# Lyme Disease Causing Complex Bullous Lesions: A Case Report

**Authors:** Carlos E Levischi

PMC · DOI: 10.7759/cureus.92859 · Cureus · 2025-09-21

## TL;DR

A Brazilian patient with Lyme disease developed a rare skin condition called epidermolysis bullosa, which was treated with antibiotics and immunomodulators.

## Contribution

This case report highlights the rare autoimmune complication of Lyme disease and the effectiveness of combined antibiotic and immunomodulatory treatment.

## Key findings

- The patient showed subepidermal cleavage and linear IgG deposits, confirming acquired epidermolysis bullosa.
- Treatment with doxycycline and dapsone led to lesion regression and improved inflammatory markers.
- Immunomodulation with colchicine and hydroxychloroquine helped control the autoimmune response.

## Abstract

Lyme disease (LD), caused by the spirochete Borrelia burgdorferi, 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.

## Linked entities

- **Chemicals:** doxycycline (PubChem CID 54671203), dapsone (PubChem CID 2955), colchicine (PubChem CID 2833), hydroxychloroquine (PubChem CID 3652)
- **Diseases:** Lyme disease (MONDO:0019632), epidermolysis bullosa (MONDO:0006541)

## Full-text entities

- **Genes:** COL7A1 (collagen type VII alpha 1 chain) [NCBI Gene 1294] {aka EBD1, EBDCT, EBR1, NDNC8}
- **Diseases:** autoimmune response (MESH:D001327), autoimmune complications (MESH:D020274), autoimmune manifestations (MESH:D012877), inflammatory (MESH:D007249), LD (MESH:D008193), EBA (MESH:D004820), erythema migrans (MESH:D005929)
- **Chemicals:** doxycycline (MESH:D004318), dapsone (MESH:D003622), colchicine (MESH:D003078), hydroxychloroquine (MESH:D006886)
- **Species:** Borreliella burgdorferi (Lyme disease spirochete, species) [taxon 139], Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

8 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12542265/full.md

## References

39 references — full list in the complete paper: https://tomesphere.com/paper/PMC12542265/full.md

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Source: https://tomesphere.com/paper/PMC12542265