Author: Helen Yasmin Sultan / Editor:  Adrian Boyle / Reviewer: Sarah Hickin, Mehdi Teeli / Codes: DC1, DC5, DC6, DP2, IP1, IP3, RP6, SLO1, SLO5Published: 15/02/2021

Impetigo, erysipelas, cellulitis and necrotising fasciitis represent a spectrum of soft tissue infections. Most are of mild to modest severity, but a few are life-threatening.

This module aims to explain important clinical differences in presentation and to enable the clinician to differentiate those patients with life-threatening features from those who can be safely managed in the community.



Impetigo is caused by Staphylococcus aureus (usual causative agent of the bullous type), Group A beta-haemolytic Streptococcus pyogenes (usual causative agent of the non-bullous type), or both. Minor abrasions and skin lesions, associated with a wide variety of skin diseases, allow bacterial introduction into the skin. These bacteria colonise and then infiltrate the superficial layers of the skin, initially creating a small erythematous macule (a flat, discoloured area of skin), which soon becomes vesicular. MRSA can be a causative organism and is seen more often in cases of non-bullous impetigo.

Clinical classification

Bullous impetigo: bullae are fluid-filled lesions >0.5 cm in diameter.

Non-bullous impetigo: impetigo without bullae.

Learning Bite

Don’t forget MRSA as a cause of infection not responding to treatment.

Clinical features

Several clinical forms of impetigo exist. All forms are more common in children, with the bullous form seen mainly in the under twos and the non-bullous two to five year-olds. Adult contacts may develop crusting impetigo or folliculitis around shaved areas on the face and axillae.

1. Non-bullous impetigo is the usual form. Red macules form initially, then golden crusts. It is itchy but not painful. Regional lymphadenopathy is common.


Fig 1: Non-bullous impetigo. Reproduced with permission from Wellcome Images.

2. Bullous impetigo. Here there is sloughing of the epidermis due to toxin production. Vesicles/bullae may be on face, buttocks, nappy area or trunk.


Fig 2: Bullous impetigo. Reproduced with permission from Wellcome Images.

3. Folliculitis is infection of the hair follicles due to Staphylococcus aureus.


Fig 3: Folliculitis. Reproduced with permission from Wellcome Images.

4. Ecthyma, which is deeper, ulcerating & associated with lympadenitis.


Fig 4: Ecthyma. Reproduced with permission from Wellcome Images.

5. Secondary infection of pre-existing skin disease or traumatized skin, also called impetiginous dermatitis.


Fig 5: Impetigenised dermatitis. Reproduced with permission from Wellcome Images.

  • Systemic upset is rarely seen.
  • Complications are rare and seen mainly in neonates or imunosuppressed patients. They include meningitis, sepsis, secondary cellulitis, pneumonia and septic arthritis. Post-streptococcal glomerulonephritis is occasionally seen in young children.


Impetigo is diagnosed clinically. However, consider swabbing for culture and sensitivities in the following:

  • Suspected MRSA: take swab from under crusts
  • Recurrent episodes: swab anterior nares, possibly axillae/perineum
  • Infected eczema: wet-swab inflamed areas


  • Use topical antibiotics for localised areas. Clean crust before applying. Fucidin, though often used, is frequently ineffective due to resistance. Mupirocin 2% is the best choice
  • To combat the resistance, antibiotic creams are often combined with antiseptics such as chlorhexidine
  • Systemic antibiotics (generally flucloxacillin) are needed for extensive areas and infected dermatitis
  • Inpatient care is required for infants with bullous impetigo and patients with widespread impetigenised dermatitis who may develop sepsis or dehydration
  • Neonates have a much higher incidence of developing sepsis and meningitis so require paediatric referral.
  • Follow-up is required if lesions have not cleared in seven days
  • Children should not return to daycare or school until the lesions clear
  • Carers should avoid contact with lesions, towels etc. Wash clothing, toys and hands frequently

Learning Bite

Use mupirocin nasal ointment to eradicate nasal carriage when treating impetigo on the face.


