A radio-detected type Ia supernova with helium-rich circumstellar material.

Type Ia supernovae (SNe Ia) are thermonuclear explosions of degenerate white dwarf stars destabilized by mass accretion from a companion star1, but the nature of their progenitors remains poorly understood. A way to discriminate between progenitor systems is through radio observations; a non-degenerate companion star is expected to lose material through winds2 or binary interaction3 before explosion, and the supernova ejecta crashing into this nearby circumstellar material should result in radio synchrotron emission. However, despite extensive efforts, no type Ia supernova (SN Ia) has ever been detected at radio wavelengths, which suggests a clean environment and a companion star that is itself a degenerate white dwarf star4,5. Here we report on the study of SN 2020eyj, a SN Ia showing helium-rich circumstellar material, as demonstrated by its spectral features, infrared emission and, for the first time in a SN Ia to our knowledge, a radio counterpart. On the basis of our modelling, we conclude that the circumstellar material probably originates from a single-degenerate binary system in which a white dwarf accretes material from a helium donor star, an often proposed formation channel for SNe Ia (refs. 6,7). We describe how comprehensive radio follow-up of SN 2020eyj-like SNe Ia can improve the constraints on their progenitor systems.

Otomycosis caused by the cryptic and emerging species Aspergillus sydowii: two case reports.

Two cases of otomycosis have been reported in patients undergoing tympanomastoidectomy. The first one had chronic otitis media, hypertrophic concha and nasal septum deviation, tympanic perforation and otorrhea. The second had otalgia, pruritus, chronic otitis media and cholesteatoma. Direct examination showed mycelial septate filaments with a branch at an angle close to 45°, later identified as Aspergillus sydowii by sequencing the BenA and CaM genes. Susceptibility testing showed low MIC of amphotericin B, itraconazole, ketoconazole and ciclopirox olamine. In both cases, ketoconazole was instituted for 10 days. Otomycosis is a challenge as it is primarily recurrent in patients undergoing surgery. The clinical implication, the identification of the emerging pathogen and the determination of MIC were necessary for the knowledge of the epidemiological profile and establishment of the treatment.

Aspergillus are fungi that can cause ear disease. In severe infections, these fungi can be present for long periods inside the ear, and commonly belong to the species Aspergillus section Nigri and Aspergillus flavus. In this work, we present two cases of ear infections by a different species, Aspergillus sydowii. Patients had obstructed nasal cavities, crooked internal separation of the nose and complaints of secretion in the ear. The efficient diagnosis allowed a treatment that resulted in the death of the fungus and the cure of the patient.

Precise genome editing using a CRISPR-Cas9 method highlights the role of CoERG11 amino acid substitutions in azole resistance in Candida orthopsilosis.

BACKGROUND: Azoles are one of the main antifungal classes for the treatment of candidiasis. In the current context of emerging drug resistance, most studies have focused on Candida albicans, Candida glabrata or Candida auris but, so far, less is known about the underlying mechanisms of resistance in other species, including Candida orthopsilosis. OBJECTIVES: We investigated azole resistance in a C. orthopsilosis clinical isolate recovered from a patient with haematological malignancy receiving fluconazole prophylaxis. METHODS: Antifungal susceptibility to fluconazole was determined in vitro (CLSI M27-A3) and in vivo (in a Galleria mellonella model of invasive candidiasis). The CoERG11 gene was then sequenced and amino acid substitutions identified were mapped on the predicted 3D structure of CoErg11p. A clustered regularly interspaced short palindromic repeat-Cas9 (CRISPR-Cas9) genome-editing strategy was used to introduce relevant mutations into a fluconazole-susceptible C. orthopsilosis isolate. RESULTS: Compared with unrelated C. orthopsilosis isolates, the clinical isolate exhibited both in vitro and in vivo fluconazole resistance. Sequencing of the CoERG11 gene identified several amino acid substitutions, including two possibly involved in fluconazole resistance (L376I and G458S). Both mutations mapped close to the active site of CoErg11p. Engineering these mutations in a different genetic background using CRISPR-Cas9 demonstrated that G458S, but not L376I, confers resistance to fluconazole and voriconazole. CONCLUSIONS: Our data show that the G458S amino acid substitution in CoERG11p, but not L376I, contributes to azole resistance in C. orthopsilosis. In addition to highlighting the potential of CRISPR-Cas9 technology for precise genome editing in the field of antifungal resistance, we discuss some points that are critical to improving its efficiency.