Impetigo: treatment and management
Although a common and usually self-limiting skin condition, impetigo needs to be treated effectively to prevent recurrence and the spread of infection
In this article…
- Causes of impetigo
- How the infection is transmitted
- How impetigo should be diagnosed and managed
Sandra Lawton is nurse consultant in dermatology, Nottingham University Hospitals Trust.
Lawton S (2014) Impetigo: treatment and management. Nursing Times; 110: 18-20.
Impetigo is the third most common skin disease in children. It is highly infectious and can be transmitted through direct and indirect contact. This article discusses the types of impetigo, its cause, diagnosis
and management, and highlights additional guidance and resources that can support practice.
- This article has been double-blind peer reviewed
- Figures and tables can be seen in the attached print-friendly PDF file of the complete article in the ‘Files’ section of this page
5 key points
- Impetigo is the third most common skin disease seen in children
- The infection can be transmitted through direct contact or indirectly through contact with fomites
- Impetigo is usually caused by Staphylococcus aureus
- Patients and their families must be given evidence-based advice to reassure them and to prevent recurrence
- If treatment is not effective within seven days, treatment and adherence should be reviewed
Impetigo is a highly contagious superficial bacterial skin infection frequently seen in children. It occurs annually in around 2.8% of children aged up to four years old and 1.6% of those aged 5-15 years (National Institute for Health and Care Excellence, 2013). The third most common skin disease seen in children after eczema and viral warts (Sladden and Johnston, 2004), it is usually transmitted by direct contact.
The condition can be classified as:
- Primary - there is a direct bacterial invasion of normal skin that has minor breaks;
- Secondary - the infection is secondary to an underlying skin disease such as eczema or scabies (Koning et al, 2012), or a result of trauma from burns, bites or lacerations (Fitzpatrick et al, 2001).
Although children are infected most often through contact with other infected children, fomites (objects or materials likely to carry infection, such as clothes, towels, utensils and furniture) can also spread impetigo. It is also more common in the summer months, and in areas with poor hygiene and crowded living conditions (Cole and Gazewood, 2007).
Types of impetigo
There are two forms of impetigo:
- Non-bullous (impetigo contagiosa or crusted impetigo) - this is the more common form, accounting for three-quarters of cases;
- Bullous impetigo (NICE, 2013; Blenkinsopp et al, 2004).
Both can be present at the same time.
Lesions present as vesicles (small fluid-filled blisters) or pustules. These commonly present around the mouth and nose, but can affect other areas of the face and the extremities. The lesions rapidly burst and develop into gold-crusted plaques, typically 2cm in diameter, which have been said to resemble “glued-on cornflakes”.
Satellite lesions may occur due to autoinoculation. Non-bullous impetigo is usually asymptomatic although there may be some itching. Systemic symptoms (such as fever) are uncommon unless the infection is widespread (NICE, 2013).
Bullous impetigo is characterised by flaccid, fluid-filled vesicles and blisters (bullae) that are 1-2cm in diameter. These rupture leaving raw skin and form thin, flat, brown-to-golden crusts. The lesions are multiple, painful and spread rapidly; patients may also experience systemic symptoms (weakness, fever and diarrhoea), and regional lymphadenopathy (swelling of lymph nodes). The face is less commonly affected; sites involved tend to be the axilla, neck folds and nappy area (NICE, 2013).
Staphylococcus aureus is the main bacteria that causes non-bullous impetigo; Streptococcus pyogenes (group A beta-haemolytic streptococcus) causes a smaller number cases, either alone or in combination with S aureus. Bullous impetigo is always caused by S aureus (Koning et al, 2012; Cole and Gazewood, 2007).
Impetigo is diagnosed by identifying clinical features and history, and by ruling out other conditions that mimic it (Table 1). Assessment should consider:
- Any pre-existing skin disease;
- Trauma to the skin;
- Onset of lesions and site;
- Localised lesions or generalisedwith spread;
- Appearance of lesions;
- Symptoms, such as itchiness, soreness and pain;
- Symptoms of systemic illness;
- Family history - other family members with symptoms or with impetigo;
- Hygiene routines and the sharing of beds and towels;
- Whether impetigo has been treated and, if so, with what and for how long, including prescribed and over-the-counter preparations (Burr, 2003).
Skin swabs are not necessary to diagnose impetigo but are taken to identify the type of bacteria causing the infection and for sensitivity if the infection is:
- Extensive or severe;
- Recurrent (consider nasal swab for staphylococcal carriage);
- Suspected to be a community outbreak;
- Suspected to be caused by meticillin-resistant S aureus (MRSA) - the patient has been in contact with a person diagnosed with MRSA (NICE, 2013).
