Cellulitis and erysipelas

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

Cellulitis usually follows a small breach in the skin barrier and is commonly caused by beta-haemolytic streptococci or Staphylococcus aureus. Routine disease is a clinical diagnosis because blood and skin cultures have low yield without systemic illness or an open lesion.

Erysipelas affects the upper dermis and superficial lymphatics, producing a raised, bright and sharply demarcated edge. The distinction does not usually alter first treatment but can help explain appearance and recurrence.

Treatment setting follows severity and host reserve. Stable adults who can absorb oral medicine usually receive narrow oral therapy; severe systemic illness, rapid progression or inability to take tablets supports admission and intravenous treatment.

A daily decision should integrate physiology, pain trajectory, marked margin, inflammatory trend and function. A static inflammatory marker or colour alone cannot demonstrate cure or failure.

Key points

Cellulitis is a spreading infection of dermis and subcutaneous tissue; erysipelas is more superficial, raised and sharply demarcated.
Typical findings are unilateral warmth, erythema, tenderness and swelling, sometimes with lymphangitis or systemic upset.
Bilateral red legs are rarely bilateral cellulitis; venous stasis, lipodermatosclerosis and oedema are common mimics.
Outline the margin and document observations, pain, portal of entry and baseline limb function before treatment.
For uncomplicated adult disease, NICE first choice is flucloxacillin 500 mg to 1 g four times daily for five to seven days.
Clarithromycin 500 mg twice daily is an option for penicillin allergy; erythromycin 500 mg four times daily is preferred in pregnancy when a macrolide is needed.
Initial redness may extend during the first 24 to 48 hours despite effective therapy, but worsening physiology or disproportionate pain is not expected.
Address tinea pedis, eczema, wounds, oedema and venous disease because antibiotics alone do not prevent recurrence.

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

Streptococcal entry

Beta-haemolytic streptococci enter through small skin breaches and spread through dermal and lymphatic planes, often without a recoverable culture.

Staphylococcal contribution

Staphylococcus aureus is more likely with wounds, penetrating trauma, purulence or injection sites and can form a drainable abscess.

Barrier and lymphatic risk

Tinea pedis, eczema, ulceration, oedema, lymphatic damage, venous disease and previous cellulitis weaken local defence and promote recurrence.

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

1
Dermal innate inflammation
Bacterial products activate complement and innate immune cells, producing vasodilatation, warmth, erythema, capillary leak and tenderness.
2
Lymphatic spread
Superficial lymphatic involvement creates a raised erysipelas edge, proximal streaking and tender regional nodes and contributes to later lymphatic damage.
3
Oedema feedback loop
Inflammation worsens tissue oedema, while impaired lymphatic clearance reduces local immune function and increases susceptibility to future episodes.

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

Unilateral inflammatory plaque

Warmth, spreading erythema, oedema and tenderness affecting one limb or local skin region is the typical clinical pattern.

Erysipelas edge

A bright, raised and sharply demarcated plaque with lymphatic involvement suggests a superficial streptococcal process.

Portal of entry

Interdigital fissures, tinea pedis, eczema, ulcer, wound, injection site, lymphoedema or oedematous skin often provides the entry point.

Systemic severityRed flag

Fever, rigors, tachycardia, hypotension, delirium or reduced urine output indicates systemic involvement and possible sepsis.

Deep infection cluesRed flag

Disproportionate pain, rapid spread, anaesthesia, bullae, crepitus or skin necrosis should override a reassuring superficial label.

Special anatomical siteRed flag

Infection near an eye, hand, joint, surgical implant, diabetic ulcer or bite requires anatomy-specific assessment and often specialist input.

Red flags requiring action

Pain out of proportion or rapidly advancing oedema suggests necrotising soft-tissue infection.
Hypotension, confusion, tachypnoea, mottling or oliguria indicates sepsis-related organ dysfunction.
Crepitus, haemorrhagic bullae, skin anaesthesia or dusky necrosis requires immediate surgical assessment.
Periorbital swelling with painful eye movements, visual change or proptosis suggests orbital cellulitis.
Hand infection, human bite, diabetic foot disease or severe immune compromise requires a different specialist pathway.

