Eighty serum samples from patients with bronchopulmonary aspergillosis {50 patients with aspergilloma, 19 with allergic bronchopulmonary aspergillosis (ABPA), 9 with Aspergillus pneumonia, and each one with tracheal aspergillosis and bronchial stump aspergillosis}, and 88 sera for controls (several kinds of fungal diseases except aspergillosis, respiratory tract diseases, healthy adults, etc.) were studied for antibody response to Aspergillus fumigatus antigens by means of counterimmunoelectrophoresis (CIE).
Two antigens, called J antigen and T antigen, were used for CIE. The former is our own crude antigen produced by a selected strain of A. fumigatus (ATCC 26430), and the latter is a semicommercial one produced by Torii pharmaceutical compancy.
The patients with aspergilloma were classified into 8 groups by the certainty of diagnosis using their chest roentgenograms and fungal cultural examinations of their sputa, in conjunction with testing their sera.
The results were as follows: Out of 50 sera from patients with aspergilloma, 45 (90%) and 44 (88%) reacted positively to J antigen and T antigen, respectively, and out of 19 sera from patients with ABPA, 5 (26.3%) reacted positively to both antigens. The sera from the other aspergillosis and those from the controls reacted negatively to both antigens. No significant statistical difference in the positive reaction rates was noted among the 8 groups of the patients with aspergilloma.
In this study, no difference was detected in sensitivity, specificity, and efficacy between J antigen and T antigen in diagnosis of bronchopulmonary aspergillosis. The author thus hopes that the A. fumigatus crude antigen used for serodiagnosis in his laboratory can be mass-produced and made available to all researchers.
CIE test was a satisfactory method for the diagnosis of aspergilloma because of its simplicity, rapidity, and specificity.

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Asp-hemolysin production of six strains of Aspergillus fumigatus, FM, K-2, K-9, AUGE, IAM and TIMM was examined. A each toxic fraction of each was prepared from a mixture of the mycelium and culture filtrate by procedures that included precipitation with ammonium sulfate, gel filtration on Sephadex G-50, and chromatography of DEAE-Sephadex.
In the hemolytic activity levels of each FI fraction, FM had very high activity but K-2, K-9 and IAM, and TIMM and AUGE showed very low or no activity, respectively. Moreover, four antigens (hemolytic activity; positive), Asp-hemolysin, FI of K-2, K-9 and IAM formed one precipitin line that completely fused against anti-Asp-hemolysin serum with Asp-hemolysin purified from the FM strain.
All the FIs of tested strains were found to possess binding ability to human erythrocytes using indirect enzyme-link immunosorbent assay under a light microscope.

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In an attempt to evaluate effects of severe liver injury on susceptibility to Candida infection, we conducted experiments on experimental Candidiasis using mice with carbon tetrachloride-induced liver injury. In the group administered carbon tetrachloride, liver injury was characterized by necrosis of liver parenchyma predominantly distributed in the centrilobular area. With intravenous inoculation of Candida, these mice died earlier and final survival was 0%. In contrast, a 20% survival rate was seen in the group with Candida and without liver injury. Candidial lesions were extensive and disseminated, involving lung and heart in the group with liver injury, but predominantly localized to kidneys in the group without liver injury. This study demonstrated that susceptibility to Candida is enhanced in the presence of severe liver injury.
In the group with liver injury, transferrin (TIBC) was significantly decreased as compared with the other group. Therefore, it is suggested that the decreased amount of TIBC may enhance the susceptibility to Candida infection; however, in the group with liver injury, administration of apotransferrin did not compensate the decreased TIBC, which was unable to reverse the carbon tetrachloride-induced Candida-enhancing activity. Thus, more studies are needed to fully understand the relationship between the roles of iron metabolism and increased susceptibility to Candida infection.

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The killer toxin of Hansenula mrakii IFO 0895 completely inhibited the growth of all of 51 Candida glabrata strains and four Candida krusei strains tested at concentrations of 10μg/ml or less. The minimum inhibitory concentration (MIC) of the killer toxin against all 74 Candida albicans strains, 12 Candida tropicalis strains, and five Candida parapsilosis strains tested was 100μg/ml or more.
C. albicans and C. glabrata are the two major yeast pathogens that cause vulvovaginal mycosis, so that isolation and identification of these two species are useful in the laboratory diagnosis of the disease. We attempted to identify the two species on the basis of their different susceptibility to the H. mrakii killer toxin. A plate with a 90-mm diameter divided into two parts with a plastic barrier was used. One contained MS medium, which was YEPD medium (2% glucose, 1% Bacto-peptone, 0.5% yeast extract, and 1.5% agar) containing 100mg of mezlocillin, 50mg of sisomicin, and 20mg of potassium tellurite per liter, which are all antibacterial substances. The other contained MS medium, with 15mg of killer toxin and 20mg of the dye amaranth per liter. This novel medium was called KMS medium.
Of 75 patients with vaginitis examined in the obstetrics and gynecology departments of the authors using the two media, only the two species of C. albicans and C. glabrata were detected in vaginal smears. Fifty of the 75 patients were infected with C. albicans and 20 with C. glabrata. Four of the 75 patients were infected with both C. albicans serotype A and C. glabrata, and one was infected with C. albicans serotypes A and B.

