Blastomycosis-like Pyoderma Arising in Lichen Planus

A 71-year-old Fitzpatrick phototype IV man with a history of hyperlipidemia and extensive travel to the Middle East presented with a mildly painful vegetative growth on his right lower leg for 1.5 months (Figure 1). In 2014, the patient reported a pruritic “rash” in the same location, which was treated with fluocinonide .05% ointment with resolution.Physical examination revealed a well-circumscribed violaceous scaly plaque with a central exophytic cerebriform soft nodule. Histopathological examination of a shave biopsy revealed papillated and endophytic acanthosis with hyperkeratosis, neutrophilic inflammation and congested granulation tissue (Figure 2). A punch biopsy from the plaque demonstrated a vacuolar interface and mild superficial perivascular dermatitis with acanthosis and dermal hemosiderin deposition, most consistent with hypertrophic lichen planus (Figure 3). Tissue cultures, PAS and T. pallidum immunostains were negative. Taken together, these features were suggestive of blastomycosis-like pyoderma arising in lichen planus.Following biopsy, the patient was treated with topical steroid clobetasol cream and the lesion resolved with post-inflammatory pigment alteration.

Blastomycosis-like pyoderma (BLP) is a rare reactive skin disease that results from an exaggerated immunological response to a prolonged inflammatory milieu. Historically, it arises in the setting of bacterial infection with Staphylococcus aureus, Pseudomonas aeruginosa and β-hemolytic streptococci as the most frequently implicated microorganisms. BLP typically affects the elderly and otherwise immunocompromised patients, though there is evidence that it can occur in normocompetent individuals, as seen with our patient.¹ Clinically, patients with BLP present with large, crusted, verrucous plaques with pustules and well-defined and raised borders. Although the etiology is unknown, it was postulated that acute inflammatory responses induce localized neutrophilic infiltrates that release connective tissue-activating peptides and trigger the rapid production of glycosaminoglycans, found in ground substance and fibroblasts. This flourish of connective tissue elongates dermal papillae, which support a larger germinative cell volume producing the pseudocarcinomatous hyperplasia seen in BLP.² Pseudocarcinomatous hyperplasia, a common histological feature of BLP, can mimic an epithelial neoplasm like squamous cell carcinoma (SCC), making this entity both clinically and pathologically challenging. This highlights the necessity for a tissue diagnosis both to identify infectious agents and rule out malignancy when confronted with BLP. Treatment for BLP includes antibiotics to which cultured organism(s) is/are sensitive, intralesional corticosteroids, acitretin, surgical excision, or local ablative measures.³Interestingly, infection was not the causative factor but rather a primary inflammatory disease. Lichen planus (LP) is a chronic inflammatory papulosquamous dermatosis that is historically characterized by pruritic, polygonal, flat-topped, violaceous papules and plaques, however numerous atypical presentations have been reported ranging from annular/atrophic to bullous.⁴ In line with the discussion above, SCC has been reported in oral LP, and also, though less commonly, in cutaneous LP.⁵ There are several reported cases in which SCC arose in hypertrophic cutaneous LP located on lower limbs.⁶ In BLP, a chronic inflammatory insult induces squamous cell proliferation in