Asynchronous application of modified biochar and exogenous fungus Scedosporium sp. ZYY for enhanced degradation of oil-contaminated intertidal mudflat sediment.

Intertidal mudflats are susceptible to oil pollution due to their proximity to discharges from industries, accidental spills from marine shipping activities, oil drilling, pipeline seepages, and river outflows. The experimental study was divided into two periods. In the first period, microcosm trials were carried out to examine the effect of chemically modified biochar on biological hydrocarbon removal from sediments. The modified biochar's surface area increased from 2.544 to 25.378 m2/g, followed by a corresponding increase in the hydrogen-carbon and oxygen-carbon ratio, indicating improved stability and polarity. In the second period, the effect of exogenous fungus - Scedoporium sp. ZYY on the bacterial community structure was examined in relation to total petroleum hydrocarbon (TPH) removal. The maximum TPH removal efficiency of 82.4% was achieved in treatments with the modified biochar, followed by a corresponding increase in Fluorescein diacetate hydrolysis activity. Furthermore, high-throughput 16S RNA gene sequencing employed to identify changes in the bacterial community of the original sediment and treatments before and after fungal inoculation revealed Proteobacteria as the dominant phylum. In addition, it was observed that Scedoporium sp. ZYY promoted the proliferation of specific TPH-degraders, particularly, Hyphomonas adhaerens which accounted for 77% of the total degrading populations in treatments where TPH removal was highest. Findings in this study provide valuable insights into the effect of modified biochar and the fundamental role of exogenous fungus towards the effective degradation of oil-contaminated intertidal mudflat sediments.

Synthesis of the Hydroxamate Siderophore Nα-Methylcoprogen B in Scedosporium apiospermum Is Mediated by sidD Ortholog and Is Required for Virulence.

Scedosporium species rank second among the filamentous fungi capable to colonize chronically the respiratory tract of patients with cystic fibrosis (CF). Nevertheless, there is little information on the mechanisms underpinning their virulence. Iron acquisition is critical for the growth and pathogenesis of many bacterial and fungal genera that chronically inhabit the CF lungs. In a previous study, we showed the presence in the genome of Scedosporium apiospermum of several genes relevant for iron uptake, notably SAPIO_CDS2806, an ortholog of sidD, which drives the synthesis of the extracellular hydroxamate-type siderophore fusarinine C (FsC) and its derivative triacetylfusarinine C (TAFC) in Aspergillus fumigatus. Here, we demonstrate that Scedosporium apiospermum sidD gene is required for production of an excreted siderophore, namely, Nα-methylcoprogen B, which also belongs to the hydroxamate family. Blockage of the synthesis of Nα-methylcoprogen B by disruption of the sidD gene resulted in the lack of fungal growth under iron limiting conditions. Still, growth of ΔsidD mutants could be restored by supplementation of the culture medium with a culture filtrate from the parent strain, but not from the mutants. Furthermore, the use of xenosiderophores as the sole source of iron revealed that S. apiospermum can acquire the iron using the hydroxamate siderophores ferrichrome or ferrioxamine, i.e., independently of Nα-methylcoprogen B production. Conversely, Nα-methylcoprogen B is mandatory for iron acquisition from pyoverdine, a mixed catecholate-hydroxamate siderophore. Finally, the deletion of sidD resulted in the loss of virulence in a murine model of scedosporiosis. Our findings demonstrate that S. apiospermum sidD gene drives the synthesis of a unique extracellular, hydroxamate-type iron chelator, which is essential for fungal growth and virulence. This compound scavenges iron from pyoverdine, which might explain why S. apiospermum and Pseudomonas aeruginosa are rarely found simultaneously in the CF lungs.

Pathobiology of Lomentospora prolificans: could this species serve as a model of primary antifungal resistance?

The number of fungal isolates resistant to antifungal drugs has increased dramatically over the last few years and has become an important concern for clinicians. Among these isolates, fungi showing multidrug resistance are particularly worrying because of the difficulties associated with their treatment. These factors hamper the successful recovery of patients and drastically raise mortality rates. Antifungal resistance is multifactorial and several mechanisms in different fungi have been described. There is a need to study these mechanisms in depth; however, the study of antifungal drug resistance separately for each individual species makes progress in the field very slow and tedious. The selection of a multiresistant microorganism as a model for understanding resistance mechanisms and extrapolating the results to other species could help in the search for a solution. In this mini-review, we describe the pathobiology of Lomentospora (Scedosporium) prolificans, paying special attention to its intrinsic resistance to all currently available antifungal agents. The characteristics of L. prolificans offer several advantages: the possibility of using a single microorganism for the study of resistance to different drugs, even cases of double and triple resistance; it is biologically safe for society in general as no new genetically-modified strains are needed for the experiments; it is homologous with other fungal species, and there is repetitiveness between different strains. In conclusion, we propose L. prolificans as a candidate for consideration as a fungal model for the study of resistance mechanisms against antifungal agents.