Cellulitis and erysipelas

Meet the patient

A 62-year-old with chronic leg oedema wakes with a hot, red, swollen, tender left shin. By evening the redness has climbed to the knee, she is febrile and shivering, and you can see a peeling, macerated fissure between her third and fourth toes. The edge of the redness is raised and sharp.[1]

That is classical lower-limb erysipelas with tinea pedis as the portal — the single commonest presentation. Three questions decide her next 48 hours: is this really cellulitis (or pseudocellulitis)?, is the fascia alive (or is this necrotising)?, and where did the bacteria get in? Mark the edge, draw the toe-web, and read on.[1][4]

Two diseases, one portal — the sharp-edge discriminator

Cellulitis and erysipelas are the same infection at different depths. Cellulitis sits in the dermis and subcutaneous tissue, so its margins are flat and ill-defined. Erysipelas involves the upper dermis and superficial lymphatics, so its edge is raised, sharply demarcated and shiny — often with proximal lymphangitis and tender regional nodes.[1][7]

Both are caused most often by β-haemolytic streptococci (especially group A, S. pyogenes) and Staphylococcus aureus; groups B, C and G streptococci contribute in diabetes and older adults. The depth distinction is an examiner favourite because it explains the morphology, not because it changes first-line antibiotics.[3][8]

[1] [7]

The discriminator line: sharp raised edge = erysipelas; flat indistinct margin = cellulitis. Both are usually streptococcal, and both start at a portal of entry.[1]

The portal of entry — find it or it will be back

Every case of cellulitis has a portal of entry — your job is to find it. Tinea pedis (the single commonest predisposing factor for leg cellulitis), interdigital fissures, chronic venous ulcers, eczema cracks, leg trauma, insect bites, IV cannulation sites, surgical wounds, and fungal nail infections all breach the barrier and seed the dermis.[1]

The portal is the cornerstone of prevention, not just acute treatment. Examine the inter-toe web spaces for maceration, fissuring and tinea — KOH microscopy of scrapings is a quick, cheap bedside test. A cellulitis that keeps coming back is almost always a portal that was never closed.[1][9]

The bedside round — MARK the edge

Bedside assessment differentiates true cellulitis from look-alikes, finds the portal, and grades severity before you decide on site of care and route of antibiotics.[1]

• Mark the edge of erythema with indelible ink or a dated photograph; spread beyond the mark at 24 to 48 hours means treatment failure or wrong diagnosis.
• Examine the inter-toe web spaces for maceration, fissuring and tinea pedis — the commonest portal in lower-limb cellulitis.
• Palpate for fluctuance suggesting an abscess (which needs incision and drainage, not antibiotics alone).
• Look for the portal of entry — wounds, ulcers, eczema, heel cracks, cannulation, bites, fungal nails.
• Check for lymphangitis (linear tracking proximally) and tender regional nodes — features that argue for streptococcal infection.
• Quantify severity — fever, tachycardia, hypotension, sepsis, pain out of proportion, bullae, crepitus and skin necrosis all flag severe (Class III to IV) disease.
• Screen comorbidity — diabetes, immunosuppression, cirrhosis, IVDU, peripheral vascular disease, lymphoedema, chronic kidney disease, sickle cell — all raise severity and lower the threshold for IV therapy.
• Apply the border sign — erysipelas has a raised, sharply demarcated edge; cellulitis has a flat, indistinct margin.[1]

[1] [1] [6]

Pseudocellulitis and the dangerous mimics

A large fraction of patients referred as "cellulitis" have an alternative diagnosis — pseudocellulitis — and misdiagnosis drives unnecessary admission and antibiotics. The bedside tells the difference: true cellulitis is unilateral, warm, tender, spreading and systemically upsetting; mimics are bilateral, chronic, pruritic, or carry a feature that points elsewhere.[1][4]

[1] [4]

The broader list holds stasis (venous) dermatitis and lipodermatosclerosis, contact and atopic dermatitis, DVT, acute gout, septic arthritis, osteomyelitis, erythema nodosum, fixed drug eruption, erythema migrans (Lyme), early herpes zoster, and carcinoma erysipeloides. The unilateral, warm, tender, spreading pattern with systemic upset distinguishes true cellulitis from most bilateral, chronic, pruritic mimics.[2][4]

