Lesions of adiaspiromycosis, a respiratory disease affecting wild animals, have been found mainly in dead mammals and free-living mammals captured for surveillance. No report has described an investigation of adiaspore formation progress in the lung. After establishing an experimental mouse model of intratracheal adiaspiromycosis infection with the causative agent Emmonsia crescens, we observed adiaspore development. The spores grew and reached a plateau of growth at 70 days post-infection. The median adiaspore diameter showed a plateau of around 40 μm. The characteristic three-layer cell-wall structure of adiaspores was observed in the lung at 70 days post-infection. We examined infection with a few spores, which revealed that adiaspores in the mouse lung progressed from intratracheal infection of at least 400 spores. Moreover, we developed adiaspores in vitro by culture in fetal bovine serum. Although most spores broke, some large spores were intact. They reached about 50 μm diameter. Thick cell walls and dense granules were found as common points between in vitro adiaspores and in vivo adiaspores. These models are expected to be useful for additional investigations of E. crescens adiaspores and adiaspiromycosis.

Adiaspiromycosis is a mycotic infection caused by thermally dimorphic fungi classified as Emmonsia parva and E. crescens (formerly Chrysosporium spp.) until recently, when new classifications were proposed. We document the pathologic findings in a severe case of adiaspiromycosis, with lymph node involvement, in a wild European rabbit ( Oryctolagus cuniculus). The rabbit exhibited granulomatous pneumonia with tracheobronchial lymph node enlargement. Histopathologically, the lung was expanded by myriad, densely cellular, heterophilic and granulomatous foci, surrounding bi- to trilaminar adiaspores. Adiaspore density was considered to be similar in all lung lobes. In the left caudal lung lobe, 80 adiaspores were counted in a 50-mm2 area using digital image analysis. The mean and median adiaspore diameters were 240 ± 52 μm and 255 μm, respectively. Tracheobronchial lymph nodes exhibited moderate numbers of similar adiaspores. PCR amplification of DNA extracted from microdissected adiaspores failed to identify Emmonsia spp.-specific DNA. These data suggest that adiaspiromycosis may result in severe granulomatous pneumonia in wild European rabbits. Although confirmation of the etiologic agent by PCR using DNA extracted from formalin-fixed tissue is not always successful, digital image analysis can be used to aid accurate assessment of adiaspore density and morphology.

Adiaspiromycosis is a rare fungal infection caused by saprophytic fungi Emmonsia spp. (type Ascomycota) occurring especially in small free-living mammals. The aim of this study was to evaluate the occurrence of histopathological lesions asscociated with adiaspiromycosis in the Eurasian beaver inhabiting Poland. In order to evaluate the presence of natural adiaspiromycosis we systematically investigated beaver populations from north-eastern Poland for adiaspores in the lungs. This study reveals for the first time the presence of pulmonary adiaspiromycosis of Eurasian beaver in Poland. As far as we know, there is no published data regarding pulmonary adiaspiromycosis in human patients in Poland.

Adiaspiromycosis is caused by pulmonary infection with Emmonsia. Inhalated spores of Emmonsia cause asymptomatic infection to necrogranulomatous pneumonia, depending on the burden of adiaspore and host immunity. For disease monitoring of wild rodents captured on Jeju Island in Korea, we examined the lung tissue of wild rodents histopathologically. Spores composed of thick three-layered walls were found following histopathological examination and were diagnosed as adiaspiromycosis. Adiaspiromycosis has been found in mammals in many parts of the world. To our knowledge, this is the first report of adiaspiromycosis of an Apodemus agrarius captured in Korea.