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
Clinical examination and marked marginFirst step
Why
Define extent, severity, portal of entry and a reproducible baseline for reassessment.
Interpretation and limitations
Record observations and pain as well as colour. Spread beyond a mark is meaningful only alongside time, physiology and expected early inflammatory evolution.
02
Swab from broken skin or discharge
Why
Identify an organism when a wound, ulcer, penetrating injury or purulent focus is present.
Interpretation and limitations
Do not swab intact cellulitic skin. Interpret surface growth cautiously because colonisers may not represent the invasive pathogen.
03
Blood cultures
Why
Detect bacteraemia when sepsis, high fever, immune compromise or unusual exposure is present.
Interpretation and limitations
Routine cultures in uncomplicated cellulitis have low yield. Obtain before antibiotics when indicated and when sampling does not delay treatment.
04
Full blood count, CRP, renal and liver profile
Why
Assess systemic inflammation, organ dysfunction and safe antimicrobial dosing in significant disease.
Interpretation and limitations
Normal markers do not exclude early infection, while slow CRP decline does not alone justify broadening treatment in an improving patient.
05
Ultrasound
Why
Distinguish cellulitis from a drainable abscess or investigate venous thrombosis when the clinical question remains.
Interpretation and limitations
A fluid collection redirects care to drainage; cobblestoning supports oedema but is not sufficiently specific to diagnose bacterial infection alone.
06
Radiograph, CT or MRI
Why
Assess gas, foreign body, osteomyelitis or deep fascial extension when red flags or anatomy warrants imaging.
Interpretation and limitations
Imaging must not delay surgical exploration for clinically suspected necrotising infection; choose modality for the specific anatomical question.

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

Venous stasis dermatitis

Bilateral itch, scale, haemosiderin pigmentation, oedema and chronic induration supports venous eczema or lipodermatosclerosis rather than acute infection.

Deep-vein thrombosis

Unilateral swelling and discomfort with thrombotic risk requires probability-based thrombosis assessment, although marked surface erythema is less typical.

Gout or septic arthritis

Pain centred on a joint with restricted movement redirects assessment to crystal aspiration and exclusion of joint infection.

Contact or inflammatory dermatitis

Itch, geometric exposure pattern, vesicles, scale or repeated antibiotic failure suggests allergic, irritant or autoimmune skin inflammation.

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

01STABLEUse narrow oral treatmentFirst stepUncomplicated cellulitis is likely, physiology is stable and oral absorption and follow-up are reliable.

1Document the site, margin, pain, observations, portal of entry, allergy reaction, renal function and factors that alter organism risk.
2AlternativeGive flucloxacillin 500 mg to 1 g orally four times daily for five to seven days when suitable, using a guideline-listed allergy alternative when needed.
3Elevate an affected limb, provide analgesia and treat fissures, tinea, eczema, wound care and oedema without applying topical antibiotics to intact skin.
4Arrange review if symptoms worsen rapidly or fail to begin improving within two to three days and provide sepsis and necrotising-infection safety-net advice.

02SEVEREAdmit and reassess sourceSystemic illness, rapid progression, significant comorbidity, special anatomy or oral-treatment failure increases complication risk.

1Use ABCDE, obtain blood cultures when indicated and begin a locally recommended intravenous regimen without delaying management of sepsis.
2Re-examine for abscess, bite, diabetic foot infection, septic joint, osteomyelitis, foreign body and necrotising soft-tissue infection.
3Seek surgical, ophthalmology, hand, podiatry or microbiology input according to anatomy and arrange source control when pus or devitalised tissue is present.
4Review intravenous treatment by 48 hours and switch to active oral therapy when physiology, absorption and trajectory allow.

03MIMICChallenge an uncertain diagnosisErythema is bilateral, chronic, sharply dependent, minimally tender or not responding as expected.

1Compare both limbs and examine for venous eczema, lipodermatosclerosis, lymphoedema, contact dermatitis, gout, thrombosis and inflammatory disease.
2Review onset, itch, scale, oedema, venous changes, inflammatory markers and ultrasound only where it answers a defined question.
3AlternativeStop antibiotics when an alternative diagnosis is established and institute compression, dermatology, rheumatology or anticoagulation assessment as appropriate.
4Avoid repeated empirical courses for recurrent red legs without documenting a credible bacterial syndrome and portal of entry.

04RECURReduce repeat episodesCellulitis recurs or persistent oedema and skin-barrier disease creates continuing risk.