Cellulitis and Erysipelas


Cellulitis is an acute, spreading bacterial infection of thedermis and subcutaneous tissue, usually complicating a wound,ulcer, or dermatitis. Affected skin becomes tender,warm, erythematous, and swollen. Any age group may be affected & numerous organisms can cause it.

Investigation of Cellulitis

Bloods such as full blood count or CRP are only generally useful in the systemically unwell patient


Learning Bite

Atypical organisms can cause severe, rapidly progressive cellulitis with marked systemic features.

Erysipelas is a superficial cellulitis with invasion of the lymphatics. It is generally caused by Streptococci, especially Streptococcus pyogenes. Lesions are classically well-demarcated, fiery red and raised. Apeau dorange appearance (dimpling) is due to tethering of hair follicles within the oedematous dermis. Infants and the elderly are more commonly affected.


Fig 6: Cellulitis. Reproduced with permission from Wellcome Images.


Fig 7: Erysipelas. Reproduced with permission from Wellcome Images.

Cellulitis Grades

The terms cellulitis and erysipelas are often used interchangeably and clinical differentiation may be difficult. In both conditions, patients may be systemically well or unwell. Cellulitis severity is graded 1-IV:

Class I No systemic toxicity and no uncontrolled co-morbidity
Class II Systemically ill OR co-morbidity complicating infection
Class III Signs of marked systemic illness (confusion, tachycardia, hypotension) or severe co-morbidity
Class IV Sepsis syndrome or life-threatening infection such as necrotising fasciitis

Clinical features

Both erysipelas and cellulitis present with the following:

  • Type of lesion
    • Red, oedematous tender spreading areas, which are well demarcated in erysipelas but diffuse in cellulitis. There may be small haemorrhagic areas.
    • Sometimes lymphangitis and regional lymphadenopathy.
    • Vesicles/bullae are fairly common.
    • Entry wound, bite, septic source or pre-existing skin pathology such as venous eczema or athletes foot is often apparent.
  • Systemic features
    • Usually mild. Fever, tachycardia, confusion, hypotension, and leukocytosis are sometimes present and may precede visible skin changes.
  • Anatomic location
    • Commonest site is the leg usually unilateral, but bilateral cellulitis does occur rarely.
    • Arm and breast cellulitis occurs after mastectomy.

Predisposing factors include:

  • Diabetes
  • Immunodeficiency (more atypical organisms, eg pseudomonas aeruginosa)
  • Varicella infection
  • Systemic illness
  • Impaired peripheral circulation (arterial or venous insufficiency)
  • Lymphoedema
  • Obesity

Learning Bite

Always consider necrotising fasciitis if the patient is systemically unwell and the cellulitis is spreading rapidly.

Differential diagnoses

Numerous conditions can mimic cellulitis. Varicose eczema (lipodermatosclerosis)

  1. Panniculitis (vasculitis such as erythema nodosum)
  2. Post-phlebitic limb (chronic venous insufficiency)
  3. Other types of eczema, (eg atopic or contact).
  4. Venous insufficiency (also called venous eczema, stasis eczema or gravitational eczema)
  5. Thrombophlebitis
  6. Deep vein thrombosis

1. Panniculitis

Panniculitis refers to a group of conditions that involve inflammation of the fat under the skin, with or without associated vasculitis. Despite having very diverse causes, most forms of panniculitis have the same clinical appearance. Affected skin feels thickened and woody to touch. There may be discolouration of the overlying skin, either reddening or darker, brownish pigmentation. The area is often tender. Most often, the affected areas appear as raised nodules or lumps under the skin, but may be a plaque or large flat area of thickened skin. Purpuric discoloration may be present and there may also be bullae and erosions.

Causes include the collagen vascular disorders such as rheumatoid arthritis, sarcoidosis, polyarteritis nodosum, also Crohns disease, steroid therapy, necrobiosis lipoidica and erythema nodosum.)


Fig 8: Panniculitis. Reproduced with permission from Wellcome Images.

2. Post-phlebitic limb

Thrombophlebitis results in chronic skin discoloration and scarring, sometimes with oedema. However there is no erythema and generally no discomfort unless there is associated eczema.

