Counterfeit Pennies: Distinguishing Chromoblastomycosis From Phaeohyphomycotic Infections
We read with great interest the case report by Zarei et al1 in the September issue of the American Journal of Dermatopathology titled “Chromoblastomycosis in a diabetic patient without a history of trauma.” This article is valuable in that it highlights the need to search for infectious organisms in diabetic patients even without known trauma and also raises the issue of possible laboratory contaminants. The authors describe a chronic verrucous plaque in a female diabetic patient in which the pathology demonstrated Medlar bodies within a granulomatous infiltrate. However, a close inspection of the photomicrographs provided revealed elongate hyphae in addition to round “copper penny”–like fungal elements. Indeed, the authors report that fungal culture grew mold with a final microbiology report of Scytalidium species. The authors maintained that “since Scytalidium species are very likely to be cultured as contaminants and Medlar bodies are pathognomonic for chromoblastomycosis, the patient was diagnosed with chromoblastomycosis.”
Many fungi once thought to be laboratory contaminants are being documented as etiological agents of phaeohyphomycosis and similar opportunistic mycotic infections.2 Three previous cases of Scytalidium dimidiatum causing deep dermal and subcutaneous infections were reported in patients with underlying diabetes.2–4 Similar to the case described by Zarei et al,1 these infections presented as recalcitrant abscesses and nodules on the lower extremity. We propose that the case presented by Zarei et al was a phaeohyphomycotic infection caused by S. dimidiatum and describe the clinical, pathologic, and mycologic features that help distinguish infections with phaeohyphomycoses from chromoblastomycosis (Table 1).
Scytalidium. dimidiatum, a dematiaceous ascomycete, lives on the roots of certain plants, mainly of the species Populus pinus. Human infection occurs mainly after traumatic implantation, most commonly resulting in superficial skin lesions mimicking dermatophytosis and onychomycosis. The fungus is also capable of causing deeper infections, such as subcutaneous abscesses, sinusitis, and even fungemia and disseminated infections in immunocompromised patients. It has been suggested that Scytalidium species are unique among fungi that are capable of producing keratinase enzyme, thus allowing the fungus to invade skin in a similar fashion as seen in infections caused by dermatophytes.5 Recent work has proven that members of the genus Scytalidium synthesize melanin.4
Melanized (dematiaceous) fungi are associated with a wide variety of cutaneous infections, including chromoblastomycosis, mycetoma, and phaeohyphomycosis.6 In chromoblastomycosis, the tissue form of the etiological agent is a dark, thick-walled, muriform cell that divides by both horizontal and vertical septation, whereas in phaeohyphomycosis, septate mycelia tend to predominate. The distinction is important not only for epidemiological purposes but also because of the differences in antifungal susceptibility of the causative organisms. Subcutaneous phaeohyphomycosis may be treated with oral azoles that have activity against dematiaceous fungi. Itraconazole, voriconazole, and posaconazole demonstrate the most consistent activity against these fungi. Fluconazole has negligible activity against dematiaceous molds and essentially no role in therapy. Treatment choices for chromoblastomycosis include itraconazole alone or in combination with fluconazole, flucytosine, cryosurgery or heat, amphotericin B, and terbinafine.7
Chromoblastomycosis is caused by saprophytic pigmented fungi commonly found in the soil and plant debris of tropical and subtropical climates. Accordingly, infection generally occurs after traumatic implantation in rural farmers. It occurs primarily in Central and South America, with rare cases reported in Europe, North America, Australia, and Africa. There is a predilection for the distal lower extremities, although in Australia, there is a higher incidence of lesions occurring on the hands. The primary lesion of chromoblastomycosis is a pink scaly papule that enlarges slowly into a verrucous nodule or plaque. The nodular stage may superficially resemble subcutaneous nodule of phaeohyphomycosis.