Pemphigus and Infection

Autoimmune diseases are assumed to be initiated or triggered by a complex interaction of environmental factors such as infections and drugs in a genetically susceptible individual. Among the autoimmune diseases, pemphigus is a group of organ-specific autoimmune mucocutaneous blistering disorders with an established immunological basis. The clinical hallmark of pemphigus is the presence of intraepithelial blisters and erosions of the skin and the mucous membranes. Its three major variants—pemphigus vulgaris, pemphigus foliaceus, and paraneoplastic pemphigus—are characterized histologically by cell-to-cell detachment of epidermal and mucosal epithelial cells (acantholysis) caused by IgG autoantibodies directed against desmosomal adhesion molecules of affected epithelium. These autoantibodies can be visualized using the direct IF technique. Two forms of drug-related pemphigus exist; the drug-induced pemphigus is the more frequent one. In this form, unlike more common drug eruptions, drug-induced pemphigus persists even after the withdrawal of the culprit drug because the drug induces a true autoimmune disease.