title: Adiaspiromycosis due to Emmonsia crescens is widespread in native British mammals.
abstract: Adiaspiromycosis caused by Emmonsia crescens is primarily a respiratory disease affecting small mammals, especially members of the Families Rodentia, Carnivora and Mustelidae. Although isolated reports exist of adiaspiromycosis in free-living British wildlife, the extent of infection in wild animals in the UK, and the significance of any associated pathology are unclear. Here, we report the results of histopathological examination of lungs of free-living wild mammals from the south-west UK coupled with digestion of lung material in potassium hydroxide followed by centrifugation and microscopic examination for the presence of adiaspores. The combined results showed that almost one-third (27/94, 28.7%) of animals examined had evidence of infection with E. crescens. Attempts to culture E. crescens from infected lungs were unsuccessful. However, E. crescens could be confirmed as the causative agent by PCR amplification and sequencing of DNA from adiaspores micro-dissected from animal lungs. The prevalence of adiaspiromycosis was largely independent of animal species or precise geography. Adiaspore burdens in most animals were low, consistent with transient exposure to E. crescens. However, burdens in several animals suggested heavy or repeated exposures to E. crescens, and were considered sufficient to have significantly impaired respiratory function. Finally, since E. crescens is apparently widespread in UK mammals and the first UK human case of adiaspiromycosis was reported recently, we present data obtained using a previous isolate of E. crescens demonstrating that both the mycelial and adiaspore phases of the organism are susceptible to amphotericin B, voriconazole, itraconazole and caspofungin.
authors.affiliation: Mycology Reference Laboratory, Health Protection Agency South West Regional Laboratory, Bristol, UK. Andy.Borman@uhBristol.nhs.uk
authors.forename: Andrew M
authors.initials: AM
authors.lastname: Borman
authors.forename: Vic R
authors.initials: VR
authors.lastname: Simpson
authors.forename: Michael D
authors.initials: MD
authors.lastname: Palmer
authors.forename: Christopher J
authors.initials: CJ
authors.lastname: Linton
authors.forename: Elizabeth M
authors.initials: EM
authors.lastname: Johnson
mesh_terms: D000820:Animal Diseases / Q000453:epidemiology* / Q000382:microbiology*; D000818:Animals; D000935:Antifungal Agents / Q000494:pharmacology; D002335:Carnivora; D002912:Chrysosporium / Q000235:genetics / Q000302:isolation & purification*; D004271:DNA, Fungal / Q000737:chemistry / Q000235:genetics; D006801:Humans; D008168:Lung / Q000382:microbiology / Q000473:pathology; D008826:Microbial Sensitivity Tests; D045969:Mustelidae; D009181:Mycoses / Q000453:epidemiology / Q000662:veterinary*; D011014:Pneumonia / Q000453:epidemiology / Q000662:veterinary*; D016133:Polymerase Chain Reaction; D012377:Rodentia; D017422:Sequence Analysis, DNA; D006113:United Kingdom / Q000453:epidemiology
chemical_list: D000935:Antifungal Agents; D004271:DNA, Fungal