Aspergillus lentulus was first reported in 2005 as a cryptic species of Aspergillus fumigatus, and since then, its resistance to azole drugs and the high mortality rate of infected individuals have emerged as problems. Although it has been reported that P450 14-α sterol demethylase (Cyp51) is involved in azole resistance in A. lentulus, the specific resistance mechanism has not been elucidated. In this study, we successfully introduced the entire A. fumigatus cyp51A gene into the cyp51A locus in A. lentulus using the CRISPR/Cas9 genome-editing system. The A. lentulus strains harboring A. fumigatus cyp51A showed reduced minimum inhibitory concentrations for itraconazole and voriconazole compared with those of the parent strain. This finding suggests that Cyp51A is involved in azole resistance in A. lentulus and may contribute to the elucidation of the mechanism of resistance to azole drugs via Cyp51A and to the development of new antifungal drugs. In addition, our successful application of the CRISPR/Cas9 system to A. lentulus opens the door to examination of other gene functions in this fungus.

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We herein report a case of kerion celsi of the scalp and tinea corporis due to Trichophyton tonsurans. A 17-year-old Japanese male high school student who practiced judo had alopecic patches with severe inflammation on the scalp. We performed a fungal culture and identified the causative fungus as T. tonsurans. A plate culture of T. tonsurans showed lemon-yellow colonies with yellow-green fluorescence under UVA light, which are typical findings for Microsporum canis. However, genetic analysis of the ribosomal RNA gene of the isolate facilitated differential diagnosis of T. tonsurans.
In contrast to dermatophytosis due to other dermatophytes, the clinical features of infection caused by T. tonsurans, an anthropophilic dermatophyte, are initially not very apparent and, thus, are frequently overlooked. We herein present a case of a severe type of kerion celsi caused by T. tonsurans with a fluorescence pattern mimicking M. canis colonies under UVA light. We suspect that yellow pigment metabolites, such as riboflavin, which are fluorescent under UV when secreted into the culture medium, are the virulence factors for not only M. canis, but also T. tonsurans, as shown in the present case.

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A high incidence of genital infections, such as vulvovaginal candidiasis, has been reported in patients with diabetes treated with sodium-glucose co-transporter type 2 inhibitors. This is because Candida growth and virulence are enhanced in high glucose environments. Our previous study demonstrated that the adhesive interaction between Candida complement receptors and a ligand on vaginal epithelial cells (intracellular adhesion molecule-1: ICAM-1) is a factor for Candida albicans colonization, and the high ICAM-1 expression by vaginal epithelial cells exposed to high glucose conditions increases C. albicans adhesion. In this study, we examined the effect of a sodium-glucose co-transporter type 2 inhibitor, empagliflozin, on Candida glabrata adhesion to human cells (VK2/E6E7). There was no significant difference among four conditions that contained empagliflozin at various concentrations. We demonstrated that empagliflozin does not affect C. glabrata adhesion to VK2/E6E7 cells.

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Aspergillosis is a major fungal infection in humans and animals. Penguins (Order Spheniscidae) are particularly susceptible to aspergillosis, and aspergillosis in captive penguins is presently a major problem. We were faced with the challenge of combating aspergillosis in an aquarium. As a solution, we organized a multidisciplinary aspergillosis control team, including a medical and veterinary mycologist. Since Aspergillus, including Aspergillus fumigatus, is abundant in soil, we thought it necessary to minimize contact between captive penguins and soil to prevent aspergillosis. As a countermeasure, we stopped using a route for outdoor penguin marches where the soil was exposed. Additionally, after outdoor penguin marches, the feet of penguins were washed with seawater to avoid bringing soil into the rearing facility for penguins. Furthermore, since A. fumigatus was detected on several spots in the environment of the rearing facility by swab analysis, we cleaned and sanitized the rearing facility with 0.02% sodium hypochlorite and hot water. As a result of the above measures, there has been no incidence of aspergillosis in captive penguins since 2016. These results show that our preventive measures are working well. As shown here, we presented an example of how the multidisciplinary control team, which included a mycologist, successfully implemented preventive measures against aspergillosis. Due to changes in the rearing environment and the impact of global warming on penguins, it is expected that the role of mycologists in aspergillosis control will expand in the future.

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Azole resistance in Malassezia pachydermatis has been reported in isolates from canine skin worldwide. Decreased susceptibility of M. pachydermatis to azoles has been hypothesized to potentially result from mutations in the ERG11 gene, which encodes lanosterol 14α-demethylase. To sequence the mutation hotspots of ERG11 in the isolates, we prepared primers (MPERG11hot2S and MPERG11hot2R) based on the conserved sequences of M. pachydermatis ERG11. DNA samples from azole-resistant and -susceptible strains were amplified by PCR using the primer pair. PCR amplicons were sequenced and analyzed for single-nucleotide polymorphisms (SNPs) in the target gene. Seven of the tested azole-resistant strains (16 strains) harbored ERG11 SNPs at nucleotide 904 (G→A) or 905 (C→T), resulting in the replacement of Ala 302 with Thr or Val (Ala302Thr or Val). None of the tested azole-susceptible strains had a mutation at either of those residues. Our PCR method detected SNPs at the nucleotide-905 (C→T) hotspot mutation site in M. pachydermatis ERG11. Moreover, we discovered an additional hot spot site at nucleotide 904 (G→A).

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