All of this, along with the wide resistance possessed by the pathogens to the antifungal therapies currently in medical use, presents the increased interest for researchers to further study the scedoporal infections and develop treatments.
First detectable description of a scedosporal disease arises in 1911[4] where S. apiospermum was identified as a cause of human mycetoma – a deep fungal subcutaneous infection.
In the correction to that particular case,[13] a distinction was suggested based on the arrangement of cells and shape and color of conidia, however, in practice, difficulties therein still can persist.
[citation needed] S. apiospermum was found[14] to be resistant to a wide range of the known antifungal drugs, displaying high minimal inhibitory concentration values to amphotericin B, isavuconazole and posaconazole, and is, to different extents, susceptible to voriconazole, micafungin and anidulafungin.
[2] Osteomyelitis, particularly, sternal and lower rib bone infection, caused by S. apiospermum was reported[6] in a successfully cured lung transplant patient in 2016.
[citation needed] The culmination of disseminated scedosporiosis would be a highly fatal infection (>90% mortality rate[17]) of the central nervous system.
[19] Reported as "most catastrophic", a systematic disseminated scedosporal infection happens after its infiltration of blood vessel and subsequent growth in tissues.
[citation needed] In cases of S. apiospermum-caused mycetoma, a treatment constituting a combination of surgery and terbinafine was reported[24] to be effective in 2017.
A review[25] of 162 cases of S. prolificans infection found no association with antifungal treatment (using then-currently available medications) and reduced risk of death.
One study,[26] however, argued for the efficiency of combination therapy using voriconazole and terbinafine to cure an orthopedic infection in a non-immunocompromised host without the need for a radical surgery.
[citation needed] More resent medical advances show[27] hope for more efficient antifungal therapies, however, as novel drugs like Ibrexafungerp – a glucan synthase inhibitor – is somewhat effective in treating S. prolificans infections.
Another drug, fosmanogepix, another fungal enzyme inhibitor, showed in vitro efficacy as treatment for scedosporiosis (including S. prolificans).
Olorofim, a new dihydroorotate dehydrogenase inhibitor – which disrupts pyrimidine biosynthesis – is also deserving of the reader's attention as it showed efficacy against both S. prolificans and S. apiospermum as well as other fungi known to be universally resistant to known antifungal medications.