Letters Chromomycosis MJA 2000; 173: 656
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To the Editor: A 38-year-old man presented with a hyperkeratotic,
crusting lesion on his right knee which had been present for 17 years
and had not responded to treatment (Box 1). The lesion developed in
1983 after he knelt on wood chips while cutting wood in scrub country to
the west of Mackay in Queensland. The lesion had slowly increased in
size and persisted despite various attempts at therapy. When it was
about 1 cm in diameter, local excision was offered, but, as the surgeon
was not able to guarantee the lesion would not recur, excision was not
performed.
In January 1996 a biopsy was taken. The report read "pseudoepitheliomatous hyperplasia" of the epidermis. In the dermis there was a "granulomatous inflammatory reaction in which there were collections of pigmented yeast bodies". The histological diagnosis was chromomycosis (chromoblastomycosis) (Box 2). Chromomycosis organisms are round, thick-walled brown cells, 5-12 mm in diameter, usually occurring in dermal microabscesses. After one month's culture, Cladophialophora carrionii (also known as Cladosporium carrionii) was isolated. By 1999, when the patient presented, he had been treated sequentially, without success, with ketoconazole (200 mg daily for six months), fluorocytosine (dose unknown) and terbinafine (250 mg daily). In October 1999, he was given itraconazole 100 mg daily. This dose was increased to 100 mg twice daily in November 1999 and was continued until May 2000, by which time the total dose of itraconazole administered was 54 g. (The patient was 179 cm tall and weighed 114 kg.) The drug has been well tolerated, with no abnormality of blood film or liver function. There has been a slow but steady healing of the knee lesion (Box 3). Chromomycosis (chromoblastomycosis) is a chronic mycotic infection of the cutaneous and subcutaneous tissues. It is diagnosed by the presence in the tissue of phaeoid (Greek phaeios, "dusky") muriform cells and by isolation and identification of the pathogenic fungus. The muriform cells represent an intermediate vegetative fungal form arrested between yeast and hyphal development. The dusky colour of these muriform cells results from a melanin pigment.1 The lesions produced by the infection are nodulo-verrucous. The fungal genera that can cause this infection (Cladophialophora, Fonsecaea, Phialophora, Rhinocladiella) live as saprophytes in soil and in decaying wood and vegetation. Infection is caused by inoculation, but the injury may be so minor as to go unnoticed and may have occurred years before the slow-growing lesion is noticed. It occurs most commonly on the feet or legs, but, in Australia, the upper limbs are more commonly involved. Cladophialophora carrionii infection is a common cause of chromoblastomycosis and, although the infection can be contracted from many environments, it is particularly prevalent in arid and semi-arid areas, most often in tropical and subtropical zones. It has been reported from North, Central and South America, Cuba, Jamaica, Martinique and many other countries, including India, South Africa, and Madagascar, as well as Australia and Northern Europe. It has occurred as an imported infection in the United Kingdom.2 Chromoblastomycosis is frustratingly difficult to treat, but it is becoming increasingly evident that itraconazole is the treatment of choice, at least for infections with Cladophialophora spp., partly because itraconazole accumulates in the skin and subcutaneous tissues owing to its lipophilicity.3 In adults the dose of itraconazole is 200 mg or more per day for as long as required (the dose is continued for a period two to three times longer than that required to obtain negative culture results).4 George R Crowe
Michael Martin Acknowledgements: Dr Brian Reid, Dermatologist, Townsville; Dr Andrew O'Neill, Mackay; Mr John Atkinson, Librarian, Mackay Base Hospital; and Ann James, Janssen-Cilag Australia.
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