AI Article Synopsis
- - A new genotype of the causative agent of mouse favus has emerged, showing a significant increase in itraconazole resistance and peaking in infections around 2020 in Jena, Thuringia.
- - The strains from Thuringia differ genetically from those in the IHEM collection, particularly in the ITS region and exhibit a unique amino acid change associated with their drug resistance.
- - The resistance traits may have developed through interspecies mating, suggested by nearly identical mating type fragments, while also demonstrating increased genetic diversity in related protein sequences.
Article Abstract
, the causative agent of mouse favus, has been responsible for several infections of animal owners in recent years and showed an infection peak around 2020 in Jena, Thuringia. The isolated strains from Thuringia differ in some positions of the ITS region compared to strains from the IHEM collection as well as to . All strains of the new genotype show up to a 100-fold increased itraconazole resistance as measured by microplate laser nephelometry (MLN) assays. Analysis of genes involved in azole resistance, such as , which encodes squalene epoxidase, and , one of two copies of the sterol 14-α demethylase gene, show a 100% identity between the two genotypes. In contrast, fragments differ in 15-nucleotide positions between both genotypes, resulting in the unique amino acid substitution Ala256Ser in resistant strains. The new genotype may have evolved through interspecies mating. Mating type analysis showed a nearly 100% identity of the minus type fragment for all isolates. The closely related belongs to the plus mating type and has 100% identical fragments of and . Erg11A protein sequences of and showed increased diversity.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10607888 | PMC |
| http://dx.doi.org/10.3390/jof9101006 | DOI Listing |
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