Scedosporium apiospermum: Changing clinical spectrum of a therapy-refractory opportunist

Unitat de Microbiologia, Facultat de Medicina i Ciències de la Salut, Universitat Rovira i Virgili, Spain.
Medical Mycology (Impact Factor: 2.34). 07/2006; 44(4):295-327. DOI: 10.1080/13693780600752507
Source: PubMed


Current knowledge on the opportunist Scedosporium apiospermum (teleomorph: Pseudallescheria boydii), generated over a period of more than 120 years, is reviewed. The natural environmental habitat of the fungus is unknown; nutrient-rich, brackish waters like river estuaria have been suggested. The fungus is strongly promoted by agricultural and particularly by industrial pollution.

Download full-text


Available from: Juan Luis Rodriguez-Tudela,
  • Source
    • "patients versus occurrence of the Scedosporium apiospermum complex being associated with near-drowning syndrome (Guarro et al. 2006), and as causative agent of eumycotic mycetomas. In animal models (e) S. prolificans was shown to be more virulent (Ortoneda et al. 2002). "
    [Show abstract] [Hide abstract]
    ABSTRACT: Abstract As a result of fundamental changes in the International Code of Nomenclature on the use of separate names for sexual and asexual stages of fungi, generic names of many groups should be reconsidered. Members of the ECMM/ISHAM working group on Pseudallescheria/ Scedosporium infections herein advocate a novel nomenclature for genera and species in Pseudallescheria, Scedosporium and allied taxa. The generic names Parascedosporium, Lomentospora, Petriella, Petriellopsis, and Scedosporium are proposed for a lineage within Microascaceae with mostly Scedosporium anamorphs producing slimy, annellidic conidia. Considering that Scedosporium has priority over Pseudallescheria and that Scedosporium prolificans is phylogenetically distinct fromthe other Scedosporium species, some name changes are proposed. Pseudallescheria minutispora and Petriellidium desertorum are renamed as Scedosporium minutisporum and S. desertorum, respectively. Scedosporium prolificans is renamed as Lomentospora prolificans.
    Fungal diversity 06/2014; DOI:10.1007/s13225-014-0295-4 · 6.22 Impact Factor
  • Source
    • "The antifungal activity of micafungin is through inhibition of (1,3)-β-d-glucan synthase and the subsequent disruption of fungal cell wall synthesis. This activity may enhance the action of other, less-active antifungals such as amphotericin B or itraconazole and supports the combined use of micafungin with azoles in future in vitro and in vivo studies [22]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Scedosporium apiospermum is an emerging fungal pathogen that causes both localized and disseminated infections in immunocompromised patients. Glucosylceramides (CMH, GlcCer) are the main neutral glycosphingolipids expressed in fungal cells. In this study, glucosylceramides (GlcCer) were extracted and purified in several chromatographic steps. Using high-performance thin layer chromatography (HPTLC) and electrospray ionization mass spectrometry (ESI-MS), N-2′-hydroxyhexadecanoyl-1-β-D-glucopyranosyl-9-methyl-4,8-sphingadienine was identified as the main GlcCer in S. apiospermum. A monoclonal antibody (Mab) against this molecule was used for indirect immunofluorescence experiments, which revealed that this CMH is present on the surface of the mycelial and conidial forms of S. apiospermum. Treatment of S. apiospermum conidia with the Mab significantly reduced fungal growth. In addition, the Mab also enhanced the phagocytosis and killing of S. apiospermum by murine cells. In vitro assays were performed to evaluate the CMHs for their cytotoxic activities against the mammalian cell lines L.929 and RAW, and an inhibitory effect on cell proliferation was observed. Synergistic in vitro interactions were observed between the Mab against GlcCer and both amphotericin B (AmB) and itraconazole. Because Scedosporium species develop drug resistance, the number of available antifungal drugs is limited; our data indicate that combining immunotherapy with the available drugs might be a viable treatment option. These results suggest that in S. apiospermum, GlcCer are most likely cell wall components that are targeted by antifungal antibodies, which directly inhibit fungal development and enhance macrophage function; furthermore, these results suggest the combined use of monoclonal antibodies against GlcCer and antifungal drugs for antifungal immunotherapy.
    PLoS ONE 05/2014; 9(5):e98149. DOI:10.1371/journal.pone.0098149 · 3.23 Impact Factor
  • Source
    • "state of P. boydii), Scedosporium aurantiacum, Scedosporium dehoogii and Pseudallescheria minutispora [1] [2]. These fungi are now considered as emerging opportunist pathogens due to the recent increase in reported infections [3] [4] [5]. The spectrum of S. a complex infections is broad, ranging from localized diseases to multi-organ involvement and is closely related to the immunological status of patients [6]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Background Species of the Scedosporium apiospermum complex (S. a complex) are emerging fungi responsible for chronic airway colonization in cystic fibrosis (CF) patients. Recent studies performed on Aspergillus fumigatus suggest that the colonization of the airways by filamentous fungi may contribute to the progressive deterioration of lung function. Methods We studied S. a complex seroprevalence, as a marker of close contact between patient and the fungi, in a large monocentric cohort of CF patients attended in a reference centre in Lyon, France. Results Serum samples from 373 CF patients were analysed. Antibodies against S. a complex were detected in 35 patients (9.4%). In multivariate analysis, S. a complex seropositivity was only associated with seropositivity to A. fumigatus. Conclusions This study does not suggest an association between sensitization against S. a complex and poorer lung function in CF. Prospective studies are needed to evaluate the impact of both seropositivity and S. a complex colonization on the course of CF.
    Journal of cystic fibrosis: official journal of the European Cystic Fibrosis Society 02/2014; 13(6). DOI:10.1016/j.jcf.2014.01.011 · 3.48 Impact Factor
Show more