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(described by Saccardo ex Castellani and Chalmers in 1919)
Scedosporium is a filamentous fungus which occasionally causes infections in humans.
The genus Scedosporium contains two species; Scedosporium apiospermum and Scedosporium prolificans. Pseudallescheria boydii is the telemorph of Scedosporium apiospermum. No sexual form (telemorph) is known for Scedosporium prolificans.
See the list of obsolete names, synonyms, and telemorphs for Scedosporium spp.
See our page on Pseudallescheria boydii for detailed information about Scedosporium apiospermum and its telemorph.
Scedosporium prolificans is a dematiaceous filamentous fungus isolated from soil samples.
Scedosporium prolificans can infect both immunocompetent and immunocompromised hosts. Subcutaneous infections, osteomyelitis, and arthritis are usually posttraumatic and may affect otherwise healthy individuals. Disseminated infections, on the other hand, are mostly encountered in patients who are immunosuppressed (particularly, neutropenic) due to various reasons and are often fatal [228, 908, 1090, 1405, 1826]. Scedosporium prolificans is now recognized as the most common cause of disseminated phaeohyphomycosis
. Cases with pneumonia , meningoencephalitis , and endocarditis  have been reported. Ocular infections (keratouveitis)  and colonization  by Scedosporium prolificans have also been reported.
Colonies of Scedosporium prolificans grow rapidly at 25°C and mature within 5 days. The texture is cottony and moist (yeast-like) initially which later becomes flat with fine, short, mycelial tufts. From the front, the color is light gray to black and becomes dark gray to black as the colony matures. The reverse is gray to black [1295, 2202].
Septate hyaline hyphae, conidiogenous cells (annelides), and conidia are visualized. Annelides (conidiogenous cells) may arise directly from hyphae or are formed at the tips of the conidiophores. These annelides are flask-shaped and have a swollen base part and an elongated neck. Conidia (2-5 x 3-13 µm) are unicellular, oval-shaped, olive to brown, and have a slightly narrowed, truncated base. They are formed in clusters at the apices of the annelides. In addition, some isolates may produce round, thick-walled conidia which arise directly from the hyphae [1295, 2202].
(Mats of) septate hyphae may be observed in the infected tissues [2061, 2148]. Scedosporium prolificans cannot be differentiated from Scedosporium apiospermum in tissue sections.
See also our histopathology page.
Colonies of Scedosporium prolificans are darker compared to those of Scedosporium apiospermum. The inflated conidiogenous cells (annelides) and slightly wider conidia of Scedosporium prolificans, and the inability of Scedosporium prolificans to assimilate ribitol, xylitol, and L-arabinitol also help in differentiation of the two species. Besides, unlike Scedosporium apiospermum, Scedosporium prolificans does not convert to a sexual form [531, 2202]. Differentiation of these two species has been achievable also by PCR assay and hybridization probes .
No special precautions other than general laboratory precautions are required.
Scedosporium prolificans is resistant to amphotericin B [665, 687], flucytosine,
fluconazole, and itraconazole [228, 687, 1131]. Voriconazole [495, 687], teh novel triazole Syn-2869  and caspofungin  also have no or very limited in vitro activity against isolates of Scedosporium prolificans.
While itraconazole or terbinafine alone has no activity against most Scedosporium prolificans isolates, the combination of these two drugs proved to be synergistic in vitro against 95% of the isolates after 48 h of incubation. In addition and importantly, antagonism was not observed in this combination study .
For MICs of various antifungal drugs for Scedosporium prolificans, see our susceptibility database.
Due to its primary multi-resistant nature, treatment of Scedosporium prolificans infections is difficult. Amphotericin B therapy alone or in combination with flucytosine, fluconazole, or itraconazole have so far been used in cases infected with Scedosporium prolificans. However, mortality rate has been very high in most of the cases with disseminated infection . Liposomal amphotericin B combined with G-CSF appeared to improve survival in an immunocompromised murine model with disseminated Scedosporium prolificans infection . Posttraumatic infections, such as arthritis in immunocompetent cases have responded to fluconazole or surgical debridement alone .
Conclusively, optimal treatment of Scedosporium prolificans infections remains yet unknown and there is a great demand for novel agents with favorable activity. Importantly, the clinical outcome is closely associated with the immune status of the host, extent of the infection, and feasibility of concomitant surgical debridement.
133. Arthur, S., L. L. Steed, D. J. Apple, Q. Peng, G. Howard, and M. Escobar-Gomez. 2001. Scedosporium prolificans keratouveitis in association with a contact lens retained intraocularly over a long term. J Clin Microbiol. 39:4579-4582.
228. Berenguer, J., J. L. Rodriguez-Tudela, C. Richard, M. Alvarez, M. A. Sanz, L. Gaztelurrutia, J. Ayats, and J. V. Martinez-Suarez. 1997. Deep infections caused by Scedosporium prolificans. A report on 16 cases in Spain and a review of the literature. Scedosporium Prolificans Spanish Study Group. Medicine (Baltimore). 76:256-65.
