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Author: Smriti Tandon, Paediatric Registrar, The Royal Children’s Hospital Melbourne, Australia. DermNet NZ Editor in Chief: Adjunct A/Prof. Amanda Oakley, Dermatologist, Hamilton, New Zealand. Copy edited by Gus Mitchell. January 2020.
Eczema coxsackium is an enteroviral infection typically affecting children with atopic dermatitis (eczema). It is characterised by an eruption of vesicles, bullae, and erosions affecting areas of active or inactive atopic dermatitis.
Eczema coxsackium is a form of Kaposi varicelliform eruption, and has been described as atypical hand, foot and mouth disease (HFM). Both conditions are caused by enterovirus. However, eczema coxsackium is more widespread than hand, foot and mouth disease, and presents with vesiculobullous lesions that ulcerate and scab. The term eczema coxsackium was coined by Nahmias et al in 1968 .
Eczema coxsackium most commonly affects preschool-age children with atopic dermatitis . It affects both boys and girls, and typically presents during late spring to early summer [3–4]. There have been reported cases in adults [2,5].
Enteroviral infection can also localise to sites of epidermal barrier breakdown that are not caused by eczema. Reported cases of non-eczematous conditions prone to enteroviral infection include [2,5–8]:
Coxsackievirus A6 and A16 are the most common causes of eczema coxsackium.
The reason why the enterovirus localises to sites with atopic dermatitis remains unclear. It is thought the mechanism is similar to eczema herpeticum, where afflicted patients appear to have impaired immunity to the virus and barrier dysfunction at the affected sites . This mechanism may explain how non-eczematous conditions such as Darier disease have also presented with a widespread viral infection that preferentially erupts at the sites of the skin disease .
Eczema coxsackium presents with vesicles, bullae, and erosions.
Reverse transcription-polymerase chain reaction (RT-PCR) sequencing of blister fluid, stool, and oropharyngeal swabs can be used to confirm the presence of enterovirus. Coxsackievirus is difficult to culture in vivo. Thus, viral culture is not useful and has a high likelihood of a false negative result.
The main differential diagnosis for eczema coxsackium is eczema herpeticum.
Eczema coxsackium self resolves and does not usually require hospital admission.
Whilst waiting for microbiological confirmation, oral antiviral therapy (eg, aciclovir or valaciclovir) can be prescribed to treat herpes simplex but enterovirus does not respond to this. Specific anti-enteroviral medications or vaccines for enterovirus are not currently available (2020).
Children can become dehydrated if they are not drinking due to painful oral ulcers and they may need admission for intravenous or nasogastric rehydration.
Non-medicated emollients are recommended to treat active eczema. Topical steroids are generally not recommended during the acute illness but can be reintroduced to treat the associated eczema once the child is afebrile.
Common complications during the convalescence phase of eczema coxsackium include desquamation of the palms and soles and nail changes.
Nail changes occur 1–2 months after the acute infection and include:
Unlike other enteroviral infections, multiorgan involvement is rare in children with cutaneous coxsackievirus A6/16 infection.
Numerous outbreaks of enterovirus have occurred worldwide. Enterovirus is highly infectious and easily spreads via vesicle fluid, respiratory secretions, and faecal-oral contamination. Children should be excluded from school until all blisters have dried up.
Good hand hygiene is paramount in preventing spread from other bodily secretions. Stools remain infectious for up to one month after the acute illness.
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