Campylobacter, Salmonella, Shigella and STEC

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

Campylobacter, non-typhoidal Salmonella, Shigella and Shiga toxin-producing Escherichia coli cause overlapping fever, pain and diarrhoea but differ critically in transmission, complication pattern and antimicrobial benefit. A shared label of bacterial gastroenteritis is therefore unsafe.

Campylobacter and Salmonella are often foodborne zoonoses. Shigella spreads efficiently between people, including through sexual contact, and resistant lineages circulate in the UK. STEC is acquired through food, animals, environmental contact and person-to-person spread.

The immediate priority is hydration and severity assessment. Bloody stool triggers testing but does not by itself identify the organism; STEC must remain in the differential before antibiotics or loperamide are given.

Treatment decisions integrate clinical severity, age, pregnancy, immunity, bloodstream invasion, vascular or prosthetic risk and susceptibility. Public-health teams manage linked cases, exclusion from high-risk work and additional sampling.

Key points

Campylobacter commonly causes fever, cramping and sometimes bloody diarrhoea after poultry, unpasteurised milk, animal or water exposure; most cases need fluids only.
Non-typhoidal Salmonella usually produces self-limiting gastroenteritis after food or animal exposure, but bacteraemia can seed arteries, bone and prostheses.
Shigella has a very low infectious dose and causes fever, cramps, tenesmus and small-volume bloody or mucoid stool with important person-to-person spread.
STEC produces severe cramping and bloody diarrhoea, often with little fever; antibiotics and antimotility drugs may increase toxin exposure and are avoided.
Send stool culture or PCR in bloody, severe or outbreak-associated disease and ensure culture and susceptibility follow molecular detection when required.
Take blood cultures for sepsis, enteric fever differential, immunosuppression or suspected invasive Salmonella disease.
Antibiotics are not routine for Campylobacter or uncomplicated non-typhoidal Salmonella; selected severe or high-risk disease is treated from susceptibility and local guidance.
Notify and coordinate with the health-protection team for STEC, Shigella, outbreaks and occupational or institutional transmission concerns.

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

Campylobacter zoonosis

Undercooked poultry, raw milk, contaminated water and animal contact transmit curved Gram-negative organisms to the small and large bowel.

Salmonella food and animal exposure

Eggs, meat, reptiles and contaminated produce transmit non-typhoidal serovars that occasionally invade beyond intestine. in susceptible exposed adults.

Shigella person-to-person spread

A very low infectious dose enables household, institutional, travel-related and sexual-network transmission through faecal contamination. in susceptible exposed adults.

STEC toxin-producing strains

Ruminants, contaminated food, farm environments and close contact transmit E coli strains carrying Shiga toxin genes.

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

1
Campylobacter invasion
Mucosal invasion and inflammation produce fever, cramping and inflammatory diarrhoea, with later immune-mediated neurological sequelae. during active invasive disease.
2
Salmonella translocation
Organisms invade intestinal lymphoid tissue and may survive within macrophages, enabling bacteraemia and focal seeding. during active invasive disease.
3
Shigella colitis
Direct epithelial invasion and intense colonic inflammation cause ulceration, tenesmus, mucus and blood. during active invasive disease.
4
Shiga toxin endothelial injury
Absorbed toxin binds susceptible microvascular endothelium, particularly renal tissue, causing platelet activation and microangiopathic haemolysis. during active invasive disease.

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

Campylobacter pattern

Fever, marked cramping and diarrhoea that may become bloody follow undercooked poultry, animal contact, unpasteurised milk or untreated water.

Salmonella gastroenteritis

Nausea, fever, abdominal pain and watery stool follow eggs, poultry, reptiles or contaminated food; bacteraemia risk rises in vulnerable hosts.

Shigella dysenteryRed flag

Fever, urgency, tenesmus and frequent small-volume stool containing blood or mucus suggest invasive distal colitis and easy transmission.

STEC syndromeRed flag

Severe abdominal cramps and bloody diarrhoea with limited fever after farm, animal, food or linked-case exposure raises toxin-mediated risk.

Invasive SalmonellaRed flag

Persistent fever, positive blood cultures, focal bone pain or aortic-region pain indicates extra-intestinal infection requiring imaging and prolonged treatment.

Post-infectious complicationRed flag

Weakness after Campylobacter or arthritis after Campylobacter, Salmonella or Shigella may begin after bowel symptoms improve.

Red flags requiring action

Bloody diarrhoea with falling platelets, fragmented red cells or rising creatinine suggests STEC-associated haemolytic uraemic syndrome.
Severe abdominal tenderness, guarding, distension or absent bowel sounds indicates possible perforation, ischaemia or toxic megacolon.
Persistent non-typhoidal Salmonella bacteraemia with back, abdominal or chest pain suggests infected arterial tissue or vascular graft.
Shigellosis in a sexual network or after international travel may be extensively drug resistant and needs susceptibility-led treatment.
Campylobacter illness followed by ascending weakness, areflexia, facial weakness or breathing difficulty suggests Guillain–Barré syndrome.
Any invasive disease in pregnancy, older age, immunosuppression, haemoglobinopathy or major vascular disease needs early specialist review.

