Multiple asymptomatic verrucous plaques over the legs

Cutaneous Chromoblastomycosis caused by Cladosporium carrionii

Discussion

Chromoblastomycosis is a localized, chronic subcutaneous mycosis caused by any of the several species of dematiaceous fungi with melanin-type pigment in the wall, commonly seen in tropical and subtropical climates. It usually occurs in the lower extremities following traumatic implantation of the organism. The condition is characterized by verrucoid, ulcerated and crusted lesions, either flat or raised above the skin surface. Although dematiaceous fungi have a world-wide distribution, it has a higher prevalence in areas of tropical and sub-tropical climate. Chromoblastomycosis was first described in Brazil in 1914 by Max Rudolph, a German physician. He published a report of six cases and isolated a dark, grey to black-colored fungus. Medlar, in 1915, described the characteristic histologic appearance of sclerotic bodies, which thereafter named as Medlar bodies. Other synonyms include "copper-penny" bodies or "muriform" cells. They are globose-shaped, cigar-colored, thick-walled structures that are 4-12 μm in diameter. These structures multiply by septation, and they induce a purulent and granulomatous inflammatory reaction in tissue. Six species or genera are accepted to cause chromoblastomycosis-Fonsacea pedrosoi, Phialophora verrucosa, Cladophialophora carrionii and Fonsacea compacta are common causes. Rarely caused by Rhinocladiella aquaspersa and Exphiala species, ^[1] the disease is characterized by the presence, in infected tissue, of sclerotic bodies or Medlar bodies.

Clinically, plaque type of cutaneous chromo blastomycosis may resemble cutaneous tuberculosis, warts, cutaneous phaeohyphomycosis or cutaneous sarcoidosis. Histopathological differential diagnoses would be other subcutaneous mycoses and foreign body granuloma. But, KOH mount of the crust will clinch the diagnosis of chromoblastomycosis. Histopathological examination is highly characteristic.

The taxonomy of the organism that causes chromoblastomycosis is complex. Their identification is based on somewhat distinct microscopic morphologic features. Cladosporium is characterized by long chains of elliptical conidia (2 to 3 μm Χ 4 to 5 μm) borne from erect, tall, branching conidiophores. Hyphae are septate and brown in color. Conidiophores are long and branched, and give rise to chains of darkly pigmented budding conidia. Conidia are usually single-celled and exhibit prominent attachment scars (disjunctors) that may resemble "shield" cells. This organism may often fail to reveal chains of conidia on wet mounts because conidia are easily dislodged. Phialophora verrucosa produce tube-like or flask-shaped phialides each with a distinct colarette. Conidia are produced endogenously and occur in clusters at the tip of phialide. Fonsacea pedrosoi and Fonsacea compacta show conidial heads with sympodial arrangement of conidia, with primary conidia giving rise to secondary conidia. ^[2]

There are many case reports of chromoblastomycosis from India caused by agents other than Cladosporium carrionii. ^[3],[4] Even though, it has been mentioned in the literature that Cladosporium carrionii is one of the common agents causing cutaneous chromoblastomycosis, we could not find many case reports in the literature and in India, it appears to be rare.

The main treatment of chromoblastomycosis involves the use of antifungal chemotherapy. Itraconazole with or without flucytosine is often successful, although responses to itraconazole alone are thought to be better if the causative organism is Cladosporium carrionii. Flucytosine alone or combined with amphotericin B may also be effective. Other options include terbinafine 250 mg/day, thiabendazole, cryotherapy or local application of heat. Surgery is indicated in very small lesions, and even in these should be combined with chemotherapy. ^[5]