Deep Infections Caused by Scedosporium prolificans: A Report on 16 Cases in Spain and a Review of the Literature

Abstract

Scedosporium prolificans, a mold morphologically similar to Scedosporium apiospermum, may cause asymptomatic colonization or localized or disseminated infection following trauma, surgery, and immunosuppression. S. prolificans is normally resistant to available antifungal agents, and prognosis depends largely on the host's immune status, extent of infection, and feasibility of surgical debridement. We report on 16 patients with deep S. prolificans infections, focusing on predisposing factors, clinical characteristics, outcome, postmortem findings, and antifungal susceptibility testing to 6 antifungal agents. Between 1989 and 1994, 16 cases of deep infections by S. prolificans were documented in 6 clinical centers in Spain (15 adults and 1 child: male/female = 0.77). Fifteen patients had underlying hematologic malignancy (14 with neutropenia) and 1 had a prosthetic cardiac valve. Syndromes included disseminated infection in 14 patients (1 with prosthetic valve endocarditis) and fungal pneumonia and meningoencephalitis in 1 patient each. S. prolificans was isolated from 2 specimens in 14 patients and from 1 specimen in 2 patients (blood, n = 12; respiratory tract, n = 4; CNS, n = 4; and skin biopsy, n = 3). Antifungal susceptibility testing by a micromethod with RPMI-2% glucose medium was performed in 8 isolates, all of which were resistant to amphotericin B, flucytosine, ketoconazole, fluconazole, itraconazole, and miconazole. All patients received antifungal therapy (amphotericin B, n = 9; amphotericin B+ flucytosine, n = 1; amphotericin B+ itraconazole, n = 2; liposomal amphotericin B+ itraconazole, n = 1; amphotericin B+ fluconazole, n = 1 and 2 underwent surgical procedures. Two patients survived coinciding with hematologic recovery and 14 (87.5%) patients died in a median time of 4 days after the first positive culture (range, 0-60 d). Necropsy was performed in 10 patients, and disseminated infection was found in 9. In conclusion, S. prolificans is an emerging multiresistant fungal pathogen that may cause asymptomatic colonization, localized infection related to trauma or surgery, and rapidly fatal disseminated infection in immunocompromised hosts, particularly those with neutropenia. This mycosis underscores the urgent need for new antifungal agents.

Fungal communities in pressmud composting harbour beneficial and detrimental fungi for human welfare

“…However, it is noteworthy that, L. prolificans along with C. tropicalis accounted for more than 50 % of the sequences in the fresh pressmud, and both are classified as In particular, L. prolificans is an emerging opportunistic pathogen with high levels of resistance to most antifungal drugs, and infections caused by this fungus are often fatal (Berenguer et al, 1997;Song et al, 2011). However, basic aspects of its biology, such as the natural reservoir, are still poorly known; clarifying these issues is necessary to prevent exposure of immuno-compromised individuals to this fungus (Thornton et al, 2015).…”

Molecular Typing of AustralianScedosporiumIsolates Showing Genetic Variability and NumerousS. aurantiacum

“…On the basis of genetic data, a new species, S. aurantiacum, was proposed for a subset of isolates previously identifi ed as S. apiospermum (11). S. prolifi cans infections are geographically more restricted than those caused by S. apiospermum, being most prevalent in Australia, Spain, and the United States (12)(13)(14)(15). S. prolifi cans typically causes localized infections in immunocompetent hosts but rapidly fatal disseminated infections in the immunocompromised among whom it has been associated with nosocomial outbreaks (3,(12)(13)(14)(15)(16)(17).…”

Comparison of the E-test with the NCCLS M38-P Method for Antifungal Susceptibility Testing of Common and Emerging Pathogenic Filamentous Fungi

“…A higher incidence of fungal infections has been documented since the 1980s with the parallel emergence of either new fungal pathogens or fungi that were considered nonpathogenic as etiologic agents of systemic disease, especially in the immunocompromised host (2,4,8,16,27,28,31). Although the volume of disseminated infections caused by the filamentous fungi (molds) is lower than that caused by yeasts, their higher incidence and the increased resistance of molds to established antifungal agents (2, 4, 9, 10, 14-16, 18, 27, 31) warrant the evaluation of the in vitro susceptibilities of these fungi to both established and investigational agents.…”

“…Aspergillus fumigatus is responsible for the majority (85 to 90%) of the different clinical manifestations of severe mold infections (9). However, other Aspergillus spp., Fusarium spp., Scedosporium apiospermum (Pseudallescheria boydii), Scedosporium prolificans, and less common molds have become important emerging pathogens (2,4,15,18,27,28).…”