1Treat tinea pedis, eczema, ulcers and wounds and optimise lymphoedema and venous-oedema care after the acute pain settles.
2Review weight, mobility, footwear, diabetes control and self-management of early skin breaks with the relevant multidisciplinary services.
3Refer repeated episodes for specialist assessment and consider antibiotic prophylaxis only under current recurrence guidance after modifiable factors are addressed.
4Give a personalised action plan that distinguishes expected post-inflammatory colour from new warmth, tenderness and spreading swelling.

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

NICE first-choice narrow treatment targeting streptococci and methicillin-susceptible Staphylococcus aureus in typical non-purulent infection.

Flucloxacillin

Give 500 mg to 1 g orally four times daily for five to seven days for uncomplicated adult cellulitis; use intravenous dosing when severity requires admission.

Clarify immediate penicillin allergy, adjust route to severity, review hepatic dysfunction and interactions, and extend beyond seven days only after clinical reassessment.

Provides a NICE-listed oral alternative for selected non-pregnant adults with penicillin allergy.

Clarithromycin

Give 500 mg orally twice daily for five to seven days when penicillin allergy makes flucloxacillin unsuitable.

Review QT prolongation, liver disease and interactions including statins, warfarin, colchicine and other CYP3A4 substrates; local macrolide resistance may alter suitability.

NICE-preferred macrolide alternative in pregnancy when penicillin cannot be used.

Erythromycin in pregnancy

Give 500 mg orally four times daily for five to seven days when a macrolide is required during pregnancy.

Confirm allergy and pregnancy status, review QT risk, gastrointestinal intolerance and interactions, and escalate severe infection rather than persisting with poorly absorbed oral therapy.

Broadens coverage for selected facial infection where anatomical complications and a different organism spectrum matter.

Co-amoxiclav near eyes or nose

Give 625 mg orally three times daily for seven days when NICE guidance selects treatment near the eyes or nose.

Check penicillin allergy, renal function, liver injury history and Clostridioides difficile risk, and seek urgent ophthalmology assessment for orbital features.

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

Abscess formation

Localised purulence becomes walled off and may cause persistent pain, fever and treatment failure until incision and drainage.

Bacteraemia and sepsis

Invasive organisms can enter blood and trigger organ dysfunction, especially with frailty, immune compromise or delayed treatment.

Necrotising progression

A deep fascial infection may initially resemble cellulitis but rapidly produces severe pain, toxicity, bullae, anaesthesia and tissue death.

Recurrent lymphatic injury

Repeated episodes scar lymphatics, worsen chronic oedema and create a self-reinforcing cycle of impaired defence and further cellulitis.

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

Recheck temperature, pulse, blood pressure, respiratory rate, mental state and urine output according to initial severity.
Assess pain, tenderness, function and spread relative to the documented margin; worsening pain is more concerning than persistent residual colour.
Review culture results and narrow or change therapy only when clinical trajectory and specimen relevance support the decision.
Check renal and hepatic function during significant systemic illness, prolonged treatment or medicines requiring adjustment.
Before discharge confirm oral tolerance, mobility, wound and skin care, portal-of-entry management and a clear route for urgent reassessment.
Persistent swelling and pigmentation can outlast viable infection; arrange oedema management rather than automatically extending antibiotics.

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

Bilateral red legs are a warning

Symmetrical lower-leg erythema with chronic oedema and scale is more often inflammatory venous disease than simultaneous bacterial cellulitis.

A pen mark needs context

Early inflammatory extension can occur after treatment begins, so marked spread is interpreted with pain, physiology and time rather than alone.

Pus changes management

A fluctuant collection requires incision and drainage; antibiotics cannot reliably sterilise a walled-off abscess without source control.

Skin barrier care prevents recurrence

Interdigital fungal disease, eczema, ulceration and uncontrolled oedema are actionable drivers that remain after the antibiotic course ends.

Orbital signs are distinct

Painful eye movement, visual impairment, ophthalmoplegia or proptosis indicates possible post-septal infection and requires emergency specialist care.

11Common pitfallsFrequent interpretation and management errors.

01
Do not diagnose bilateral chronic red legs as bilateral cellulitis without actively considering venous and inflammatory mimics.
02
Do not swab intact erythematous skin and treat a colonising result as the invasive pathogen.
03
Do not interpret slow resolution of oedema or colour as automatic evidence that antibiotics have failed.
04
Do not allow imaging to delay surgical assessment when disproportionate pain, bullae, anaesthesia or crepitus suggests necrotising infection.
05
Do not prescribe prophylaxis for recurrence before addressing tinea, wounds, eczema, venous disease and lymphoedema.