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. This aligns with the patient profile in this case, where a male farmer, primarily with right lower extremity involvement, presented symptoms. However, the specific history of trauma leading to the infection remained unclear, suggesting the possibility of neglected or unnoticed causative factors [1].
CBM manifests in various forms, including nodular, verrucous, tumorous, cicatricial, plaque, and mixed forms [1]. In this case, the patient primarily presented with plaques, accompanied by crusting, scaling, and erythema.
The current diagnostic approach for CBM involves clinical presentation, mycological examination, and histopathological study. However, fungal culture and histopathology require extended timeframes. Dermoscopy and reflectance confocal microscopy, as noninvasive techniques, offer rapid detection of characteristic abnormalities, making them suitable for assessing efficacy and monitoring disease progression. Dermoscopic findings may reveal dark brown to black pitting, crusting, scaling, and orange-yellow coloration, with multiple irregular reddish-black pits indicating the elimination process of inflammatory cells and fungal elements [3–6]. Reflectance confocal microscopy, providing real-time images, can visualize sclerotic bodies as bright white spherical vesicles due to melanin presence [7].
These imaging methods are crucial for early identification and differential diagnosis, particularly in atypical CBM cases. Although they contribute to the initial diagnosis, the final confirmation relies on mycologic examination and histopathologic study. The combination of direct microscopy, dermoscopy, and reflectance confocal microscopy findings facilitates early clarification of the diagnosis and the development of a treatment plan. This patient represents the first reported case in China with typical reflectance confocal microscopy findings, characterized by small round hyperreflective bodies.
The treatment of CBM encompasses a spectrum from traditional antifungal medications such as itraconazole and terbinafine to physical therapies, including surgery and photodynamic therapy. The disease often induces hypertrophic scarring or tissue fibrosis due to the formation of sclerotic bodies, presenting a challenge for drug penetration. Traditional treatment options involve extended treatment durations and may also be poorly tolerated. Additionally, physical therapy has its limitations and, in the absence of treatment, CBM may progress into skin cancer [8].
Imiquimod, functioning as a Toll-like receptor agonist, has demonstrated efficacy in treating external anogenital warts, actinic keratoses, and superficial basal cell carcinomas. Moreover, studies have indicated its benefits in CBM treatment by modulating immunity and shortening the treatment course [8–14]. 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, including imiquimod [15]. 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 [16, 17].
In the presented case, a combination of traditional antifungal drugs (itraconazole and terbinafine) and topical imiquimod was employed to regulate immunity. Itraconazole and terbinafine acted on the cell membrane and cell wall structure, complemented by the application of topical imiquimod. Initially, 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. Imiquimod, as an immune response modifier, enhanced the local immune response and proved effective in the short term, establishing it as an efficient therapy for CBM.