Scedosporiosis is the general name for anymycosis – i.e., fungal infection – caused by afungus from the genusScedosporium. Current population-based studies suggestScedosporium prolificans (also known and recently more commonly referred to asLomentospora prolificans) andScedosporium apiospermum to be among the most common infecting agents from the genus,^[1] although infections caused by other members thereof are not unheard of.^[2] The latter is an asexual form (anamorph) of another fungus,Pseudallescheria boydii. The former is a "black yeast" (akadematiaceous fungus),^[3] currently not characterized as well, although both of them have been described assaprophytes.^[4]

The fungi of thisgenus are more and more recognized as significant human pathogens.S. apiospermum is described as anemerging and even an "underrated" opportunistic pathogen.^[2] It was reported^[5] in a 2003 US study that Scedosporiosis had been associated with 25% of all non-Aspergillus fungal infections fororgan transplant patients. In a similar 2005 study^[4] scedosporal infections caused a 58%mortality rate for transplant recipients affected with it. Among the patients withcystic fibrosis, it is the second most common fungal infection.^[6][7] Moreover, a certain difficulty has been reported with correctly identifying the pathogen as, for example, scedosporal infections are in some cases almost indistinguishable^[8] from infections with otherfilamentous fungi, like the already-mentionedAspergillus – 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 theantifungal 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] whereS. apiospermum was identified as a cause of humanmycetoma – 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.^[8]S. prolificans, on the other hand, was discovered more recently, in 1974, under the nameL. prolificans.^[9]

There has been a series of name changes for bothS. apiospermum and its teleomorphP. boydii. It has also been reported that at different timepoints, both, at some point, have been referred to asPetriellidium boydii,Allescheria boydii,Pseudallescheria sheari andMonosporium apiospermum^[10]. S. prolificans, likewise, went through a name change, and in the most recent literature, the original nameL. prolificans is generally preferred as proposed^[11] 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 whereinAcrophialophora fusispora was mistaken forS. prolifcans. The identification^[12] performed by the researchers based on the specifics of the pathogen'smorphology was shown to be erroneous. In the correction to that particular case,^[13] a distinction was suggested based on the arrangement of cells and shape and color ofconidia, 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 highminimal inhibitory concentration values toamphotericin B,isavuconazole andposaconazole, and is, to different extents, susceptible tovoriconazole,micafungin andanidulafungin.S. prolificans was found to be consistently resistant to all of these drugs and the effectiveness of voriconazole against itin vitro is limited.^{[citation needed]}

Interestingly, it was recently established^[15] that the growthS. prolificans can be inhibited by non-mucoid strains ofPseudomonas aeruginosa.

BothS. apiospermum andS. 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.^{[citation needed]}

It was reported^[2] that solid organ transplant andhematopoietic stem cell transplant patients are a significant proportion of those at risk ofScedosporium mycoses.

Localized scedosporiosis can occur in a vast range ofinternal organs and injoints 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), affectingsubcutaneous tissue, joints and evenmuscles andbones, although foot or leg is a common location of such an infection.^[2] 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.^[2]Osteomyelitis, particularly,sternal and lowerrib bone infection, caused byS. apiospermum was reported^[6] in a successfully cured lung transplant patient in 2016.

Scedosporal eye infection, specifically,keratitis, arises usually after an injury of thecornea, bothS. apiospermum andS. prolificans are known to be able to cause it. It presents itself in a form of painful lesions within theretina accompanied by symptoms likephotophobia and blurred vision.^[2]

Severely immunocompromised patients, patients onimmunosuppressive therapy, as well as those suffering from cancers includingleukemia, have a risk of developing an infection that would constitute a spread of the extant localized infection throughout the organism.^[2] Additional and highly significant risk factor isneutropenia, found especially in leukemia patients.^[16]

Disseminated infections present a significant challenge to manage and result in consistently high mortality. Some studies suggest overall mortality rates for disseminated infections to be within 58-75%.^[17] A review of 25 cases published in 2006 reported mortality rates of disseminated infections withS. apiospermum andS. prolificans to be 70 and 100%, respectively. A 2002 review^[3] of 72 cases of disseminatedphaeohyphomycosis reported poor outcomes for the antifungal treatment usingamphotericin B with the overall mortality being 79% among all patients, with a likewise 100% mortality for infections byS. prolificans.^{[citation needed]}

The culmination of disseminated scedosporiosis would be a highly fatal infection (>90% mortality rate^[17]) of the central nervous system. This development is possible in both immunocompromised and immunodeficient individuals. Studies report the former group develops the condition after anear-drowning experience in water contaminated with the pathogen's conidia.^[2][18] An extreme manifestation of this highly lethal case of scedosporiosis would be abrain abscess.^[19]

Reported as "most catastrophic", a systematic disseminated scedosporal infection happens after its infiltration of blood vessel and subsequent growth in tissues. In neutropenic patients and patients withHIV, this produces most severe case of the infection and fatality.^[2]

Effective treatment against scedosporiosis continues to present a challenge to modern medicine – as do many other fungal infections. It is still being researched and can vary depending on the localization and type of infection. Factors like immunodeficiency can significantly hinder the chances of a successful outcome. Studies suggest^[20] Voriconazole to be effective as clinical treatment for infections caused byS. apiospermum. A study of 107 patients with saw the treatment successfully working in 57% in patients infected with scedosporiosis with best effects in localizedS. apiospermum skin and bone infections.^[21] A 2003 review^[22] confirms its effectiveness for treating invasive mycosis ofS. apiospermum while also citing evidence for efficacy ofravuconazole. A 2007 case report likewise shows^[23] the effectiveness of voriconazole in a renal transplant patient with disseminated scedosporiosis.^{[citation needed]}

In cases ofS. apiospermum-caused mycetoma, a treatment constituting a combination of surgery andterbinafine was reported^[24] to be effective in 2017. An immunocompromised patient suffering from an intense subcutaneous infection in his right leg was successfully treated using this method.^{[citation needed]}

S. prolificans treatment presents a more significant challenge due to its wider array of antifungal resistance. Localized limb infections might require extensive surgery or evenamputation. A review^[25] of 162 cases ofS. 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 likeIbrexafungerp – a glucan synthase inhibitor – is somewhat effective in treatingS. prolificans infections. Another drug,fosmanogepix, another fungal enzyme inhibitor, showedin vitro efficacy as treatment for scedosporiosis (includingS. prolificans).Olorofim, a newdihydroorotate dehydrogenase inhibitor – which disruptspyrimidine biosynthesis – is also deserving of the reader's attention as it showed efficacy against bothS. prolificans andS. apiospermum as well as other fungi known to be universally resistant to known antifungal medications.^{[citation needed]}

• Aspergillosis
• Mycetoma
• Mycosis
• Immunodeficiency

• Animal fungal diseases
• Fungal diseases
• Tropical diseases
• Neglected American diseases

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