Lyme Disease Causing Complex Bullous Lesions: A Case Report

Lyme disease (LD), caused by the spirochete <i>Borrelia burgdorferi</i>, is a multisystemic zoonosis that can progress to severe autoimmune manifestations in its advanced stages. This article describes the case of a Brazilian patient who developed acquired epidermolysis bullosa (EBA) following an LD diagnosis. Initially, the patient presented with atypical erythema migrans, which later evolved into multiple bullous lesions characterized by cycles of exacerbation and remission. Histopathological investigation revealed subepidermal cleavage with linear IgG deposits along the basement membrane, confirming the diagnosis of EBA. Treatment consisted of doxycycline and dapsone for 90 days, leading to regression of the lesions, normalization of inflammatory markers, and significant clinical improvement. After completing antibiotic therapy, immunomodulation with colchicine and hydroxychloroquine was initiated to control the autoimmune response. This case highlights the immune-mediated impact of LD, where autoantibodies, such as anti-collagen VII, can play a central role in perpetuating symptoms. These findings emphasize the importance of a personalized diagnostic and therapeutic approach, incorporating both antibiotics and immunomodulators, to manage LD-associated autoimmune complications. The complexity of the disease underscores the necessity of multidisciplinary care and integrated interventions to minimize sequelae and improve the quality of life for affected patients.