The main pathogens of CBM include Fonsecaea pedrosoi, Fonsecaea monophora, Fonsecaea nubica, and Fonsecaea pugnacious [1]. Fonsecaea monophora has emerged as a significant pathogen in the southern region, responsible for a considerable number of reported cases in Guangdong [2]. Typically, the infection originates from breaches in the skin barrier, such as those caused by plant punctures from thorns or wood, a common occupational hazard in farming [1]. This aligns with the patient profile in this case, where a male farmer, primarily with right lower extremity involvement, presented with plaques, accompanied by crusting, scaling, and erythema. However, the specific history of trauma leading to the infection remained unclear, suggesting the possibility of neglected or unnoticed causative factors.

The current diagnostic approach for CBM involves clinical presentation, mycological examination, and histopathological study. However, these methods often necessitate considerable time. Dermoscopy and reflectance confocal microscopy offer rapid, noninvasive detection of characteristic abnormalities, aiding in early diagnoses and monitoring disease progression. Dermoscopic findings may reveal dark brown to black pitting, crusting, scaling, and orange-yellow discoloration, with multiple irregular reddish-black pits indicating inflammatory cell and fungal element elimination [3,4,5,6]. Reflectance confocal microscopy provides real-time images, visualizing sclerotic bodies as bright white spherical vesicles due to melanin presence [7]. These imaging techniques are crucial for early identification and differential diagnosis, especially in atypical CBM cases. While they aid initial diagnosis, confirmation still relies on mycologic examination and histopathologic study. Combining direct microscopy, dermoscopy, and reflectance confocal microscopy facilitates early diagnosis and treatment planning. The patient marks the first reported case in China demonstrating typical reflectance confocal microscopy findings, characterized by small round hyperreflective bodies.

CBM often induces hypertrophic scarring or tissue fibrosis due to the formation of sclerotic bodies, presenting a challenge for drug penetration. CBM might be linked to a defect in innate Toll-like receptor recognition, a deficiency that can be rectified by the exogenous administration of Toll-like receptor agonists [8]. Imiquimod, functioning as a Toll-like receptor agonist, has demonstrated efficacy in treating external anogenital warts, actinic keratoses, and superficial basal cell carcinomas. Studies have indicated its benefits in CBM treatment by modulating immunity and shortening the treatment course [9,10,11,12,13,14,15,16,17,18,19]. In addition, imiquimod inhibits collagen synthesis by promoting the production of the Th1 cytokine TNF-γ, and also inhibits the Th2 cellular immune response by inhibiting the production of the Th2 cytokines IL-4, IL-5, etc., ultimately controlling scar hyperplasia [20, 21]. In this case, conventional antifungal medications alone provided suboptimal results. However, after one month of combining imiquimod with the patient’s treatment regimen, the skin lesions exhibited significant flattening, and histopathology revealed a marked reduction in inflammatory cells. We speculate that imiquimod played a role in enhancing host immune cell function and anti-fibrotic effects during this process, thereby shortening the treatment duration.