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Author: Hon A/Prof Amanda Oakley, Dermatologist, Waikato Hospital, Hamilton, New Zealand, 1999. Updated September 2015. DermNet NZ revision August 2021.
Impetigo is a common acute superficial bacterial skin infection characterised by pustules and honey-coloured crusted erosions ('school sores').
The word 'impetiginisation' is used for superficial secondary infection of a wound or other skin condition. Ulcerated impetigo is called ecthyma.
Impetigo is most common in children (especially boys), but may also affect adults if they have low immunity to the bacteria. It is prevalent worldwide. Peak onset is during summer, and it is more prevalent in developing countries.
The following factors predispose to impetigo.
In nonbullous impetigo, staphylococci and streptococci invade a site of minor trauma where exposed proteins allow the bacteria to adhere.
Ecthyma is usually due to Strep pyogenes, but co-infection with Staph aureus may occur.
Bullous impetigo is due to staphylococcal exfoliative toxins (exfoliatin A–D), which target desmoglein 1 (a desmosomal adhesion glycoprotein) and cleave off the superficial epidermis through the granular layer. No trauma is required, as the bacteria can infect intact skin.
Primary impetigo mainly affects exposed areas such as the face and hands, but may also affect other body sites. It presents with single or multiple, irregular crops of irritable superficial plaques. These extend as they heal, forming annular or arcuate lesions.
Although many children are otherwise well, lymphadenopathy, mild fever and malaise may occur.
Nonbullous impetigo starts as a pink macule that evolves into a vesicle or pustule and then into erosions with a honey-coloured crust. Untreated impetigo usually resolves within 2 to 4 weeks without scarring.
Ecthyma starts as nonbullous impetigo but develops into a punched-out necrotic ulcer that heals slowly, leaving a scar.
Bullous impetigo presents with small vesicles that evolve into flaccid transparent bullae. It heals without scarring.
The bacteria causing impetigo can become invasive, leading to cellulitis and lymphangitis; subsequent bacteraemia might result in osteomyelitis, septic arthritis or pneumonia.
In infants under six years of age or adults with renal insufficiency, localised bullous impetigo due to specific staphylococcal serotypes can lead to a sick patient with generalised staphylococcal scalded skin syndrome (SSSS). Superficial crusting then tender cutaneous denudation on the face, in flexures, and elsewhere is due to circulating exfoliatin/epidermolysin, rather than a direct skin infection. It does not scar.
Toxic shock syndrome is rarely preceded by impetigo. It causes fever, diffuse erythematous then desquamating rash, hypotension and involvement of other organs.
Group A streptococcal infection may lead to acute post-streptococcal glomerulonephritis 3–6 weeks after the skin infection. It is associated with anti-DNase B and antistreptolysin O (ASO) antibodies.
Group A streptococcal skin infections have been linked to cases of rheumatic fever and rheumatic heart disease. It is thought that this occurs because strains of group A streptococci usually found on the skin move to the throat (the more usual site for rheumatic fever-associated infection).
Impetigo is usually diagnosed clinically but can be confirmed by bacterial swabs sent for microscopy (gram-positive cocci are observed), culture, and sensitivity.
A blood count may reveal an elevated white cell count due ot increased neutrophils when impetigo is widespread.
Suitable oral antibiotics in New Zealand are flucloxacillin 500 mg four times daily for 5 days (adult dose), and in case of allergy or bacterial resistance, trimethoprim + sulphamethoxazole 960 mg, twice daily, for five days (adult dose), erythromycin 800 mg twice daily for 5 days, or cephalexin 1 g twice daily for 5 days .
To reduce the chance of passing the infection to another person:
Books about skin diseases
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