A 36-year-old woman visited our hospital with a five month history of persistent pustulation, crusting, and alopecia on the vertex of the scalp. No pathological organisms were isolated from the lesions. Histological examination revealed non-specific changes of chronic inflammation with destroyed follicles. Antibiotic therapy produced no response, but steroid therapy was effective. From these observations, a diagnosis of erosive pustular dermatosis of the scalp (EPDS), as described by Pye et al., was made. The patient also had Hashimoto's thyroiditis, autoimmune hepatitis, and Takayasu's aortitis. The laboratory studies revealed an increased erythrocyte sedimentation rate, C-reactive protein 3+, hypergammaglobulinemia, and various auto-antibodies, suggesting the possibility of a pathogenesis common to both this dermatosis and the autoimmune diseases.

Figure 1 Total colonoscopy revealed a single ulceration (a) with several erosions in the ascending colon. Capsule endoscopy also revealed a single ulceration (b) with several erosions in the jejunum very similar to the one found in the ascending colon.

Forty-nine strains of anaerobic gram-positive rods were used in a systematic study of their biochemical and physiological reactions and morphological characteristics and were also subjected to gas chromatographic analyses in an effort to classify them as strains of Corynebacterium acnes (C. acnes). The strains were isolated both from lesions in acne vulgaris and from normal skin. According to their biochemical and physiological characters, these 49 strains were divided into six subgroups (Subgroup A-F). They were also separated into two morphological types. The larger of these two types included gram-positive, unevently staining pleomorphic rods (35 strains); the smaller type contained shorter coccal rods similar to Peptostreptococci (14 strains). The macroscopic appearance of the colonies of both types was the same. All strains of the smaller type showed the same biochemical and physiological characteristics which were of the saccharolytic type (Subgroup B) suggesting a close relationship between the microscopic appearance of the strains and their biochemical and physiological characteristics. Upon microscopical observation, the changing the pH of the media did not cause any transformation of the organism from one type to another. Between pH 6.0 and 6.5 all strains grew well but above pH 8.0 growth was poor. The gas chromatographic analyses demonstrated that selected sample strains from each of the six subgroups showed the same characteristic chromatograph, suggesting that they could be of the same species, i.e., C. acnes.

Onychomycosis caused by Candida is often accompanied by paronychia. Not only the morbid changes in the nailplate caused by the true parasitism by Candida but also the secondary changes in the nail due to candidial paronychia are sometimes handled as though they were candidial onychia. Onychomycosis caused by candidial infection, i.e., nail candidiasis, is entirely different in its pathogenetic respects from the secondary ungual changes due to candidial paronychia. The reason why both are classified together as candidial onychia appears attributable to the ambiguous characterization of their clinical and pathological features. We therefore undertook a statistical analysis of 765 cases of candidiasis who visited the Dermatological Department of Tokyo University Hospital during the period from 1969 to 1980. Of these, 25 cases of nail candidiasis (primary onychia) were sorted out, followed by clinical and pathological examinations. The results showed that nail candidiasis appeared in 14.3% of the candidial paronychia and onychia cases, and no significant differences from candidial paronychia were attributable to age or sex. On the other hand, it was found that nail candidiasis was clinically characterized by subungual hyperkeratosis, while the fungal element appeared histopathologically in the lower part of the nailplate, taking an abnormal parasitic form similar to that in dermatophytes. The pathogen causing nail candidiasis was Candida albicans and was resistant to various therapies. The only effective therapy was oral administration of Ketoconazole. Nail candidiasis is often accompanied by underlying diseases like SLE which result in cellular immunodeficiency. While chronic mucocutaneous candidiasis occurs with a background of congenital cellular immunodeficiency to Candida, nail candidiasis appears to have an acquired immunodeficiency as the background. In short, nail candidiasis can be interpreted as a candidiasis which occurs when the host/parasite relations are disturbed. In this sense, it appears that nail candidiasis can be regarded as a dermadrome which reflects cellular immunodeficiency of host.