Necrotising fasciitis — the do-not-miss

Pain out of proportion to the signs is the single sentence that should make you stop. Necrotising fasciitis is a surgical emergency, and the cost of missing it is a limb or a life. The classic features are cutaneous pain out of all proportion to examination, rapid progression beyond the mark, dusky or violaceous skin, haemorrhagic bullae, skin necrosis, systemic toxicity disproportionate to the skin, anaesthesia over the affected area (cutaneous nerve death), and crepitus from gas-forming organisms.[1][2]

The natural history evolves through recognisable bedside stages, and naming them improves early recognition:[1]

• Stage 1 (early, 0 to 2 days) — tender erythema with swelling and warmth disproportionate to findings; pain that exceeds the signs; fever, tachycardia and a rising CRP. Misdiagnosis as uncomplicated cellulitis is common; the LRINEC score may still be low.
• Stage 2 (intermediate, 2 to 4 days) — tense oedema, dusky or violaceous discolouration, haemorrhagic bullae, and serosanguinous "dishwater" drainage from any breach; cutaneous anaesthesia appears as superficial nerves infarct; systemic toxicity mounts (lactate over 2 mmol/L, AKI, confusion).
• Stage 3 (late, 4 to 7+ days) — frank skin necrosis with eschar, crepitus from gas-forming organisms, septic shock and multi-organ failure; mortality now exceeds 50 percent even with surgery.

[2] [4]

Recognition at Stage 1 is the only route to a good outcome. Any cellulitis with pain out of proportion, rapid spread beyond the marked edge, bullae, anaesthesia or a rising lactate mandates urgent senior surgical review and operative exploration — do not wait for confirmatory imaging.[4][5]

Orbital versus periorbital — the septum is the line

Periorbital (preseptal) cellulitis is a dermal-subcutaneous infection anterior to the orbital septum; orbital (postseptal) cellulitis is posterior to it and threatens vision. The septum is a fibrous sheet anchoring the orbital rim to the tarsal plates, and because it is a physical barrier, preseptal infection leaves vision, ocular motility and pupil reflexes normal — the key bedside discriminator.[1][11]

In children under 9, the commonest antecedent of periorbital cellulitis is bacteraemic seeding from ipsilateral ethmoid or maxillary sinusitis (the ethmoid bone is fenestrated, allowing direct venous communication); in older children and adults the portal is more often local trauma, an insect bite, impetigo or a hordeolum. Orbital cellulitis is usually from adjacent sinusitis and presents with proptosis, painful or limited eye movements (ophthalmoplegia), reduced visual acuity and chemosis — an ophthalmic and ENT emergency needing urgent contrast CT and IV antibiotics.[11][15]

[1] [11]

Mild childhood periorbital cellulitis without systemic features is treated with oral co-amoxiclav (or cephalexin in penicillin allergy) for 7 days with review at 48 hours. Children under 1 year, the systemically unwell, those who cannot tolerate oral therapy, or any in whom orbital extension cannot be excluded clinically are admitted for IV ceftriaxone plus metronidazole plus urgent contrast CT.[1][15]

How common, who, why it spreads

Group A β-haemolytic streptococci (S. pyogenes) are the commonest cause of erysipelas and a leading cause of cellulitis; groups B, C and G contribute, especially in diabetes and older adults. Staphylococcus aureus is the other principal pathogen, and MRSA matters in endemic regions, recurrent or severe disease, and specific exposures (athletes, incarcerated populations, IVDU).[1][8]

Infection enters through a skin-barrier breach — tinea pedis (the commonest predisposing factor for leg cellulitis), fissures, ulcers, eczema, trauma, bites, cannulation or surgery. Bacteraemia is uncommon in uncomplicated cellulitis and erysipelas (around 1 to 2 percent), so routine blood cultures are low-yield in immunocompetent adults with mild-to-moderate disease — but warranted in severe disease, sepsis, immunocompromise and specific exposures.[6][8][11]

Investigations — calibrated to severity

The diagnosis is clinical. Adjuncts are reserved for severity, diagnostic uncertainty and special exposures.[1]