495. Cuenca-Estrella, M., B. Ruiz-Diez, J. V. Martinez-Suarez, A. Monzon, and J. L. Rodriguez-Tudela. 1999. Comparative in-vitro activity of voriconazole (UK-109,496) and six other antifungal agents against clinical isolates of Scedosporium prolificans and Scedosporium apiospermum. J Antimicrob Chemother. 43:149-151.
527. de Granda, M. E. C., C. Richard, E. Conde, A. Iriondo, F. M. de Lucas, R. Salesa, and A. Zubizarreta. 2001. Endocarditis caused by Scedosporium prolificans after autologous peripheral blood stem cell transplantation. Eur. J. Clin. Microbiol. Infect. Dis. 20:215-217.
531. de Hoog, G. S., J. Guarro, J. Gene, and M. J. Figueras. 2000. Atlas of Clinical Fungi, 2nd ed, vol. 1. Centraalbureau voor Schimmelcultures, Utrecht, The Netherlands.
558. Del Poeta, M., W. A. Schell, and J. R. Perfect. 1997. In vitro antifungal activity of pneumocandin L-743,872 against a variety of clinically important molds. Antimicrob. Agents Chemother. 41:1835-1836.
665. Ellis, D. 2002. Amphotericin B: spectrum and resistance. J Antimicrob Chemother. 49:7-10.
687. Espinel-Ingroff, A. 2001. In vitro fungicidal activities of voriconazole, itraconazole, and amphotericin B against opportunistic moniliaceous and dematiaceous fungi. J Clin Microbiol. 39:954-958.
908. Groll, A. H., and T. J. Walsh. 2001. Uncommon opportunistic fungi: new nosocomial threats. Clin Microbiol Infect. 7:8-24.
1090. Idigoras, P., E. Perez-Trallero, L. Pineiro, J. N. Larruskain, M. C. Lopez-Lopagtegui, N. Rodriguez, and J. M. Gonzalez. 2001. Disseminated infection and colonization by Scedosporium prolificans: A review of 18 cases, 1990-1999. Clin Infect Dis. 32:E158-E165.
1131. Johnson, E. M., A. Szekely, and D. W. Warnock. 1999. In vitro activity of Syn-2869, a novel triazole agent, against emerging and less common mold pathogens. Antimicrob. Agents Chemother. 43:1260-1263.
1295. Larone, D. H. 1995. Medically Important Fungi - A Guide to Identification, 3rd ed. ASM Press, Washington, D.C.
1405. Maertens, J., K. Lagrou, H. Deweerdt, I. Surmont, G. E. G. Verhoef, J. Verhaegen, and M. A. Boogaerts. 2000. Disseminated infection by Scedosporium prolificans: an emerging fatality among haematology patients. Case report and review. Ann. Hematol. 79:340-344.
1512. Meletiadis, J., J. W. Mouton, J. L. Rodriguez-Tudela, J. Meis, and P. E. Verweij. 2000. In vitro interaction of terbinafine with itraconazole against clinical isolates of Scedosporium prolificans. Antimicrob. Agents Chemother. 44:470-472.
1697. Ortoneda, M., J. Capilla, I. Pujol, F. J. Pastor, E. Mayayo, J. Fernandez-Ballart, and J. Guarro. 2002. Liposomal amphotericin B and granulocyte colony-stimulating factor therapy in a murine model of invasive infection by Scedosporium prolificans. J Antimicrob Chemother. 49:525-529.
1793. Pickles, R. W., D. E. Pacey, D. B. Muir, and W. H. Herrell. 1996. Experience with infection by Scedosporium prolificans including apparent cure with fluconazole therapy. J. Infect. 33:193-197.
1826. Ponton, J., R. Ruchel, K. V. Clemons, D. C. Coleman, R. Grillot, J. Guarro, D. Aldebert, P. Ambroise-Thomas, J. Cano, A. J. Carrillo-Munoz, J. Gene, C. Pinel, D. A. Stevens, and D. J. Sullivan. 2000. Emerging pathogens. Med Mycol. 38:225-236.
1902. Revankar, S. G., J. E. Patterson, D. A. Sutton, R. Pullen, and M. G. Rinaldi. 2002. Disseminated phaeohyphomycosis: Review of an emerging mycosis. Clin Infect Dis. 34:467-476.
2061. Schwartz, D. A. 1989. Organ-specific variation in the morphology of the fungomas (fungus balls) of Pseudallescheria boydii. Development within necrotic host tissue `see comments. Arch Pathol Lab Med. 113:476-80.
2148. Stanley, M. W., M. Deike, J. Knoedler, and C. Iber. 1992. Pulmonary mycetomas in immunocompetent patients: diagnosis by fine-needle aspiration. Diagn Cytopathol. 8:577-9.
2202. Sutton, D. A., A. W. Fothergill, and M. G. Rinaldi (ed.). 1998. Guide to Clinically Significant Fungi, 1st ed. Williams & Wilkins, Baltimore.
2389. Wedde, M., D. Muller, K. Tintelnot, G. S. De Hoog, and U. Stahl. 1998. PCR-based identification of clinically relevant Pseudallescheria/Scedosporium strains. Med Mycol. 36:61-67.
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