Disrupted
skin in patients with atopic dermatitis permits viral implantation.
Once the virus is implanted (and it may be implanted at multiple
sites) it spreads from cell to cell producing extensive lesions
dependent only on the extent of the abnormal skin.
An underlying T-cell immunologic defect is suspected in some
patients with atopic eczema on the basis of their propensity
to develop cutaneous viral and fungal infections and a decreased
sensitivity to contact dermatitis which is T-cell mediated.
Some patients with T-cell immune deficiencies have atopic
dermatitis as a feature, also suggesting a link between the
two. Laboratory findings support this hypothesis. The T-cell
defects are a contributory factor to the severity of vaccinia
infection and help explain lesions in ěhealedî skin.
If early diagnosis is not established and treatment with VIG
is delayed, viremia ensues allowing for the spread of virus
to other parts of the body, including skin that is not affected
by eczema. Bacterial and fungal invasion may occur as a late
stage of untreated eczema vaccinatum.
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