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Childhood atopic dermatitis and skin infections Dr Graham Thom, Dermatologist, Southbank Dermatology, Suite 14a, 38 Meadowvale Ave, South Perth. Tel 6162 1864
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he relationship between microbial pathogens and atopic dermatitis can be complex, where the impaired skin barrier encourages colonisation and infection by pathogens, and pathogens themselves may exacerbate or modify the inflammation of atopic dermatitis (AD).
Staphylococcus aureus Staph aureus on the skin is extremely common in AD, usually as colonisation rather than infection. True secondary infection of pre-existing eczema will tend to manifest as weeping and yellowish crusting, or follicular pustules / furuncles, together with an exacerbation of the AD. On the other hand, eczema itself may appear moist, weepy and crusted, in the absence of infection (e.g. cheeks of infants; older children with thickened discoid eczema) and may be mistaken for impetigo, with a resultant tendency to over-treat infection with repeated courses of oral antibiotics and undertreat inflammation.
Figure 1
Figure 2
n In both these cases (severe eczema on the
cheeks of an infant, and discoid eczema on the limbs), secondary infection is likely to be present, but it is essential that the underlying eczema is treated with a topical corticosteroid of appropriate potency.
Bacteriological swabs of apparently infected eczema and anterior nares should be taken for two main reasons; to demonstrate Staph aureus infection and/or colonisation and to pick up any cases of community acquired MRSA (which require more stringent decolonisation procedures). For suspected Staph aureus infection (nonMRSA) a 7-10 day course of oral antibiotics (e.g. flucloxacillin/dicloxacillin; cephalexin) may be indicated. Topical steroids should generally not be withheld when treating infected AD, as treatment of the underlying inflammation is essential to facilitate healing of the skin. This can be a source of confusion for parents, who have often been instructed not 46
to apply topical steroids to broken skin. In the presence of folliculitis/furunculosis, occlusive ointment-based emollients are best avoided. Topical antibiotics (e.g. mupirocin) have a limited role for short-term use on localised areas of infected eczema, but indiscriminate use is to be avoided to prevent bacterial resistance developing, given that mupirocin use is important in MRSA decolonisation. Children whose AD has been persistently severe, or repeatedly complicated by secondary infection, often benefit from attempts at reducing the bacterial load (or decolonisation, if MRSA). Even in the absence of overt infection, high bacterial loads of Staph aureus may exacerbate AD through mechanisms including the production of toxins, which act as superantigens, causing widespread activation of T-cells. Positive nasal swabs are followed by mupirocin 2% nasal ointment bd for 7 days. Ideally this should be combined with an antiseptic skin wash (e.g. 2% chlorhexidine or 1% triclosan) for 7 days, but in practice these preparations are often rather drying and irritating to the skin. Similarly, some of the proprietary bath oils with added antiseptic agents can be irritating, particularly in infants. ‘Bleach baths’ are a cheap and simple adjunct – ¼ cup of household bleach is added to a normal bath (to give a final concentration of 0.005% sodium hypochlorite), together with a bland emollient bath oil (e.g. QV TM oil, Alpha KeriTM oil). The child is bathed for 10 minutes 1-2 times per week, before rinsing off in the shower. An additional strategy in recurrently infected AD, where culture sensitivities are confirmed, is a 3-4 week course of an oral antibiotic (e.g. cephalexin). If MRSA is isolated, then further advice from a clinical microbiologist or infectious diseases physician may be helpful.
Figure 3
n Eczematised molluscum contagiosum in the popliteal fossae.
Herpes simplex Herpes simplex virus superinfection (eczema herpeticum) is always borne in mind in cases of acute severe exacerbations of eczema. The herpes simplex virus spreads rapidly on broken skin; multiple scattered small vesicles appear, which rapidly develop into erosions and crusts, with a miliary ‘shotgun-like’ appearance. These cases often require hospital management. For facial involvement, seek an ophthalmologic evaluation for corneal ulceration. After swabs for viral PCR, an oral antiviral (e.g. acyclovir) is given (although not PBS listed for this purpose), and topical corticosteroids withheld while there are active vesicles or moist ulcers (usually a few days). A topical astringent such as very dilute Condy’s crystals (potassium permanganate) can be helpful to dry up moist, exudative areas. Some cases can be recurrent. Figure 4
Occasionally, a localised or regional eczematous reaction may complicate a primary skin infection (such as impetigo or folliculitis) in individuals without a prior history of AD. This may be termed an ‘infective dermatitis’ and generally requires a combination of antibiotic and topical corticosteroid treatment.
n Eczema herpeticum on the face of an infant.
Molluscum contagiosum
Dermatophyte fungi
The lesions of molluscum contagiosum often become irritated and eczematised. This can be quite pronounced in children with preexisting AD, but can also be seen in patients without a prior history of AD. New cases of localised ‘eczema’ should always be examined for molluscum, treatment of which presents its own challenges but first priority is usually treatment of the secondary eczematous reaction.
Dermatophyte infections are uncommon in atopic dermatitis. Tinea corporis can mimic discoid eczema, so fungal scrapings are helpful if there is clinical uncertainty. Dermatophyte infections can cause a secondary generalised hypersensitivity reaction (‘id reaction’), which usually presents as pompholyx or papular eczema rather than classical atopic dermatitis. n
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