Limited genetic diversity among Malassezia furfur isolates during two one-year neonatal and pediatric bloodstream infection surveys confirms preference for one specific IGS1 genotype in deep-seated infections

In recent years, multiple reports indicated that Malassezia fungemia may be of emerging concern in immunocompromised patients and neonates. In combination with observations of reduced antifungal susceptibility, this highlights the need for a better understanding of the extent of Malassezia etiology in deep seated infections. The use of media without lipid supplementation in most clinics underlines the likelihood of underdiagnosis. Here, we utilize multiple genetic markers to explore the genetic diversity of number one Malassezia fungemia species Malassezia furfur, observed from two one-year surveys investigating neonatal and pediatric bloodstream infections. All strains isolated from skin and deep seated neonatal or pediatric sites belong to IGS1-genotype A, except for nine isolates from one pediatric patient. This confirms previous observations of a preferential genotype for deep seated body sites. The mitochondrial cox3-nad3 intergenic region provided additional typing resolution, and including ITS, translation elongation factor 1-, chitin synthase 2, and the mating type, 16 genotypes (MF1-16) could be distinguished among all isolates from both surveys and reference isolates. These results present a promising MLST scheme that requires further testing. We observed a decreased genetic variation of M. furfur isolates among NICU and pediatric surgery patients over the course of 5 years and showed that the skin likely serves as a reservoir for resident M. furfur strains from where they can enter the bloodstream, causing infections among susceptible patient groups. Overall, reduced susceptibility for amphotericin B and specifically fluconazole was observed.