A novel elastase inhibitor from Aspergillus nidulans NBRC 4340, Asnidin, was isolated, and biochemical properties and partial amino acid sequence were examined. Column chromatography using diethylaminoethyl (DE) 52-Cellulose and reversed-phase HPLC were used to purify the inhibitor. Purified Asnidin was found to be homogeneous as indicated by reversed-phase HPLC and TOF-MS (Time of Flight Mass Spectrometry). Asnidin has a molecular weight of 4,181.63 as determined by TOF-MS. The elastolytic activities of elastases from A. fumigatus, A. flavus, and human leukocytes but not chymotrypsin, and elastases from snake venom and bacteria were inhibited by Asnidin. The fibrinogenase and collagen type IV hydrolytic activities of the elastase from A. fumigatus were inhibited by Asnidin. Asnidin was found to be stable under heat treatment and over a wide pH range. The elastolytic inhibitory activity of Asnidin was inhibited by dithiothreitol (DTT), while no inhibition was observed with ethylenediaminetetraacetic acid (EDTA-2Na) and benzamidine. Since there is a possibility of Asnidin becoming another drug in the arsenal of weapons against aspergillosis or interstitial pneumonia, further studies are warranted.

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 A 50-year-old man with chronic renal failure (hemodialysis treatment) and interstitial pneumonia (IP) was referred to our hospital for exacerbation of IP. We immediately administered a mechanical ventilation, broad spectrum antibiotics, steroid pulse therapy, and endoxan pulse therapy in the intensive care unit, but alveolar opacities became worse. Subsequently, an intrapulmonary cavity appeared in the left middle lung field on the chest X-ray and we also administered amphotericin B. However he died of tension pneumothorax on the tenth day of hospitalization. In an autopsy the rupture of the intrapulmonary cavity of the left S3 region was detected and we diagnosed as invasive pulmonary mucormycosis by Grocott stain of the cavitary lesion. We report a rare case that complicated by fatal tension pneumothorax during treatment with a ventilator in invasive pulmonary mucormycosis and review the literature.

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 In April 2012 an 88-year-old woman, who was receiving oral prednisolone (15 mg/day) for the treatment of chronic inflammatory demyelinating polyneuropathy, was admitted to our hospital with suspected pneumonia. The patient was diagnosed with pulmonary cryptococcosis based on the findings from chest radiography and computed of tomographic imaging and observation of a high cryptococcal antigen titer. The general condition of the patient, including her fever, improved after initiation of an intravenous infusion of fluconazole (200 mg/day). However, the skin ulcers on all the limbs, which were present at the time enlarged since her admittance, were found to have rapidly enlarged. The patient underwent a detailed examination by a dermatologist. Skin ulcers measuring 4 × 6 cm on the dorsal surface of the left hand and understood without reporting 2 × 3 cm on the left thigh were noted, and she was diagnosed as having cutaneous cryptococcosis based on the results of skin biopsy, direct microscopic examination of pus, and mycological culture. For treatment of the skin ulcers, fluconazole was administered by intravenous infusion at 200 mg/day for 7 days. The treatment was then changed to oral itraconazole (200 mg/day). However, after 1 week, the patient exhibited a liver disorder, and the treatment was switched back to oral fluconazole (200 mg/day). After 2 months of treatment, the ulcers began to diminish. Thus, we believe that deep mycosis, including cutaneous cryptococcosis, should be considered during differential diagnosis if the patient is either elderly or undergoing corticosteroid/immunosuppressant therapy and has an ulcer.

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A 58-year-old Japanese woman who was engaged in dairy farming presented with multiple subcutaneous nodules and abscesses on the dorsum of her left hand from 5 months ago. These had been unsuccessfully treated with oral itraconazole. The patient had a history of Sjögren syndrome and diabetes mellitus, for which she had been taking oral prednisolone for 10 years. Direct microscopy of a pus sample treated with potassium hydroxide (KOH) showed brownish-red branching hyphae. In fungal culture, black colonies covered with gray-white villi were formed. Slide culture showed conidiogenesis from an annellide. The fungal strain was identified as Exophialia oligosperma by molecular biological techniques. Histopathological examination revealed abscesses and surrounding granulomatous infiltration in the dermis and subcutis, and hyphae in the granulomatous infiltration in the outer area. However, no eumycotic granules were observed. The diagnosis was phaeohyphomycosis caused by E. oligosperma. Since the previous treatment with itraconazole had not been effective, we performed daily hyperthermia using a disposable body warmer and drainage of the pus, which ceased after 3 weeks. After approximately 4 months, the skin eruptions became scarred. To the best of our knowledge, this is the second case of phaeohyphomycosis caused by E. oligosperma reported in Japan which was successfully treated with hyperthermia.

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 The prevalence of cerebral meningitis caused by Cryptococcus neoformans in HIV-infected patients in Eastern Thailand is high. However, little is known about the occurrence of this pathogenic yeast in the environment of this region.
 The aim of our study was to characterize the prevalence of C. neoformans, its serotypes and antifungal drug susceptibilities in environmental isolates from Chon Buri, Eastern Thailand.
 C. neoformans was isolated from 10% of fifty pigeon excreta examined from this province. All C. neoformans isolates were of serotype A and although the isolates displayed slightly decreased susceptibility towards fluconazole, all tested sensitive to amphotericin B, fluconazole and itraconazole. This study is the first report of the occurrence of C. neoformans in pigeon excreta in eastern Thailand.

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