Scedosporiosis is the general name for any mycosis – i.e., fungal infection – caused by a fungus from the genus Scedosporium. Current population-based studies suggest Scedosporium prolificans (also known and recently more commonly referred to as Lomentospora prolificans) and Scedosporium apiospermum to be among the most common infecting agents from the genus, although infections caused by other members thereof are not unheard of. The latter is an asexual form (anamorph) of another fungus, Pseudallescheria boydii. The former is a "black yeast" (aka dematiaceous fungus), currently not characterized as well, although both of them have been described as saprophytes. The fungi of this genus are more and more recognized as significant human pathogens. S. apiospermum is described as an emerging and even an "underrated" opportunistic pathogen. It was reported in a 2003 US study that Scedosporiosis had been associated with 25% of all non-Aspergillus fungal infections for organ transplant patients. In a similar 2005 study scedosporal infections caused a 58% mortality rate for transplant recipients affected with it. Among the patients with cystic fibrosis, it is the second most common fungal infection. Moreover, a certain difficulty has been reported with correctly identifying the pathogen as, for example, scedosporal infections are in some cases almost indistinguishable from infections with other filamentous fungi, like the already-mentioned Aspergillus – this difficulty could have potentially contributed to the "underrating" of the pathogen. 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.
Background First detectable description of a scedosporal disease arises in 1911 where S. apiospermum was identified as a cause of human mycetoma – a deep fungal subcutaneous infection. S. apiospermum is, indeed, not a recently discovered human pathogen and data about it have been aggregated over a period of more than 120 years. S. prolificans, on the other hand, was discovered more recently, in 1974, under the name L. prolificans. There has been a series of name changes for both S. apiospermum and its teleomorph P. boydii. It has also been reported that at different timepoints, both, at some point, have been referred to as Petriellidium boydii, Allescheria boydii, Pseudallescheria sheari and Monosporium apiospermum. S. prolificans, likewise, went through a name change, and in the most recent literature, the original name L. prolificans is generally preferred as proposed by Lackner et al. in 2014. The risk of misidentification of the fungi for other infecting agents is, as previously mentioned, extant and significant as a given treatment will be differently applicable to different fungal infections, especially considering resistance patterns. In 2002, a corneal disease case was reported wherein Acrophialophora fusispora was mistaken for S. prolifcans. The identification performed by the researchers based on the specifics of the pathogen's morphology was shown to be erroneous. In the correction to that particular case, a distinction was suggested based on the arrangement of cells and shape and color of conidia, however, in practice, difficulties therein still can persist. S. apiospermum was found 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. S. prolificans was found to be consistently resistant to all of these drugs and the effectiveness of voriconazole against it in vitro is limited. Interestingly, it was recently established that the growth S. prolificans can be inhibited by non-mucoid strains of Pseudomonas aeruginosa.
Infection Both S. apiospermum and S. prolificans are capable of causing a wide range of infections, both in immunocompromised and immunocompetent individuals. Infections arising therefrom can be both localized and disseminated. It was reported that solid organ transplant and hematopoietic stem cell transplant patients are a significant proportion of those at risk of Scedosporium mycoses.
Localized mycosis Localized scedosporiosis can occur in a vast range of internal organs and in joints and limbs. It can commonly be found on the surface of the skin in a form of white and yellow papules. Among the other most common manifestations would be mycetoma, specifically, eumycetoma (a mycetoma caused by a fungus), affecting subcutaneous tissue, joints and even muscles and bones, although foot or leg is a common location of such an infection. A typical cause could be an open wound or surgery and both immunocompetent and immunocompromised patients can develop the infection. Eumycetoma grows in a granular fashion, is usually painless at first and grows steadily, causing complications and even disability if left untreated. Osteomyelitis, particularly, sternal and lower rib bone infection, caused by S. apiospermum was reported in a successfully cured lung transplant patient in 2016. Scedosporal eye infection, specifically, keratitis, arises usually after an injury of the cornea, both S. apiospermum and S. prolificans are known to be able to cause it. It presents itself in a form of painful lesions within the retina accompanied by symptoms like photophobia and blurred vision.
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