If herpes simplex is suspected, a viral culture should be taken. Further investigations may be needed if there is still doubt over the diagnosis or systemic symptoms (Blenkinsopp et al, 2004; Burr, 2003).
Hygiene measures are crucial to prevent impetigo from spreading so it is important that patients and families receive advice and treatment based on current evidence (Box 1).
Non-bullous impetigo should be treated with topical or oral antibiotics and the underlying cause addressed if appropriate. If the impetigo is localised it should be treated with topical fusidic acid 3-4 times a day for seven days (eMC, 2013). Before application, lesion crusts should be removed by soaking in soapy water - providing this does not cause discomfort. This allows the antibiotic to come into direct contact with the bacteria rather than being wasted on inert, dry, exfoliating skin (Watkins, 2005).
Topical mupirocin, retapamulin and antiseptics are not recommended as first-line treatments (Box 2); there is a lack of evidence that topical antiseptics are effective and they can cause skin reactions. Alcohol-based antiseptics can also exacerbate skin dryness and fissures (Watkins, 2005). If the impetigo is bullous, extensive or severe with systemic symptoms, oral antibiotics should be the first-line treatment (Table 2) (NICE, 2013).
Treatment outcomes and follow-up
Most controlled trials have shown positive results from topical and oral antibiotics after one week, so follow-up is unnecessary unless there is no significant improvement seven days after starting treatment - or sooner if the condition deteriorates (Koning et al, 2012). If this happens, the diagnosis, underlying cause and adherence to treatment and hygiene measures should be reviewed. A swab should be taken and oral antibiotics considered if topical fusidic acid was used and the impetigo has spread; if it has not spread, consider using topical retapamulin for five days. If an oral antibiotic was used, this can be extended for a further week until the swab results are available.
Switching from one oral antibiotic to another is unlikely to be beneficial; there is the possibility that the infection is caused by MRSA, which the skin swab will confirm or exclude. In cases of recurrent impetigo, nasal swabs should be taken from the patient and their immediate family to detect staphylococcal carriage. If S aureus is detected, advise on hygiene measures and eliminate the bacteria from the nasal carriage with mupirocin or chlorhexidine plus neomycin.
Referral is rarely necessary unless thediagnosis is uncertain or the impetigo is extensive with systemic symptoms, unresponsive to optimal treatment or recurring. Referral should then be made to a dermatologist or paediatrician and microbiology teams.
Complications of non-bullous impetigo are rare but local and systemic spread of infection can occur that may result in cellulitis, lymphangitis or septicaemia. Non-infectious complications of S pyogenes infection include guttate psoriasis, scarlet fever and glomerulonephritis (an inflammation of the kidney that can lead to kidney failure) (Koning et al, 2012). Exotoxins produced by some strains of S aureus may rarely result in staphylococcal toxic shock syndrome or scalded skin syndrome (DermNetNZ, 2013).
Impetigo can be successfully treated with evidence-based interventions. However, if the infection is recurring, health professionals should offer hygiene and lifestyle advice and assess the underlying cause, including taking nasal swabs from the patient’s immediate family. Box 3 lists sources of further information.
British Association of Dermatologists (2011) Impetigo.
Blenkinsopp A et al (2004) Impetigo. Primary Health Care; 14: 5, 33-34.
Burr S (2003) ‘Impetigo’. In: Barnes K (ed)Paediatrics: A Clinical Guide for Nurse Practitioners. London: Butterworth Heinemann.
Cole C, Gazewood J (2007) Diagnosis and treatment of impetigo. American Family Physician; 75: 6, 859-864.
DermNetNZ (2013) Staphylococcal Scalded Skin Syndrome.
eMC (2013) SPC Fucidin Cream.
Fitzpatrick TB et al (2001) Color Atlas and Synopsis of Clinical Dermatology. New York, NY: McGraw-Hill.
Health Protection Agency and British Infection Association (2013) Management of Infection Guidance for Primary Care for Consultation and Local Adaptation. London: HPA.
Koning S et al (2012) Interventions for Impetigo. Cochrane Review.
National Institute for Health and Care Excellence (2013) Impetigo. NICE Clinical Knowledge Summaries.
Sladden MJ, Johnston GA (2004) Common skin infections in children. British Medical Journal; 329: 7457, 95-99.
Watkins P (2005) Impetigo: aetiology, complications and treatment options. Nursing Standard; 19: 36, 50-54.
Yang LP, Keam SJ (2008) Retapamulin: a review of its use in the management of impetigo and other uncomplicated superficial skin infections. Drugs; 68: 6, 855-873.