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Impetigo

Impetigo is a very common superficial infection of the skin. It an be divided into non-bullous and bullous forms. The non-bullous types represent about 70%. The infecting organism is usually Staphylococcus aureus or a Beta haemolytic streptococcus although other organisms or mixed flora may be implicated. Over the past 50 years there has been a considerable move from streptococci to staphylococci as the principle causative organism.
Usually the predisposing factor is a breech of the skin but bullous impetigo may affect intact skin and is almost invariably caused by S aureus
Another classification is as primary and secondary impetigo. In the latter it occurs on top of other dermatological disease or extensive breaks in the skin.

Epidemiology: It is extremely common and occurs in all parts of the world but precise figures are not available. It is commoner in hot areas where sweating can macerate the skin and biting insects may also break it. In the UK impetigo seems to be commonest in late summer.¹
Impetigo is most often found in pre-school children but is also quite common in young adults, especially in military training environments where a number of factors may be predisposing. The elderly are also more susceptible to skin infections.²

Presentation:

• Non-bullous lesions usually start as tiny pustules that evolve rapidly into honey-coloured crusted plaques that tend to be under 2cm in diameter. It is usually on exposed areas of the face and extremities where bites, abrasions, lacerations, scratches, burns or trauma has occurred. It spreads rapidly. There may be some itching. There is little or no surrounding erythema or oedema. Regional lymph nodes are often enlarged.
• Bullous lesions have a thin roof and tend to rupture spontaneously. They are usually on the face, trunk, extremities, buttocks, or perineal regions. They are more likely to occur on top of other disease like atopic eczema. There is little erythema and usually no regional lymphadenopathy.

Investigation: Diagnosis is usually purely clinical but a swab for culture and sensitivity may be useful.

Differential diagnosis:

• Contact dermatitis
• Scabies
• Various viral skin infections including herpes zoster and varicella
• Ecthyma is a deeper form of impetigo caused by streptococci that extends into the dermis

Management:

• Local treatment involves cleansing, removal of crusts, and frequent application of wet dressings
• If the condition is localised topical mupirocin or fusidic acid is applied to affected skin.^3,6 For nasal carriers, mupirocin or chlorhexidine & neomycin cream may be used. Mucpirocin should not be used for more than 10 days for fear of development of resistance. (BNF advice)
• Oral flucloxacillin or erythromycin may be required. Co-amoxiclav, clarithromycin and azithromycin are alternatives, but cephalosporins and cephamycins vary in their activity against staphylococci
• Community acquired MRSA is uncommon in children but can usually be treated with clindamycin or co-trimoxazole (depending on sensitivities).⁴
• Emollients in bath water may help improve the intergrity of the skin but antispetics are so highly diluted that they are unlikely to be effective
• If itching is a problem then oral antihistamines may help to prevent scratching which spreads the infection. Topical antihistamines should be avoided because of risk of allergy. The old-fashioned, sedating types are required as the efficacy is related to sedation rather than antihistamine effect

Complications:

• Complications of group A beta haemolytic streptococci like scarlet fever or glomerulonephritis are much rarer nowadays but also impetigo is most often caused by staphylococci.
• Cellulitis, lymphangitis, suppurative lymphadenitis, and staphylococcal scalded skin syndrome may occur in as many as 10% of patients with impetigo. Cellulitis rarely follows bullous impetigo.
• Mortality in infants with staphylococcal scalded skin syndrome is low but it can be as high as two thirds in adults.⁵ It represents a serious clinical challenge and will usually require admission to hospital.

Prognosis: The condition usually resolves without complications but it is highly contagious and may recur due to re-infection from family members with shared towels etc.

References Used

1. Loffeld A, Davies P, Lewis A, et al; Seasonal occurrence of impetigo: a retrospective 8-year review (1996-2003).;Clin Exp Dermatol 2005 Sep;30(5):512-4.[abstract]
2. Laube S; Skin infections and ageing.;Ageing Res Rev 2004 Jan;3(1):69-89.[abstract]
3. George A, Rubin G; A systematic review and meta-analysis of treatments for impetigo.;Br J Gen Pract 2003 Jun;53(491):480-7.[abstract]
4. Ladhani S, Garbash M; Staphylococcal skin infections in children: rational drug therapy recommendations.;Paediatr Drugs 2005;7(2):77-102.[abstract]
5. Patel GK; Treatment of staphylococcal scalded skin syndrome.;Expert Rev Anti Infect Ther 2004 Aug;2(4):575-87.[abstract]
6. Sladden MJ, Johnston GA. Common skin infections in children. BMJ. 2004 Jul 10;329(7457):95-9. Review. [Full Text]

Internet:

• Lewis LS Impetigo, from e-medicine

Historical:

• First named staphylococcus by Sir Alexander Ogston in 1881 in recognition of the grape-like clusters of bacteria he observed in pus from human abscesses.
• Rosenbach described the 2 pigmented colony types of staphylocoocus in 1884, naming then S. aureus and S. albus (now known as S. epidermidis). He also showed that S. aureus was responsible for wound infections and furunculosis.
• The streptococcus was first described by Billroth (the famous surgeon who introduced the concept of audit) in 1874, Frederick Fehleisen isolated the bacteria in 1883, and was named Streptococcus pyogenes by Rosenbach in 1884.
• William Tilbury Fox (1836-1879) wrote a classical description of impetigo contagiosa which appeared in Wilson's Journal. William Wilson (1809-1884) was a self-taught dermatologist, who famously transported Cleopatra's needle at his own expense from Alexandria to the Thames embankment.

Acknowledgements EMIS is grateful to the Mentor authoring team for updating this article from an original by Dr D J Ward and doctoronline.nhs.uk. The final copy has passed peer review of the independent Mentor GP authoring team. © EMIS 2006.

Last issued 14 Feb 2006