INTRODUCTION. Biofilms are complex organized communities composed by microbial cells and an extracellular polymeric matrix (Kaur and Singh, 2014; Davies, 2003). Studies regarding fungal biofilms are recent, especially in the context of fungal infections where it confers protection against host immune defense and resistance to the current antifungal drugs available in the clinical practice (Borghi et al, 2016). Aspergillus fumigatus and Candida albicans are the most studied pathogenic fungi causing biofilm-related invasive fungal diseases (Sherry et al, 2014; Fan et al, 2015). The ability of C. albicans to adhere to medical devices and form biofilms is commonly associated to bloodstream infections (Kojic and Darouiche, 2004). A. fumigatus can form biofilm in patients presenting aspergilloma and invasive aspergillosis (Muller et al, 2011). To establish these invasive infections, A. fumigatus conidia germinate into mycelia embedded in an extracellular matrix forming a complex biofilm structure inside the host (Filler and Sheppard, 2006; Kaur and Singh, 2014). Although fungi from the complex Pseudallescheria/Scedosporium are known to present a pathogenesis similar to Aspergillus species, little is known about their biofilm structures. Also, the increasing descriptions of the biofilm importance for fungal infections make its study for Pseudallescheria/Scedosporium an interesting need. Recently, it was described that some Pseudallescheria/Scedosporium species can form biofilms (Mello et al, 2016). 
OBJECTIVES. This study aimed to report the ability of nine different strains from Pseudallescheria/Scedosporium complex to form biofilm structures and the influence of fungal growth and biofilm formation in virulence and susceptibility to antifungals.
METHODS. To evaluate biofilm formation, staining techniques were used, such as violet crystal, concanavalin A, calcofluor white and XTT-reduction assay. Also, confocal and scanning electron microscopy was performed to analyze biofilm structures. Galleria mellonella model of infection was performed for virulence analysis, and susceptibility assay was realized to test antifungal resistance.
RESULTS. It was observed that all strains from Scedosporium aurantiacum formed biofilms faster than Pseudallescheria species, indicating that it could be a reason why S. aurantiacum emerges as more virulent species from the complex. In addition, the clinical strains presented a more robust biofilm and more virulence in G. mellonella model comparing to environmental strains, suggesting that biofilms could be an important structure for Pseudallescheria/Scedosporium pathogenesis. Moreover, biofilms displayed significantly more resistance to different antifungal agents than planktonic cells.
CONCLUSIONS. Growth speed and biofilm formation are related to fungal virulence and susceptibility to antifungal drugs. Also, clinical isolates tend to grow faster and form a more robust biofilm than the environmental strains. We believe that this study helps the understanding of pseudallescheriosis/scedosporiosis and opens a new field of researches for this fungal complex.

Biofilm formation by Pseudallescheria/Scedosporium complex: a comparison study