3. Leg eczema. Various forms can affect the leg

Discoid eczema can arise at any age and results in round or oval plaques. Dry discoid eczema is often relatively non-itchy, and is often due to over-dry skin. Exudative or wet discoid eczema is often triggered by an injury to the skin (insect bite, burn or cut), and colonised or infected by Staphylococcus aureus. Discoid eczema starts with a single patch on one leg, but soon multiple lesions appear on both lower legs and may later affect the trunk and arms.

Atopic eczema is seen mainly in children. In older children and adults it is commonly found behind the knees, but can affect large areas during flares or if secondarily infected. Characteristically, atopic dermatitis is very itchy.


Fig 10: Leg eczema. Reproduced with permission from Wellcome Images.

4. Venous insufficiency

(also called venous eczema, stasis eczema or gravitational eczema) develops secondary to poor venous drainage in the leg. Episodes of cellulitis or deep vein thrombosis damage the valves, back pressure develops and fluid collects in the tissues, resulting in chronic skin inflammation. The affected leg is usually swollen, due to both inflammation and lymphoedema. Dermatitis is usually bilateral, with yellow crusting, scaling, and marked itching. It may become secondarily infected, in which case discomfort and erythema would increase, helping to differentiate acute cellulitis from the chronic appearance.


Fig 11: Venous insufficiency.

5. Thrombophlebitis

This is an inflammation of the superficial leg veins, resulting in a tender red or purple subcutaneous cord and associated swelling along the track on the vein. It may be secondary to deep vein insufficiency, cannulation or injection (eg in iv drug abusers) or malignancy (causing migratory thrombophlebitis known as Trousseau Syndrome).


Fig 12: Thrombophlebitis. Reproduced with permission from Wellcome Images.

6. Deep vein thrombosis

This does not usually cause significant erythema or blistering, though there may be associated superficial thrombophebitis. Similarly it is not generally tender, though there may be tenderness along the deep veins. Pitting oedema may be present, and swelling may be marked compared to the unaffected side (more than three cm).


Fig 13: Deep vein thrombosis. Reproduced with permission from Wellcome Images.

Investigation and management

Patients with Class I cellulitis can be managed in the community with oral antibiotics (1,3).
Admission for intravenous antibiotics is recommended for patients with:

  • Systemic upset (fever, nausea, malaise)
  • Immunosuppression (due to disease, medication)
  • Haematological malignancy
  • Co-morbidity (cardiac failure, diabetes mellitus, renal impairment)
  • Factors affecting healing (iv drug abuse, obesity, peripheral vascular disease)
  • Age extremes (below 1 year or elderly)
  • Facial and orbital cellulitis. These require urgent assessment by the appropriate specialities because of the high risk of local complications.


Yield from blood cultures in cellulitis is actually very low (generally <5 % in most series) unless infection is severe. Guidelines recommend taking them in Class III or IV infections only (1,2.)

Swab any broken skin. Culture blister fluid.


Patients with Class I cellulitis can be managed in the community with oral antibiotics [5,7-9].

Arrange urgent hospital admission if the person:

  • Has Class IV cellulitis (sepsis or severe life-threatening infection, such as necrotizing fasciitis).
  • Has Class III cellulitis (significant systemic upset, such as acute confusion, tachycardia, tachypnoea, hypotension, or unstable comorbidities, or a limb-threatening infection due to vascular compromize).
  • Has severe or rapidly deteriorating cellulitis (for example extensive areas of skin).
  • Is very young (under 1 year of age) or frail.
  • Is immunocompromized.
  • Has significant lymphoedema.
  • Has facial cellulitis (unless very mild).
  • Has suspected orbital or periorbital cellulitis (admit to ophthalmology).
  • Has Class II cellulitis (systemically unwell or systemically well but with a comorbidity).
    • Admission may not be necessary if the facilities and expertise are available in the community to give intravenous antibiotics and monitor the person (check local guidelines).
  • Has symptoms or signs suggesting a more serious illness or condition (such as osteomyelitis, or septic arthritis).

Facial and orbital cellulitis, require urgent assessment by the appropriate specialities because of the high risk of local complications.