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 and cultureFirst step
Why
Detect Campylobacter, Salmonella, Shigella and Shiga toxin genes and preserve isolates for susceptibility and public-health typing.
Interpretation and limitations
State bloody stool, travel, animal, food, sexual and outbreak exposures. A Shiga toxin result drives immediate HUS monitoring and treatment avoidance.
02
Full blood count and platelets
Why
Assess inflammation, anaemia, thrombocytopenia and evolving microangiopathic haemolysis.
Interpretation and limitations
Falling haemoglobin and platelets after bloody diarrhoea require blood film, LDH, bilirubin and haptoglobin rather than attributing anaemia to stool loss alone.
03
Urea, electrolytes and creatinine
Why
Identify dehydration, electrolyte loss and acute kidney injury, including HUS.
Interpretation and limitations
Serial trend is essential when STEC is suspected because renal injury may develop after diarrhoea starts improving.
04
Blood cultures
Why
Detect invasive Salmonella, Shigella or alternative enteric fever in sepsis and high-risk hosts.
Interpretation and limitations
Collect before antibiotics where possible; persistent Salmonella growth warrants endocardial, vascular, bone and prosthetic source investigation.
05
Antimicrobial susceptibility testing
Why
Guide treatment of severe Campylobacter, invasive Salmonella or Shigella amid macrolide, fluoroquinolone and multidrug resistance.
Interpretation and limitations
Do not infer susceptibility from species or travel region; ensure molecularly detected Shigella is cultured when treatment or transmission decisions require it.
06
Haemolysis panel and urine assessment
Why
Confirm microangiopathic haemolysis and renal involvement in possible HUS.
Interpretation and limitations
Schistocytes, high LDH, low haptoglobin, thrombocytopenia, haematuria and proteinuria support the syndrome and require urgent renal input.
07
CTA, MRI or focal imaging
Why
Investigate invasive Salmonella complications or post-infectious neurological and joint disease.
Interpretation and limitations
Use CTA for focal aortic pain, MRI for spinal symptoms and appropriate neurological testing for ascending weakness.

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

Clostridioides difficile

Antibiotic or healthcare exposure with watery diarrhoea and colitis requires toxin-pathway testing and different treatment. on focused clinical assessment.

Inflammatory bowel disease

New ulcerative colitis or Crohn disease causes blood, urgency and systemic inflammation and may coexist with enteric infection.

Ischaemic colitis

Abrupt pain and haematochezia in vascular-risk patients requires urgent imaging and surgical assessment rather than routine gastroenteritis care.

Amoebic dysentery

Entamoeba histolytica after travel causes blood and mucus and requires tissue plus luminal anti-parasitic therapy. on focused clinical assessment.

Enteric fever

Typhoid and paratyphoid cause sustained systemic fever with variable gastrointestinal symptoms and need blood cultures and directed treatment.

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

01BLOODProtect against STEC harmFirst stepAn adult has bloody diarrhoea, severe cramping or epidemiological exposure compatible with STEC.

1Isolate, rehydrate and send urgent stool testing that includes Shiga toxin detection and culture.
2AlternativeAvoid antibiotics and antimotility drugs until STEC is excluded or a specialist identifies a compelling alternative indication.
3Obtain baseline and serial full blood count, platelets, creatinine, blood film and haemolysis markers according to severity.
4EscalationEscalate falling platelets, haemolysis, reduced urine or neurological change to renal and critical-care teams immediately.

02CAMPYTreat Campylobacter selectivelyTesting supports Campylobacter and illness severity or host risk makes antimicrobial benefit plausible.

1Use hydration and analgesia for uncomplicated illness because spontaneous resolution is usual.
2Consider early azithromycin for severe, prolonged or high-risk infection after local guidance and travel-resistance review.
3Do not use fluoroquinolones empirically where resistance probability is high; use susceptibility when available.
4Safety-net for dehydration, persistent blood and later ascending weakness or areflexia.

03SALMONELLASeparate gut-limited from invasive diseaseNon-typhoidal Salmonella is detected in stool or blood.

1Avoid antibiotics in uncomplicated gastroenteritis because benefit is limited and carriage may be prolonged.
2Treat severe systemic or high-risk infection with a susceptibility-directed regimen and obtain blood cultures.
3Search for endocardial, arterial, prosthetic, bone or joint seeding when bacteraemia persists or focal symptoms occur.
4Use prolonged focus-specific therapy plus procedural source control for infected aneurysm, graft, bone or joint disease.

04SHIGELLAControl transmission and resistanceShigella is suspected or confirmed through dysentery, travel, contact or sexual-network exposure.

1Notify the health-protection team, reinforce hand and sexual hygiene and obtain occupational advice for food, care and healthcare roles.
2Use susceptibility-led antimicrobial treatment for severe disease or to shorten transmission where guidance supports it.
3Discuss extensively drug-resistant or treatment-failure infection with microbiology rather than cycling empirical oral agents.
4Confirm symptom resolution and complete any clearance sampling required for the organism, occupation or outbreak.

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

Shortens susceptible Campylobacter illness when started early in carefully selected patients.

Azithromycin for selected Campylobacter

Give 500 mg orally once daily for three days when severe or prolonged Campylobacter disease or host risk justifies treatment and local guidance supports macrolide therapy.

Check QT risk, liver disease, pregnancy context, interactions and local resistance; most uncomplicated cases do not need an antimicrobial.

Treats systemic Salmonella disease while vascular, endocardial, bone and prosthetic complications are assessed.

Ceftriaxone for susceptible invasive Salmonella

Give 2 g intravenously once daily for susceptible invasive non-typhoidal Salmonella when selected by infection specialists; duration depends on bloodstream clearance and seeded focus.

Review allergy, biliary adverse effects, renal and liver context and culture susceptibility; arterial or prosthetic infection requires source control and a longer course.

Treats severe shigellosis and may reduce transmission when public-health benefit is established.

Susceptibility-led Shigella therapy

Use the exact UKHSA and local recommended adult agent, dose and duration only after illness severity, travel or sexual network and isolate susceptibility are reviewed.

Extensively drug-resistant strains make blind ciprofloxacin or azithromycin unsafe; obtain microbiology advice in treatment failure, pregnancy or immunosuppression.

Treats fluid and electrolyte depletion across all four infections while definitive results are pending.

Oral rehydration solution

Give frequent small volumes prepared to the manufacturer instructions and increase intake to replace each loose stool.

Use intravenous sodium-containing crystalloid for shock, impaired consciousness or failure to retain oral fluid; monitor renal and cardiac comorbidity.

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

Haemolytic uraemic syndrome

STEC toxin causes microangiopathic haemolytic anaemia, thrombocytopenia, kidney injury and sometimes neurological involvement. without timely definitive management.

Guillain–Barré syndrome

Post-Campylobacter antibodies cross-react with peripheral nerves, producing ascending weakness, areflexia and possible respiratory failure. without timely definitive management.

Reactive arthritis

Immune inflammation of joints, entheses or eyes follows Campylobacter, Salmonella or Shigella in susceptible individuals. without timely definitive management.

Metastatic Salmonella infection

Bacteraemia seeds damaged arteries, valves, bone, joints and prosthetic material, causing relapse and structural emergencies. without timely definitive management.

Toxic colitis

Severe Shigella or other inflammatory infection can cause dilatation, systemic toxicity, perforation and emergency surgical need.

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

Record stool frequency, blood, abdominal pain, intake, urine output and physiological response to rehydration.
In suspected STEC repeat platelets, haemoglobin, creatinine, blood film and haemolysis markers during the risk window.
Repeat blood cultures until clearance in invasive Salmonella or systemic shigellosis.
Review susceptibility promptly and stop or change empirical therapy when the isolate indicates resistance or no benefit.
Examine persistent Salmonella bacteraemia for aortic pain, murmur, prosthetic pain, focal bone or joint findings.
Check Campylobacter recovery for ascending weakness, reduced reflexes or respiratory symptoms requiring neurological admission.
Follow health-protection advice on exclusion, contact management and clearance testing for high-risk work or settings.

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

Bloody stool is not one disease

Campylobacter, Shigella, Salmonella, STEC, inflammatory bowel disease and ischaemia overlap, so treatment waits for risk-aware differentiation.

STEC fever may be modest

Severe cramps and blood with little fever should increase rather than lower suspicion of toxin-mediated disease.

Salmonella can reveal vascular disease

Recurrent or sustained bloodstream infection in an older atherosclerotic adult may be the first sign of an infected aneurysm.

Shigella dose is low

Very few organisms can transmit disease, making meticulous hand hygiene and contact management essential.

Resistance follows networks

Travel and sexual-contact epidemiology can predict resistant Shigella lineages, but actual susceptibility should determine treatment.

Complications can follow recovery

Guillain–Barré syndrome and reactive arthritis often begin after diarrhoea is settling, so delayed symptoms need explicit safety-netting.

11Common pitfallsFrequent interpretation and management errors.

01
Do not give antibiotics reflexively before STEC has been considered in bloody diarrhoea.
02
Do not use loperamide for dysentery, suspected STEC or toxic colitis.
03
Do not treat uncomplicated non-typhoidal Salmonella solely to eradicate stool carriage.
04
Do not assume ciprofloxacin will treat Shigella without susceptibility evidence.
05
Do not overlook vascular infection when Salmonella bacteraemia persists with focal pain.
06
Do not reassure after Campylobacter if ascending weakness or breathing difficulty develops.