Dermatopathology of COVID-19 infection and vaccination

Many peculiar skin changes have been described in relation to both coronavirus disease 2019 (COVID-19) infection and vaccination.

This paper provides an overview of these dermatologic manifestations, focusing on their dermatopathological appearances.

Most COVID-19 patients develop variegated maculopapular eruptions with a combination of histological patterns commonly including keratinocyte apoptosis and eosinophilia. Urticaria-like lesions often show a combination of spongiotic and lichenoid patterns and are more frequent in individuals with severe disease. Vesicular lesions can be disseminated; in some cases, they become pustular and in others show dyskeratosis and a peculiar form of ballooning. Some patients develop vesicular Grover disease on the trunk. Young patients with a strong immunological response can eliminate the virus easily but may develop chilblains as a consequence of the high interferon response. Conversely, older individuals with immunosenescence and a tendency toward hypercoagulability can present livedoid and ischemic areas. Regarding COVID-19 vaccination, hypersensitivity reactions are most frequent, including “COVID-arm.” Nonetheless, a combination of local and systemic cutaneous manifestations (reactogenicity) is commonly seen. Histopathologically, lichenoid and spongiotic changes and a variable number of eosinophils are typical of rashes characterized by papules and plaques. Other dermatological side effects of COVID-19 vaccination include lesions mimicking well-defined dermatoses such as lichen planus or bullous pemphigoid and triggering of collagenous diseases.

Well-characterized skin manifestations of coronavirus disease 2019 (COVID-19) include chilblains, livedo necrotic lesions, vesicular eruptions, urticarial lesions, and maculopapular eruptions. Hypersensitivity reactions are common after SARS-CoV‑2 mRNA vaccination. Vaccine reactions may also mimic other dermatosis such as bullous pemphigoid or lichen planus, stimulate herpes reactivation, or trigger the development of autoimmune diseases.