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An evaluation of the mycological effect after treatment by culture and direct examination, and a study of the rate of recurrence in Pityriasis versicolor were carried out.
Patients were treated for 1 to 4 weeks. After treatment they were examined every month for up to 6 months. Positive rates of Malassezia furfur after treatment were very low by direct examination but relatively high by culture. Imidazole cream was found to be more effective in relief of the condition than lotion. The rate of recurrence was more than 60% after 6 months. Patients who were negative by culture on completion of treatment seldom recurred within 2 months. Positive rates of Malassezia by culture in patients who did not recur were higher than that of controls after 3 months.

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We reported earlier on a 59-year-old man with generalized granuloma trichophyticum caused by Trichophyton rubrum (Mycopathologia, 82, 77-82, 1983).
Since the definitive diagnosis of generalized granuloma trichophyticum was made, the patient was treated with griseofulvin, and the multiple cutaneous nodules, indurative plaques and ulcers apparently disappeared. But a few years later, ulcers recurred and developed on his right axilla, back and left upper extremity. A biopsy specimen taken from the ulcers was cultured on Sabouraud's dextrose agar. Colonies from the specimen grew at 37°C but were not successful grown at room temperature within two weeks. This isolate had no sensitivity to griseofulvin, but did have sensitivity to ketoconazole, and the patient was completely healed by using oral ketoconzaole.

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The in vitro antifungal activity of rimoprogin, a new 3-iodopropargyl derivative containing a pyrimidine moiety, was studied compared with that of another active 3-iodopropargyl derivative, haloprogin and an imidazole antimycotic, isoconazole, and the following results were obtained:
1) Rimoprogin was found to have a broad antimicrobial spectrum, inhibiting growth of various fungal pathogens including yeasts, dermatophytes, aspergilli, zygomycetous fungi, dimorphic fungi and dematiaceous fungi, as well as Gram-positive bacteria, at low drug concentrations. Of these fungi, dimorphic fungi were the most susceptible to rimoprogin. Then, dermatophyte fungi, aspergilli, dematiaceous fungi, yeasts and zygomycetous fungi were susceptible in this order.
2) The antifungal activity of rimoprogin was influenced to a slight extent by the inoculum size and the period of incubation. However, the activity varied remarkably with pH of the culture medium; it was significantly enhanced at low (acidic) pH values. Addition of serum to the medium reduced the activity of rimoprogin.
3) Rimoprogin exerted fungicidal action toward Candida albicans and Trichophyton mentagrophytes exposed for 6 hours to 2.5μg/ml or greater concentrations of the drug.
From the above results, we are able to state that rimoprogin is promising for treatment of dermatomycoses.

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A 74-year-old man with chromomycosis exacerbated by long term topical corticosteroid application is reported. A scaly eruption of the same region followed the abrasion. He had been treated with topical corticosteroid for about one year and the eruption had progressively worsened. When he visited our department in January, 1986, the eruption had grown into a large erythematous plaque, 5×26cm in size, with thick scales. KOH-mount examination revealed numerous fungal elements in the scales, especially an unusually large number of hyphae. Histopathological study revealed abundant sclerotic cells in the epidermis and the dermis. Fonsecaea pedrosoi was isolated from both the scales and the biopsy specimen. After the topical corticosteroid application was discontinued, the number of hyphae in the scales and those of sclerotic cells in the biopsy specimen decreased remarkably. In addition, histopathological study showed a decrease of PMNs in contrast with an increase of lymphocytes, histiocytes and plasma cells. The skin lesion was treated successfully with topical hyperthermia by a warm bath (43°C) for 2 hours twice a day and oral 5-FC. This case demonstrates that topical corticosteroid application can exacerbate chromomycosis including increasing the number of fungal elements, especially the number of hyphae in the scales. These results may be explained by the reduced function of cell mediated immunity associated with humoral immunity produced by topical corticosteroid application.

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A case of cutaneous nocardiosis associated with hemolytic anemia and generalized ringworm is presented. A 54-year-old man noticed a subcutaneous nodule on the right thigh without any history of trauma in January 1988. Since that time he had been treated with oral administration of corticosteroid for hemolytic anemia and topical antifungal ointment for generalized ringworm. Physical examination revealed a 67×54mm, firm, subcutaneous nodule on the inner part of the right thigh, and many scaled erythemas with or without infiltration on the trunk and extremities. His fingernails and toenails were thickened and discolored. Trichophyton rubrum was isolated from the erythematous lesions. Biopsy of the subcutaneous nodule revealed extensive abscesses with numerous Gram-positive filaments in the subcutaneous fat tissue. The organism isolated from the biopsy specimen yielded folded, orange-colored colonies on Sabouraud's dextrose agar, later identified as Nocardia asteroides by cell wall composition and physiological characteristics. He was successfully treated with griseofulvin for generalized ringworm, surgical drainage and administration of antibiotics for the nocardial subcutaneous abscess. However, a nocardial metastatic abscess was noted in the abdominal wall 2.5 months after therapy was discontinued.
A review of 11 reported cases of secondary cutaneous nocardiosis in Japan and taxonomic comments on the isolated Nocardia asteroides are presented.

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Spores of Absidia corymbifera were inoculated orally into sheep with ruminal acidosis produced by feeding on barley. Lesions, which developed in the forestomachs of all four inoculated cases, included desquamation of superficial layers of the mucosae and focal necrosis from the lamina propria to muscular layers. Granulomatous lesions were found in the submucosa of three sheep. Lesions in the abomasum (two sheep) included focal necrosis, diffuse hemorrhages, and infiltration of neutrophils. All lesions were accompanied by mycotic proliferation. These results show that A. corymbifera can invade forestomach mucosae through degenerated epithelium resulting from ruminal acidosis.

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