Dermatophytosis is a fungal infection that affects the skin, hair, and nails, impacting approximately 25% of the global population. Nannizzia gypsea is a geophilic fungus that can cause infections in humans and animals. Several studies have been conducted regarding its virulence, or ability to cause disease. This species may produce keratinolytic enzymes and form biofilms, which can increase resistance to treatment. Thus, this study focuses on investigating the biofilm formation of N. gypsea isolated from canine dermatophytosis using an ex vivo hair model, its biofilm extracellular matrix macromolecular contents, and the expression of genes involved in the colonization of keratinized surfaces. The biofilm was analyzed for metabolic activity using the XTT reduction assay, crystal violet staining to measure biofilm biomass, scanning electron microscopy (SEM), and the presence of polysaccharides, proteins, and extracellular DNA in the biofilm extracellular matrix. The virulence genes subtilisin 7, fungalysin (extracellular metalloproteinase), and efflux pump (Multidrug and Toxin Extrusion Protein 2) were evaluated by qPCR, comparing the planktonic and biofilm phenotypes. N. gypsea formed a robust biofilm, which matured after 5 days. Scanning electron microscopy (SEM) revealed the presence of an extensive extracellular matrix. In the hair model, the characteristic ectothrix parasitism of the species is observable. The gene expression analysis revealed a higher expression of all evaluated genes in the biofilm form compared to the planktonic form. Thus, N. gypsea exhibits a biofilm characterized by a robust extracellular matrix and high gene expression of factors related to pathogenesis and resistance.

Candidozyma auris has emerged as one of the most formidable fungal pathogens of the modern era, designated a critical priority pathogen by the World Health Organization due to its multidrug resistance, thermotolerance, and capacity to cause prolonged outbreaks in healthcare settings. Unlike most fungal pathogens, C. auris exhibits a remarkable tropism for human skin, where it persists asymptomatically, forms biofilm-like structures resistant to conventional antiseptics, and serves as a reservoir for nosocomial transmission. Invasive infections, particularly candidemia, carry mortality rates of 40-60% and disproportionately affect immunocompromised individuals and those with prolonged healthcare exposure. Six geographically distinct clades have been described, each differing in antifungal susceptibility, colonization capacity, and virulence. Despite the clinical urgency, the molecular and immunological mechanisms governing cutaneous colonization, persistence, and the transition to invasive infection remain poorly understood. This review examines the biology, virulence, and skin colonization dynamics of C. auris, with emphasis on experimental models (i.e. murine, porcine, and human skin systems) that have advanced our understanding of host-pathogen interactions, immune responses, and the efficacy of antifungal and decolonization strategies, highlighting critical knowledge gaps and future research priorities.