General measures

  • The affected limb should be elevated and a bed cradle used
  • Analgesia and antipyretics as required
  • Maintain good hydration
  • Mark the extent of erythema present on admission
  • Non-adherent saline dressings for weeping areas

Choice of antibiotics

Beta-haemolytic streptococci or Staphylococcus aureus cause almost all infections, so therapy must cover these.

Flucloxacillin is bacteriocidal against both organisms so is recommended as monotherapy for Class I (mild) infections at 500mg QDS and for moderate (Class II and III) infections at a dose of 2gm qds. (Level of evidence A III). (1.)

Patients with Class IV infections need broad spectrum intravenous cover according to local guidelines (eg benzylpenecillin and ciprofloxacin). Co-amoxiclav has a broad spectrum of activity and is therefore recommended for patients with cellulitis from bites (at a dose of 625mg TDS). Ciprofloxacin 750mg bd should be added to flucloxacillin to cover fresh water infections (3.)

Recurrent cellulitis

About 29% of patients admitted with cellulitis have a recurrent episode within 3 years. Recurrence is associated with chronic lymphoedema and venous eczema. Antibiotic prophylaxis should be considered for patients with recurrent cellulitis. Penicillin V 250 mg twice daily or erythromycin 250 mg twice daily have shown benefit in several small studies(4).

Emerging treatments


Brilacidin, a member of a novel class of antibiotics called defensin-mimetics, is in phase 3 testing for skin and skin-structure infection.


Delafloxacin is a fluoroquinolone antibiotic that is approved for the treatment of acute bacterial skin and skin-structure infections caused by designated susceptible bacteria.


Necrotising fasciitis


Necrotising fasciitis is a rapidly spreading infection of the subcutaneous tissues, with characteristic widespread fascial destruction. There may also be necrosis of the underlying muscle, depending on the organisms involved.


It may be caused by single bacterial species (Clostridium perfringens or Group A Streptococci, Bacteroides and Staphylococcus aureus), or be polymicrobial. Anaerobic organisms are often present in addition to aerobes and can form gas (gas gangrene). A saltwater variant also exists, in which a minor skin wound becomes infected with a vibrio species. All varieties are rapidly progressive, resulting in massive tissue loss, multiorgan failure and death if not rapidly treated with surgical debridement. Initially diagnosis may be very difficult with presentations similar to cellulitis so a high clinical index of suspicion is required.


Fig 14: Necrotising fasciitis.

predisposing factors

Groups at increased risk of necrotising fasciitis include IV drug abusers, alcoholics, those with immunosuppression, chronic disease and haematological malignancies. However, half of cases occur in young and previously healthy individuals.

Clinical features

Early differentiation of necrotising fasciitis from cellulitis is challenging. However, delay in diagnosis results in higher mortality, so early clinical diagnosis is the priority. There are features which would point you towards a diagnosis of necrotising fasciitis:

a) Patient complains of severe pain but there is no visible skin change.
This is one of the best early diagnostic features when present, however the condition is not always very painfu so absence of severe pain does not rule it out. Pain may be severe before any skin changes are seen, & very marked tenderness may be present, despite apparently normal skin appearance, due to the deep nature of the infection. Spread is characteristically rapid and response to antibiotics poor. Systemic toxicity develops, manifested by high fever, hypotension, leucocytosis, delirium, and renal failure. Later, more obvious, signs are visible skin bruising, then necrosis, and gas in the tissues detected on palpation or imaging (eg x-ray). On average the patient has been unwell for several days by this point.

b) Increasing discomfort 48 hours after liposuction, necrotising fasciitis is well recognised complication of liposuction

c) Laboratory markers: some studies have suggested that the following features are associated with necrotising fasciitis: (see also LRINEC score -below)

  • White cell count of > 14
  • Hyponatraemia (< 135)
  • Raised urea (> 15)
  • CRP > 16
  • CK > 600

Bullae and pre-existing diabetes are not helpful in distinguishing cellulitis from necrotising fasciitis. Bullae alone are not diagnostic of deep infections, because they also occur with erysipelas, cellulitis, scalded skin syndrome, disseminated intravascular coagulation, purpura fulminans, some toxins, and primary bullous dermatological conditions. While diabetics are at greater risk of necrotising fasciitis, they are also at greater risk of all soft tissue infections, especially cellulitis. Diabetics with cellulitis may also have osteomyelitis or septic arthritis especially when their cellulitis is secondary to chronic skin ulceration.

