Scedosporium prolificans


Scedosporium prolificans

Description, Causes and Risk Factors:

During the past two decades opportunistic fungal infections have emerged as important causes of morbidity and mortality in patients with severe underlying illness and compromised host defense. Collectively Aspergillus and Candida account for the majority of these infections, but recent epidemiologic trends indicate a shift towards infections caused by previously uncommon opportunistic fungi (1). These previously uncommon hyaline filamentous fungi (such as Fusarium species, Acremonium spp., Paecilomyces spp., Pseudallescheria boydii, and Scedosporium prolificans) are increasingly encountered in life threatening invasive infections that are often refractory to therapy.

The genus Scedosporium consists of two medically important species: Scedosporium apiospermum (and its teleomorph or sexual state Pseudallescheria boydii) and Scedosporium prolificans (formerly S. inflatum). S. apiospermum/P. boydii and S. prolificans are ubiquitous filamentous fungi present in soil, sewage, and polluted waters. Scedosporium infection represents a broad spectrum of clinical diseases caused by the agents of the genus Scedosporium. These fungi can be colonizers of previously damaged bronchopulmonary trees (as in old pulmonary tuberculosis cases, cystic fibrosis, or bronchiectatic lungs of any etiology). Infections caused by these organisms can be localized, extend to the surrounding tissues (deep extension), or disseminate (hematogenously) to distant organs. The range of diseases caused by these fungi is broad, ranging from transient colonization of the respiratory tract to saprophytic involvement of abnormal airways, allergic bronchopulmonary reaction, invasive localized disease, and at times disseminated disease. These infections include skin and soft tissue infections with extension to tendons, ligaments, and bone (mycetoma); septic arthritis; osteomyelitis; lymphocutaneous syndrome; pneumonia; endocarditis; peritonitis; meningoencephalitis; meningitis; brain abscess; parotiditis; thyroid abscess; otomycosis; sinusitis; keratitis; chorioretinitis; and endophthalmitis. The disseminated form of the disease is mostly seen among immunocompromised patients; however, even in immunocompetent individuals, cases of disseminated disease have been reported. In patients suffering near-drowning events in particular, P. boydii/S. apiospermum should be considered in the differential diagnosis as potential causes of infections, especially if pneumonia or brain abscess ensues.

In most cases the implicated portal of entry is the skin, in others the aerodigestive tract. Nosocomial airborne outbreaks were also described with disseminated fatal cases in patients with hematologic malignancies. In this patient the most probable portal of entry was the skin, possibly during gardening activities, since no fungal lesions were detected in the lungs or gastrointestinal tract.

The overall frequency of Scedosporium infections is relatively low in most geographic areas; however, hospital-based clusters in patients with hematological malignancies have been described.

Treatment of Scedosporium infections is especially challenging because of their resistance to many antifungal agents.

Symptoms:

Signs &Symptoms:

    Otitis.

  • Small, hard, painless ulcerative nodules.

  • Arthritis.

  • Fever.

  • Osteomyelitis.

  • Eye infection and endophthalmitis.

  • Corneal ulcerationand hypopyon.

  • Decreased visual acuity.

  • Photophobia.

  • Onychomycosis.

  • Lymphocutaneous infection.

  • Sinusitis.

  • Cystic fibrosis.

  • Endocarditis.

Diagnosis:

Diagnosis of a Scedosporium infection is difficult,because clinical features and histopathology are similarto those of Aspergillus, Fusarium and other relativelycommon hyaline hyphomycetes. Sporulation inculture is required for a correct diagnosis, but even thenconfusion with other morphologically similar species ispossible.

Microbiological diagnosis of Scedosporium spp. currently depends upon culture and morphological characterization. Molecular tools for clinical microbiological detection of Scedosporium spp. are currently investigational.

PCR-based assays from infected tissue are useful forrapid diagnosis of S. apiospermum infections, evenbefore fungal cultures become positive.

Laboratory diagnosis:

    Direct microscopy and staining. The fungus grows well on routine mycologicalmedia such as Sabouraud's glucose agar, blood agarand chocolate agar, Leonian's agar.

  • Histopathology.

  • Radiology. In most pulmonary or cerebral cases the lesions aremultiple and have low density. The fungal mass is notseparated from the wall of the cavity by an airspace.The `air-crescent' appearance is more likely to indicateinvasive pulmonary aspergillosis. The difference between the CT may be explained by rapid andfatal evolution of Scedosporium infections.

  • Serology. Immunodiffusion may be useful in the diagnosis ofScedosporium infections, but reagents are not commercially available and antigenic extracts have to be madein the laboratory.

Treatment:

Infections caused by S. apiospermum and P. boydii in patients and animals may respond to antifungal triazoles. By comparison, infections caused by S. prolificans seldom respond to medical therapy alone. