MRSA colonisation and infection

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

MRSA is S. aureus with resistance to most conventional beta-lactams through altered PBP2a. It retains the capacity for abscess, toxin production, bloodstream invasion and metastatic seeding. Healthcare exposure, previous MRSA, wounds, devices, dialysis, long-term care, antibiotic exposure and close-contact outbreaks increase carriage and infection risk, but community acquisition also occurs.

A positive screen changes infection prevention and procedural planning, not automatically clinical treatment. A positive clinical specimen must be matched to inflammation and specimen quality. Chronic ulcers and sputum are often colonised; blood, joint fluid, bone or another sterile site represents invasive infection. The treatment plan is determined by anatomical focus, severity, source control and susceptibility.

Infection control decisions are local and risk based. Standard precautions apply universally; transmission-based contact precautions, side-room placement, equipment, screening of contacts and decolonisation are led by the IPC team from setting, wound containment, procedure and outbreak status. Repeated unsupervised mupirocin courses select resistance and rarely create permanent eradication.

Key points

MRSA carries mecA or mecC-mediated altered penicillin-binding protein, making standard anti-staphylococcal beta-lactams ineffective despite otherwise typical S. aureus virulence.
Colonisation means MRSA is present on nose, throat, perineum, skin or a wound without attributable inflammation or systemic disease; systemic antibiotics are not used to sterilise carriage.
Culture blood and the true infection focus before antimicrobials when safe, then request full susceptibility because MRSA resistance beyond beta-lactams is variable.
An abscess needs incision and drainage; antibiotics are not routinely necessary after complete drainage of a small lesion below 5 cm without cellulitis, systemic response or immunodeficiency.
First-line treatment for severe MRSA skin and soft-tissue infection is intravenous vancomycin or teicoplanin with concentration-guided dosing; linezolid or daptomycin is an alternative.
MRSA pneumonia can be treated with intravenous vancomycin or linezolid 600 mg orally or intravenously every 12 hours; daptomycin must not be used because lung surfactant inactivates it.
MRSA bacteraemia needs repeat blood cultures to clearance, line and source review, echocardiography when indicated, at least 14 days for rigorously uncomplicated disease and longer for deep infection.
Decolonisation is an IPC-directed intervention, commonly nasal mupirocin 2% three times daily plus chlorhexidine 4% body wash daily for five days, with resistance and skin tolerance considered.

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

mec-mediated resistance

mecA or mecC encodes altered PBP2a with low beta-lactam affinity, producing resistance to standard penicillins and most cephalosporins.

Healthcare exposure

Hospitalisation, surgery, dialysis, devices, wounds, long-term care and previous antibiotics increase acquisition and subsequent invasive infection.

Community transmission

Close contact, shared equipment, skin trauma and crowded settings permit community strains to spread and cause recurrent purulent skin disease.

Toxin-producing strains

Some strains carry Panton-Valentine leucocidin or other toxins associated with recurrent abscesses, tissue necrosis and severe cavitating pneumonia.

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

1
Colonisation niche
MRSA adheres to nasal and skin epithelium, creating a reservoir for self-inoculation, wound contamination and contact transmission.
2
Abscess formation
Coagulase, adhesins and immune evasion localise neutrophilic inflammation into pus-filled collections that antimicrobial penetration cannot reliably sterilise.
3
Bloodstream seeding
Entry through skin, line or deep focus permits adherence to endothelium and prosthetic material with metastatic spread to valves, bone and joints.
4
Toxin injury
Cytotoxins damage leukocytes and tissue, amplifying necrosis, haemorrhage and inflammatory shock beyond the bacterial burden alone.

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

Colonisation

Screening swabs grow MRSA from nose, throat, perineum or skin without local inflammation, fever or organ dysfunction attributable to the organism.

Purulent skin infection

A painful fluctuant abscess, furuncle, carbuncle or purulent wound is common and requires drainage assessment rather than antibiotics alone.

Bloodstream infectionRed flag

Fever, rigors, hypotension or an otherwise unexplained inflammatory syndrome with MRSA in blood is always clinically significant.

Necrotising pneumoniaRed flag

Rapid respiratory failure, haemoptysis, shock and cavitation, often after influenza in a younger person, suggests toxin-mediated severe disease.

Metastatic infectionRed flag

New murmur, focal spine, joint or bone pain, embolic lesions, visual symptoms or persistent fever after bacteraemia suggests deep seeding.

Red flags requiring action

Persistent positive blood cultures beyond 48 to 72 hours on active therapy suggests uncontrolled source, endocarditis, infected thrombosis, prosthetic material or inadequate drug exposure.
Severe pain, bullae, skin anaesthesia, systemic toxicity or rapidly spreading necrosis requires immediate surgical exploration for necrotising soft-tissue infection.
Haemoptysis, leucopenia, shock and multilobar cavitating pneumonia after influenza can indicate Panton-Valentine leucocidin-associated disease and needs toxin-suppressing specialist therapy.
Back pain, focal bone or joint pain, new neurology or implanted hardware during bacteraemia suggests metastatic osteomyelitis, epidural abscess or prosthetic infection.
MRSA in urine without a urinary explanation should prompt blood cultures and evaluation for bacteraemia rather than reflex treatment as simple cystitis.
Severe immediate glycopeptide reaction, renal failure, thrombocytopenia or serotonergic interactions can change the safest anti-MRSA agent and require pharmacy 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
First-line culture and susceptibilityFirst stepFirst line
Why
Confirm MRSA at the infection focus and identify active oral and intravenous options.
Interpretation and limitations
Sample pus, deep tissue or sterile fluid rather than an intact surface when possible. mecA or mecC detection or cefoxitin resistance confirms the phenotype.
02
Blood cultures
Why
Detect bacteraemia in systemic illness, deep infection, pneumonia or unexplained MRSA urinary isolation.
Interpretation and limitations
Any S. aureus in blood is significant. Repeat paired cultures 24 to 48 hours after active treatment begins and thereafter until documented clearance.
03
Echocardiography
Why
Identify infective endocarditis in MRSA bacteraemia and define need for prolonged therapy or surgery.
Interpretation and limitations
Use transthoracic imaging promptly and transoesophageal imaging when prosthetic valve, device, persistent bacteraemia, emboli or inadequate transthoracic views increase probability.
04
Source and metastatic imaging
Why
Find drainable abscess, infected thrombus, vertebral infection, prosthetic focus or septic emboli.
Interpretation and limitations
Select ultrasound, CT, MRI or nuclear imaging from symptoms; whole-body investigation is not routine but low-threshold targeted imaging is appropriate with persistence.
05
MRSA screening
Why
Identify carriage before selected surgery, on admission to defined high-risk units or during contact and outbreak investigation.
Interpretation and limitations
Culture or validated PCR can be used. A negative screen does not rule out a separately sampled clinical infection, and staff screening requires an epidemiological reason.
06
Antibiotic exposure monitoring
Why
Achieve effective vancomycin or teicoplanin exposure while limiting renal and other toxicity.
Interpretation and limitations
Follow the local AUC or concentration protocol and renal trend; an MIC, level and source-control review is required when bacteraemia persists.

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

MSSA infection

Clinical disease is identical, but susceptibility permits more effective anti-staphylococcal beta-lactams, making accurate resistance identification crucial.

Streptococcal cellulitis

Diffuse non-purulent rapidly spreading erythema without abscess often reflects streptococci and requires a different empirical emphasis.

Clostridial myonecrosis

Extreme pain, gas, crepitus, haemolysis and shock suggest clostridial muscle infection requiring immediate surgery and broad toxin-active therapy.

Contaminant coagulase-negative staphylococcus

Coagulase-negative species may contaminate blood cultures, but true S. aureus bacteraemia should never be dismissed by analogy.

Inflammatory skin disease

Eczema, hidradenitis, gout and venous inflammation mimic infection, while damaged skin can also become secondarily colonised with MRSA.

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

01CULTURE FIRSTAssess colonisation versus infectionFirst stepMRSA is detected from screening or a clinical specimen.

1Identify the exact specimen and examine for pain, erythema, purulence, systemic illness or organ dysfunction; do not infer disease from the organism name.
2Before antibiotics, obtain blood cultures when systemically unwell and a deep or sterile-site specimen from the focus when sampling is safe.
3Review prior MRSA, antimicrobial exposure, devices, implants, surgery and healthcare contacts and notify the local IPC team.
4Treat clinical infection according to site and severity; use decolonisation and screening only under the IPC or perioperative pathway.

02SOURCE CONTROLDrain skin and deep fociA fluctuant abscess, infected collection, necrotic tissue, removable infected line or prosthetic focus is present.

1Incise and drain a cutaneous abscess and send pus for culture; add antibiotics for systemic response, surrounding cellulitis, large or multiple lesions, immune compromise or incomplete drainage.
2Use urgent surgical debridement for necrotising infection and radiological or operative drainage for deep collections.
3Remove an implicated vascular catheter when feasible and discuss infected prosthetic material with the relevant surgical and infection multidisciplinary team.
4Re-culture persistent drainage or blood and reassess anatomy rather than repeatedly changing antibiotics without controlling the focus.

03SEVERETreat invasive MRSABacteraemia, severe soft-tissue infection, pneumonia, bone or joint disease, endocarditis or sepsis is suspected or confirmed.

1Use intravenous vancomycin with an exact local weight, renal and AUC or concentration protocol, or teicoplanin with full loading, while susceptibility and source are established.
2AlternativeUse linezolid 600 mg orally or intravenously every 12 hours as an alternative for pneumonia or when glycopeptides are unsuitable; review blood count and serotonergic drugs.
3Use daptomycin under specialist direction for bacteraemia or right-sided endocarditis when appropriate, but never for pneumonia.
4Narrow, define route and set duration after clearance cultures, echocardiography, metastatic-focus assessment and source control.

04BACTERAEMIAProve uncomplicated diseaseOne or more blood-culture bottles grow MRSA.

1Repeat blood cultures within 24 to 48 hours and continue until negative; conduct a daily search for line, skin, joint, spine, cardiac and prosthetic sources.
2Arrange echocardiography and infection-specialist review; remove implicated intravascular access and drain any focus whenever feasible.
3Treat for at least 14 days from first negative culture only if endocarditis is excluded, follow-up cultures clear promptly, fever resolves, no prosthesis remains and no metastatic focus exists.
4Use at least 28 days and commonly four to six weeks for complicated bacteraemia, endocarditis, osteomyelitis or retained infected material according to site and surgery.

05DECOLONISEReduce carriage when indicatedIPC or a perioperative pathway recommends decolonisation for a colonised patient or a defined outbreak or high-risk procedure.

1Apply mupirocin 2% nasal ointment to both nostrils three times daily for five days and use chlorhexidine 4% body wash daily for five days under the local protocol.
2Include hair washing on protocol-specified days, clean dentures and personal equipment, use clean towels and clothing, and cover draining wounds.
3AlternativeUse an alternative when mupirocin or chlorhexidine resistance, allergy, broken skin or mucosal site makes the standard course unsuitable.
4Do not repeat courses indefinitely; rescreen only when the pathway requires it and investigate household, staff or environmental sources only with IPC epidemiological direction.

Key medicines and prescribing safety6 treatments · regimens, roles and cautions

First-line glycopeptide for MRSA bacteraemia and many severe invasive infections.

Vancomycin

Use an intravenous weight-based loading and maintenance regimen from the local AUC or concentration protocol, commonly beginning around 15 to 20 mg/kg every eight to twelve hours with renal adjustment.

Measure exposure early, monitor renal function and infusion reaction, review MIC and source control with persistent bacteraemia, and do not use oral vancomycin for systemic MRSA.

Alternative glycopeptide for severe MRSA when local policy and susceptibility support it.

Teicoplanin

For severe infection, a common regimen is 12 mg/kg intravenously every 12 hours for three to five loading doses, then 12 mg/kg once daily with level-guided renal adjustment.

Adequate loading is essential; monitor pre-dose levels, renal function, blood count and liver tests, and avoid underdosing deep or bloodstream infection.

Alternative for MRSA pneumonia and severe soft-tissue infection and selected step-down or glycopeptide-intolerant scenarios.

Linezolid

Give 600 mg orally or intravenously every 12 hours; oral bioavailability permits route conversion without dose change.

Monitor FBC at least weekly, especially beyond 10 to 14 days; review serotonergic drugs, lactic acidosis, optic and peripheral neuropathy and MAOI interactions.

Bactericidal alternative for bloodstream, endovascular and some deep infections when glycopeptides are unsuitable or failing.

Daptomycin

Use 8 to 10 mg/kg intravenously every 24 hours for selected complicated MRSA bacteraemia under infection-specialist direction, with renal interval adjustment.

Do not use for pneumonia because surfactant inactivates it; monitor creatine kinase, muscle symptoms, statin exposure, eosinophilic pneumonia and susceptibility.

Narrow oral treatment for a clinically infected site when culture confirms susceptibility and bacteraemia or deep disease has been excluded.

Oral susceptible-isolate options

For mild infection or specialist step-down, options include doxycycline 100 mg twice daily, clindamycin 300 to 450 mg four times daily, or co-trimoxazole 960 mg twice daily.

Check pregnancy, age, C. difficile risk, inducible clindamycin resistance, renal function, potassium, blood count and interactions; none replaces drainage.

Temporarily suppresses nasal and skin carriage before selected procedures or during defined transmission-control pathways.

Mupirocin and chlorhexidine

Use mupirocin 2% nasal ointment three times daily plus chlorhexidine 4% body wash once daily for five days when IPC recommends decolonisation.

Avoid eyes and damaged skin, stop for significant irritation and review resistance after failure; decolonisation does not treat bloodstream or deep infection.

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

Infective endocarditis

Valve or device adherence causes persistent bacteraemia, emboli, heart failure and peri-valvular extension requiring prolonged therapy and often surgery.

Metastatic osteoarticular infection

Haematogenous spread produces vertebral osteomyelitis, epidural abscess, septic arthritis and prosthetic-joint infection with prolonged pain and disability.

Necrotising pneumonia

Rapid toxin-associated lung destruction causes extensive cavitation, haemoptysis, leucopenia, respiratory failure and shock, often following influenza.

Recurrent colonisation

Persistent household or healthcare reservoirs and mupirocin resistance can cause decolonisation failure and repeated skin infection or transmission.

Antibiotic toxicity

Renal injury, cytopenia, neuropathy, serotonin toxicity and myopathy can substantially limit prolonged glycopeptide, linezolid or daptomycin courses.

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

Repeat blood cultures until clearance and restart the duration clock from the first negative set only after all uncomplicated criteria are verified.
Track temperature, haemodynamics and focal symptoms daily and investigate new spine, joint, eye or neurological features as possible metastatic seeding.
Monitor vancomycin or teicoplanin exposure and renal function, linezolid blood counts and daptomycin creatine kinase according to drug and duration.
Review every device, wound and drain for source control and document the reason any implicated prosthetic material remains.
IPC should review room placement, wound containment, screening, transfer communication and whether decolonisation or repeat screens are required.
MRSA is not a routine clinician-notifiable disease in England, but NHS providers submit mandatory MRSA bacteraemia surveillance; clusters require prompt IPC and health-protection escalation.
After discharge, ensure antibiotic completion, toxicity bloods, wound or surgical review and immediate reassessment for recurrent fever or focal pain.

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

Blood culture is never carriage

S. aureus in blood represents invasive disease even when only one bottle is positive and the patient appears to improve rapidly.

Drainage can be definitive

A small, completely drained abscess without systemic response or immune compromise may need no antibiotic, limiting unnecessary resistance pressure.

Urinary MRSA is unusual

Before treating an apparent UTI, exclude bloodstream seeding, urinary instrumentation, obstruction and chronic catheter colonisation.

Decolonisation is suppression

Mupirocin and antiseptic washes often suppress carriage temporarily rather than permanently, and repeated exposure selects biocide or mupirocin resistance.

Pneumonia excludes daptomycin

Pulmonary surfactant neutralises daptomycin activity, so an agent suitable for MRSA bacteraemia can fail when the primary focus is alveolar.

11Common pitfallsFrequent interpretation and management errors.

01
Do not treat a positive screening swab or colonised chronic wound with systemic antibiotics in the absence of clinical infection.
02
Do not treat an abscess with antibiotics alone when incision, drainage or debridement is required.
03
Do not call MRSA bacteraemia uncomplicated before follow-up cultures, echocardiographic assessment, source control and metastatic-focus review are complete.
04
Do not use daptomycin for MRSA pneumonia and do not use oral vancomycin for systemic infection.
05
Do not repeat mupirocin decolonisation courses indefinitely without IPC review and resistance consideration.
06
Do not delay surgery for a necrotising soft-tissue phenotype while waiting for final culture or toxin-gene testing.