Clinical Decision Rules

Clinical decision rules have looked at investigations that may assist in early diagnosis of necrotising fasciitis.

Several studies have suggested that patients with the following are more likely to have necrotising fasciitis than cellulitis: the laboratory indicators of necrotising fasciitis (LRINEC) score is the most widely known, but is not validated (Table 1). A score of six or greater is considered to be suggestive of necrotising fasciitis. However, multiple studies have shown poor sensitivity and specificity for the detection of necrotising fasciitis so it should be used with caution.

Table 1: Laboratory indicators of necrotising fasciitis (14)

Important: Although a score of six or greater suggests necrotising fasciitis, this decision rule has not been convincingly validated and should not override clinical judgement.

Investigation and management of necrotising fasciitis comprises of the following:

  • Blood cultures and arterial blood gases should be performed
  • Empiric broad spectrum antibiotics should be administered immediately
  • Other investigations that may assist diagnosis are plain x-ray (showing gas in tissues) and CT (showing gas dissecting along fascial planes)

However, any suspicion of necrotising fasciitis requires immediate surgical referral and assessment by an experienced surgeon. The patient will also require intensive care, so early involvement of intensivists is necessary.

Learning Bite

Any patient with suspected necrotising fasciitis requires immediate surgical referral for debridement and exploration in theatre.

  • Severe pain with minimal skin changes is suggestive of necrotising fasciitis.
  • Blood cultures are only indicated in class III or class IV cellulitis.
  • Use mupirocin nasal ointment to eradicate nasal carriage when treating impetigo on the face.
  • Dont forget MRSA as a cause of infection not responding to treatment.
  1. Clinical Resource Efficiency Support Team. Guidelines on the management of cellulitis in adults. 2005; Belfast: CREST.
  2. Eron LJ & Lipsky BA. Use of cultures in cellulitis: when, how, and why? Eur J Clin Microbiol Infect Dis 2006; 25:615-617.
  3. Koning S, Verhagen AP, van Suijlekom-Smit LWA et al. Interventions for impetigo. Cochrane Database Syst Rev 2004:CD003261.
  4. Cole C, Gazewood J. Diagnosis and treatment of impetigo. Am Fam Physician 2007;75:859-864.
  5. Swartz MN. Cellulitis. N Eng J Med 2004;350:904-912.
  6. Su YC, Chen HW, Hong YC, Chen CT, Hsiao CT, Chen IC. Laboratory risk indicator for necrotising fasciitis score and the outcomes. ANZ J of Surgery 2008;78:968-972.
  7. Stevens DL, Bisno AL, Chambers HF et al. Practice guidelines for the diagnosis and management of skin and soft-tissue infections. Clin Infect Dis 2005;41:1373-1406.
  8. Stanway A. Cellulitis. Hamilton: DermNet NZ, 2009.
  9. NICE, NHS Clinical Knowledge Summaries, Cellulitis – acute [NICE CKS]. Last revised: 2019.
  10. British Lymphology Society and Lymphoedema Support Network. Consensus Document on the Management of Cellulitis in Lymphoedema. London: BLS, LSN. 2016
  11. NICE, NHS Clinical Knowledge Summaries. Impetigo [NICE CKS]. Last revised 2020.
  12. NICE, Scenario: Management of acute cellulitis [NICE CKS]. Last revised: 2019
  13. George A, Rubin G. A systematic review and meta-analysis of treatments for impetigo. Br J Gen Pract 2003;53:480-487.
  14. Vijayakumar A, Pullagura R, Thimmappa D. Necrotizing Fasciitis: Diagnostic Challenges and Current Practices. ResearchGate. ISRN Infectious Diseases 2014(4):1-8.