duties follow a diagnosis, and forgetting them is a common way to lose marks in an otherwise sound clinical answer.

• Notification - clinically suspected food poisoning and infectious bloody diarrhoea are notifiable to UKHSA by the diagnosing clinician, independent of any laboratory confirmation, using the statutory notification of infectious disease process
• Exclusion from work or school - symptomatic food handlers, healthcare workers and children should stay away until 48 hours after symptoms have fully resolved; E. coli O157 and typhoid/paratyphoid require longer exclusion and microbiological clearance, agreed with the local health protection team
• Infection control on wards - patients with suspected infective diarrhoea are isolated in a side room, and staff use soap and water rather than alcohol gel for hand hygiene, since alcohol does not reliably kill norovirus or C. difficile spores
• Outbreak recognition - two or more linked cases should prompt early involvement of the local health protection team, particularly where a shared food source, water supply or institutional setting (a care home, school or cruise ship) is suspected

Complications

• Haemolytic uraemic syndrome - thrombocytopenia, microangiopathic haemolytic anaemia and acute kidney injury, mainly after Shiga toxin-producing E. coli or Shigella infection in young children
• Guillain-Barré syndrome - can follow Campylobacter jejuni infection by 1-3 weeks, one of the best-recognised infectious triggers of this condition
• Reactive arthritis - after Salmonella, Shigella, Campylobacter or Yersinia, classically with the triad of arthritis, conjunctivitis and urethritis
• Post-infectious irritable bowel syndrome - can follow any significant episode of infective diarrhoea
• Amoebic liver abscess and, rarely, other extra-intestinal amoebiasis
• Bacteraemia and metastatic infection - particularly non-typhoidal Salmonella seeding bone, joints or a diseased aorta

Red flags

Prognosis

Most infective diarrhoea resolves within a week with supportive care alone. Outcomes are driven less by the organism itself than by how well dehydration is managed and how promptly complications - haemolytic uraemic syndrome, bacteraemia, an amoebic liver abscess - are recognised when they do occur. Persistent symptoms beyond 2-4 weeks warrant a fresh look for a parasitic cause, post-infectious IBS, or an alternative, non-infective diagnosis.