[A case of chromomycosis arising in a Japanese-Brazilian patient].

A 41-year-old Japanese-Brazilian man, living in Japan since 1991, visited our hospital in August 1998 complaining of a scaly annular erythema which had been present on his right forearm since 1996. Granulomatous inflammation was revealed in the dermis upon skin biopsy. Sclerotic cells were present within the granulomatous lesions. Fonsecaea pedrosoi was isolated from tissue cultures. The restriction fragment length polymorphism pattern of mitochondrial DNA of the causative fungus was compatible with F. pedrosoi type 1, the commonest type in Japan. Since type 4 is usually found in South America, the patient was assumed to have become infected in Japan. An oral dose of terbinafine at 125 mg/day was ineffective. 125 mg/day single dose of terbinafine reaches an average plasma concentration of only 0.69 g/ml, where as 250 mg/day reaches 0.96 micro g/ml. Because the minimum inhibitory concentration (MIC) of terbinafine against the isolated fungus was found to be 0.76 micro g/ml, the terbinafine dose was increased from 125 mg/day to 250 mg/day, which slowly led to remission. Chromomycosis is caused by several species of dematiaceous fungi, and terbinafine efficacy may vary depending on the causative fungus. MIC values may differ even within the same species. It is important to isolate the pathogenic fungus in each case and measure the MIC value to determine the optimal dose of terbinafine.

Ultrastructural localization of Brazilian pemphigus foliaceus (fogo selvagem) antigens in cultured human squamous cell carcinoma cells.

The ultrastructural localization of Brazilian pemphigus foliaceus (BPF) (fogo selvagem) antigen(s) in cultured human squamous cell carcinoma cells was studied using immunogold electron microscopy. Five of six BPF sera, which showed positive cell-surface reactivity on immunofluorescence, bound to the cell-cell contact area of cytoplasmic projections. This binding pattern was apparently different from that of non-endemic pemphigus foliaceus and pemphigus vulgaris sera, and mouse monoclonal anti-human E-cadherin antibody. The results suggest that BPF autoantibodies recognize a molecule(s) which is different from non-endemic pemphigus antigens, or different epitope(s) of a molecule identical with non-endemic pemphigus antigens, and that the epitope(s) to which BPF autoantibodies bind is expressed on cell-cell contact areas at a relatively early stage of cell-cell adhesion formation.