Comment
Distribution
Chromoblastomycosis, also known as chromomycosis and verrucous dermatitis,3 is a chronic subcutaneous mycosis found in tropical and subtropical regions.3,4 It is caused by traumatic inoculation of any of several members of a specific group of dematiaceous fungi through the skin.2,3 Common causative organisms include Fonsecaea pedrosoi, C carrionii, Fonsecaea compacta, and Phialophora verrucosa, all of which are saprophytes in soil and plants. Fonsecaea pedrosoi is the most common causative agent worldwide (70%–90% of cases).2Cladosporium carrionii tends to be the predominant pathogen isolated in patients who present in drier climates, with F pedrosoi in humid forests.1-4
In India, chromoblastomycosis has been reported from the sub-Himalayan belt and western and eastern coasts.1,5 Our patient resided in Ahmednagar, Maharashtra, India, which has a predominantly hot and dry climate. The history might include vegetational trauma, such as a thorn prick. Time between inoculation and development of disease is believed to be years.
Clinical Presentation
Chromoblastomycosis is characterized by a slowly enlarging lesion at the site of inoculation. Five morphological variants are known: nodular, tumoral, verrucous, plaque, and cicatricial; verrucous and nodular types are most common.3,4
The disease is limited to the skin and subcutaneous tissue, growing in extent rather than in depth and not directly invading muscle or bone.4 Lymphatic and hematogenous dissemination can occur.3,4 Secondary bacterial infection is common. The most common affected site is the lower limb, especially the foot.1,3 The upper limb and rarely the ear, trunk, face, and breast can be affected.
Diagnosis
Routine laboratory investigations are usually within reference range. Diagnosis is made by histopathological and mycological studies. Preferably, scrapings or biopsy material are taken from lesions that are covered with what is described as “black dots” (an area of transepidermal elimination of the fungus) where there is a better diagnostic yield.2-4 Routine histopathology shows hyperkeratosis, pseudoepitheliomatous hyperplasia of the epidermis, a mixed granulomatous neutrophil response with multinucleated giant cells and neutrophil abscesses, refractile fungal spores, typical sclerotic cells around abscesses or granulomas, and a dense fibrous response in the dermis and subcutaneous tissue.
Extensive fibrosis, coupled with a chronic inflammatory infiltrate and increased susceptibility to secondary infection, leads to obstruction of lymphatic flow and lymphedema below the affected site.2-4 Periodic acid–Schiff and Gomori methenamine silver stains confirm the presence of fungus. Direct microscopic examination of a 10% potassium hydroxide mount of scrapings reveals spherical, thick-walled, darkly pigmented, multiseptate sclerotic cells known as medlar bodies, copper pennies, and muriform cells that are pathognomonic for chromoblastomycosis.1-4Cladosporium carrionii culture on Sabouraud dextrose agar at 37°C shows olive green, dark, rugose, smooth, hairy, leathery or velvety colonies with pigmentation front and reverse. Direct microscopic examination of the colonies shows dematiaceous septate hyphae and sparsely branching conidiophores bearing ellipsoidal, smooth-walled conidia in long acropetal chains.1,4
Treatment
Treatment options for chromoblastomycosis can be divided into antifungal agents and physical methods.Antifungal agents include itraconazole (200–400 mg daily),3 terbinafine (250–500 mg daily),3 5-fluorocytosine (100–150 mg/kg daily),3 amphotericin B (intravenous/intralesional), and others (eg, fluconazole, ketoconazole, posaconazole [800 mg daily],6,7 potassium iodide, voriconazole). Physical methods include CO2 laser, cryosurgery, local heat therapy, Mohs micrographic surgery, and standard surgery.3 There is no evidence-based treatment protocol. Itraconazole and terbinafine are considered drugs of first choice1,8; however, combination therapy is the best option.9