• Skin swabs and microbiology are useful only when there is a wound, ulcer or purulent drainage — culture the portal of entry. Add PVL PCR for recurrent or family-clustered abscesses.
• Blood cultures for severe disease, sepsis, immunocompromise, recurrent cellulitis, piercing or tattoo exposure, IVDU, or suspected bacteraemia (low yield otherwise).
• Blood tests — FBC, CRP, U&E, glucose, HbA1c, venous and arterial gas, lactate — for sepsis and severity.
• Imaging — ultrasound for suspected abscess; CT or MRI if necrotising fasciitis or orbital cellulitis is suspected; plain radiographs if gas or osteomyelitis is suspected.
• Immunocompromise screen — HIV, HbA1c, hepatitis B/C, immunoglobulins — for recurrent disease.
• Blood-culture contamination minimisation — clean skin with 2 percent chlorhexidine, draw two sets from different sites, never from an existing cannula.[1][6]

Risk stratification — the Eron/Lewis classes

Use a severity framework to guide site of care and route of antibiotics.[2][5]

[1]

Management — antibiotics, and the edge that judges them

Empiric therapy targets streptococci and methicillin-susceptible S. aureus; broaden for MRSA only when the setting demands it. A network meta-analysis of cellulitis and erysipelas trials supports beta-lactam first-line, and a systematic review of antibiotic duration supports five days for most uncomplicated cases.[4][12][13]

Oral therapy for uncomplicated cellulitis and erysipelas (Class I):[1]

• Flucloxacillin 500 mg QDS for 5 days — the standard first-line in the UK and Australia for non-severe cellulitis and erysipelas.
• Cephalexin 500 mg TDS for 5 days — alternative with reliable streptococcal cover; an option in penicillin-allergic patients who tolerate cephalosporins.
• Clarithromycin 500 mg BD for 5 days — for true penicillin allergy.
• Amoxicillin 500 mg TDS — when streptococcal infection predominates (classic erysipelas) and staphylococcal cover is not required.

[1] [14]

IV therapy for moderate-to-severe cellulitis (Class II to III):[1]

• Flucloxacillin 1 to 2 g IV 6-hourly — switch to oral once afebrile and improving.
• Cefazolin 1 to 2 g IV 8-hourly — alternative where cephalosporin cross-reactivity is tolerable.
• Benzylpenicillin (penicillin G) 1.2 to 2.4 g IV 6-hourly PLUS flucloxacillin — when both S. pyogenes and S. aureus must be covered in a hospitalised patient.
• Clindamycin 300 to 450 mg IV 6-hourly — for penicillin-allergic patients, for toxin suppression in invasive group A streptococcal infection, or as an adjunct in necrotising fasciitis.
• Vancomycin 25 to 30 mg/kg loading then 15 to 20 mg/kg 12-hourly (trough 15 to 20 mg/L) — for suspected MRSA, severe sepsis or treatment failure.
• Linezolid 600 mg IV or orally 12-hourly — alternative to vancomycin with excellent oral bioavailability; reserve for MRSA or vancomycin intolerance.

[1] [12]

Suspected MRSA — add vancomycin, linezolid, daptomycin, or clindamycin (if susceptible) for purulent infection, recurrent disease, prior MRSA, IVDU, severe sepsis or endemic regions. Purulent infection (abscess) is treated primarily by incision and drainage; antibiotics are adjunctive depending on size, systemic signs and immune status.[1][4]

[1] [10]

Paediatric doses (per kg, approximate):[1]

• Flucloxacillin 12.5 to 25 mg/kg QDS orally (max 500 mg/dose); 25 to 50 mg/kg QDS IV (max 2 g/dose).
• Cephalexin 12.5 to 25 mg/kg TDS orally (max 1 g/dose); cefazolin 25 mg/kg 8-hourly IV.
• Co-amoxiclav (for periorbital cellulitis) — 0.5 mL/kg of 125/31 suspension TDS, or 25/5 mg/kg TDS.

