柴田 紗帆

Abstract Allodiploid hybrid species,Aspergillus latus, belonging to sectionNidulantes, is a hybrid ofA. spinulosporusand unknown species closely related toA. quadrilineatusandA. subltus. This hybrid has often been misidentified as the species in sectionNidulantes, such asA. nidulans,A. spinulosporus,A. sublatus, or other cryptic species. A. latushas not been reported in Japan as well as Asia so far. In this study, we screened 23 clinical strains identified asA. spinulosporusisolated in Japan from 2012 to 2023 and found sevenA. latusstrains. To characterize theA. latusstrains, we conducted comprehensive phenotyping including morphological observation, whole genome sequences and phylogenetic analysis based on calmodulin (CaM) gene. In addition, we conducted antifungal susceptibility testing forA. latusstrains. As a result, the morphological characters ofA. latuswere more similar to those ofA. spinulosporuscompared toA. sublatus. However, the ascospore ofA. latusdiffered from that ofA. spinulosporus.A. latusphylogenetically clustered withA. spinulosporusandA. sublatus. Furthermore,A. latusstrains showed reduced susceptibility to caspofungin and amphotericin B compared toA. spinulosporus, while they were susceptible to azoles. Our results suggest thatA. latushas been a causative pathogen of aspergillosis in Japan since 2013.

Abstract Aspergillus fumigatus is a pathogenic fungus with a global distribution. The emergence of azole-resistant A. fumigatus (ARAf) other than the TR-mutants is a problem in Japan. Additionally, the genetic diversity of A. fumigatus strains in Japan remains relatively unknown. Here we show the diversity in the A. fumigatus strains isolated in Japan as well as the complexity in the global distribution of the pathogenic strains. First, we analyzed the genome sequences of 171 strains from Japan as well as the antifungal susceptibility of these strains. Next, we conducted a population analysis of 876 strains by combining the available genomic data for strains isolated worldwide, which were grouped in six clusters. Finally, a genome-wide association study identified the genomic loci associated with ARAf strains, but not the TR-mutants. These results highlight the complexity of the genomic mechanism underlying the emergence of ARAf strains other than the TR-mutants.