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Disrupted skin in patients with eczema or 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 on the extent of the abnormal skin.
An underlying T-cell immunologic defect is suspected in some patients with atopic dermatitis 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 developing on otherwise “healed” skin following possible viremic spread.
If early diagnosis is not established and treatment with VIG is delayed, viremia may allow 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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