[1] [16]

Special scenarios — broaden the cover

Animal or human bite wounds carry Pasteurella multocida and Capnocytophaga; amoxicillin-clavulanate is first-line, and consider tetanus and rabies prophylaxis. Saltwater or brackish-water exposure means Vibrio vulnificus — doxycycline plus ceftriaxone, and remember that cirrhotic patients risk fulminant septicaemia. Freshwater exposure means Aeromonas hydrophila — doxycycline plus ciprofloxacin. Fish-tank, aquarium or fish-handling exposure means Mycobacterium marinum — biopsy and prolonged combination antibiotics.[1]

Lymphoedema-associated recurrent cellulitis demands aggressive compression, lymphoedema therapist input, and treatment of tinea pedis, plus long-term penicillin V 250 mg BD if there are two or more episodes a year (UK NICE NG141). Dermatological barrier defects — atopic dermatitis, blistering disorders, ichthyosis — must be treated at the source to prevent recurrence.[9][10]

Special populations

Children: most lower-limb cellulitis is streptococcal — empirical flucloxacillin or cephalexin; facial (periorbital) is usually S. pneumoniae, S. aureus or S. pyogenes. Pregnancy: avoid tetracyclines and fluoroquinolones; penicillins and cephalosporins are safe (amoxicillin, cephalexin, erythromycin are lactation-compatible). Diabetes and PVD: lower threshold for admission; consider mixed polybacterial infection if a chronic ulcer is the portal, and broaden cover if systemically unwell.[1]

Cirrhosis and chronic liver disease: Capnocytophaga (after dog bites) and Vibrio vulnificus (after seawater exposure) cause fulminant sepsis — aggressive empirical cover with ceftriaxone plus doxycycline. The elderly may present atypically (delirium instead of fever); blood cultures are useful, durations may be longer, and check CKD dose adjustments. The immunocompromised (HIV, transplant, chemotherapy, biologics) risk neutropenic sepsis — broader empirical cover such as piperacillin-tazobactam plus vancomycin.[1]

Regional deltas

[1]

Complications — the vicious cycle

Recurrence is the single commonest complication — about 30 percent of patients have another episode within 3 years, often from the same unaddressed portal. Beyond that: bacteraemia and sepsis (rising in immunocompromised hosts), abscess formation (needs incision and drainage — antibiotics alone fail), necrotising fasciitis (mortality around 25 percent overall, higher with delayed surgery), thrombophlebitis and DVT from inflammation and immobility, and the lymphangitis to lymphoedema vicious cycle in which recurrent episodes damage lymphatics and chronic lymphoedema further predisposes to further cellulitis.[1][9]

Two more to carry into the viva: streptococcal toxic shock — invasive GAS with hypotension and multi-organ failure, admitted to ICU, with clindamycin to suppress exotoxin production — and post-streptococcal glomerulonephritis, rare in adults but recognised after streptococcal cellulitis.[8]

Prevention of recurrence

Recurrent cellulitis is common and disabling, and prevention means eliminating the portal of entry. Aggressive treatment of tinea pedis and interdigital maceration, compression for lymphoedema and venous insufficiency, weight management, and foot care are the levers. For those with frequent recurrences despite optimisation, long-term secondary antibiotic prophylaxis — low-dose oral penicillin V 250 mg BD (or erythromycin 250 mg BD in penicillin allergy) — is supported by the ORIENT trial and the Cochrane review for reduced recurrence.[9][10]

Ward-round test

1. A 60-year-old with leg oedema has a hot, tender, red shin with a sharply raised edge and proximal lymphangitis; a macerated toe-web fissure is present. Diagnosis, organism, and the two things that prevent recurrence?[1][9]

Answer

Erysipelas (sharp raised edge, superficial lymphatic involvement), most often group A streptococcus (S. pyogenes). Recurrence is prevented by treating the tinea pedis portal (antifungal, e.g. terbinafine) and compression for the lymphoedema or venous insufficiency, with long-term penicillin V 250 mg BD if there are two or more episodes a year despite optimisation.[1][9]

2. Twelve hours into "cellulitis" the patient is in severe pain out of proportion to the redness, with a dusky patch and a lactate of 3.2. What is the diagnosis and the single most important next step?[1][4]

Answer

Necrotising fasciitis — pain out of proportion plus systemic toxicity plus a rising lactate is Stage 1 to 2 disease. The single most important step is urgent senior surgical review and operative exploration/debridement, with broad-spectrum IV antibiotics (including clindamycin for toxin suppression) started within the hour. Do not delay surgery for imaging or for the LRINEC score.[1][4]

3. A 6-year-old has eyelid swelling and redness after a mosquito bite — normal vision, full eye movements, afebrile. Diagnosis and management?[1][15]

Answer

Periorbital (preseptal) cellulitis — anterior to the orbital septum, so vision, motility and pupil reflexes are normal. Manage with oral co-amoxiclav for 7 days (or cephalexin in penicillin allergy) and review at 48 hours; admit for IV ceftriaxone plus metronidazole plus CT only if orbital extension cannot be excluded or the child is systemically unwell.[1][15]

4. A cirrhotic fisherman develops a fulminant septicaemic illness after a saltwater abrasion. Which organism, and which antibiotic combination?[1]

Answer

Vibrio vulnificus — cirrhosis is the classic high-risk host. Treat with doxycycline plus ceftriaxone and resuscitate aggressively; mortality is high without prompt cover.[1]

5. Why are blood cultures usually negative in uncomplicated cellulitis, and when must you send them?[6]

Answer

Bacteraemia is uncommon in uncomplicated cellulitis and erysipelas — about 1 to 2 percent — because the infection is localised to dermis and subcutis. Send blood cultures for sepsis, severe disease, immunocompromise, recurrent cellulitis, IVDU, piercing or tattoo exposure, or suspected bacteraemia, drawing two clean sets from different sites.[6]

References

1. [1]Raff AB, Kroshinsky D. Cellulitis: A Review JAMA, 2016.PMID 27434444
2. [2]Rrapi R, Chand S, Kroshinsky D. Cellulitis: A Review of Pathogenesis, Diagnosis, and Management Med Clin North Am, 2021.PMID 34059247
3. [3]Bystritsky RJ. Cellulitis Infect Dis Clin North Am, 2021.PMID 33494874
4. [4]Boettler MA, Kaffenberger BH, Chung CG. Cellulitis: A Review of Current Practice Guidelines and Differentiation from Pseudocellulitis Am J Clin Dermatol, 2022.PMID 34902109
5. [5]Long B, Gottlieb M. Diagnosis and Management of Cellulitis and Abscess in the Emergency Department Setting: An Evidence-Based Review J Emerg Med, 2022.PMID 34657784
6. [6]Gunderson CG, Martinello RA. A systematic review of bacteremias in cellulitis and erysipelas J Infect, 2012.PMID 22101078
7. [7]Rodrigues MA, Caetano M, Amorim I, et al. [Non-Necrotizing Acute Dermo-Hypodermal Infections: Erysipela and Infectious Cellulitis] Acta Med Port, 2021.PMID 33971117
8. [8]Stevens DL, Bryant AE. Streptococcus pyogenes Impetigo, Erysipelas, and Cellulitis 2022.PMID 36479753
9. [9]Peghin M, Graziano E, Rovelli C, et al. Prevention and treatment of recurrent cellulitis Curr Opin Infect Dis, 2023.PMID 36853755
10. [10]Dalal A, Eskin-Schwartz M, Mimouni D, et al. Interventions for the prevention of recurrent erysipelas and cellulitis Cochrane Database Syst Rev, 2017.PMID 28631307
11. [11]Yadalla D, Jayagayathri R, Padmanaban K, et al. Bacterial orbital cellulitis - A review Indian J Ophthalmol, 2023.PMID 37417106
12. [12]Shu Z, Cao J, Li H, et al. Efficacy and safety of first- and second-line antibiotics for cellulitis and erysipelas: a network meta-analysis of randomized controlled trials Arch Dermatol Res, 2024.PMID 39240378
13. [13]Mo Y, Tan WC, Cooper BS. Antibiotic duration for common bacterial infections-a systematic review JAC Antimicrob Resist, 2025.PMID 39881797
14. [14]Chambliss ML MD, MSPH, Rumball A DO, Brown CM MD Skin and Soft Tissue Infections Am Fam Physician, 2026.PMID 42202366
15. [15]Anosike BI, Ganapathy V, Nakamura MM. Epidemiology and Management of Orbital Cellulitis in Children J Pediatric Infect Dis Soc, 2022.PMID 35438766
16. [16]Clebak KT, Malone MA. Skin Infections Prim Care, 2018.PMID 30115333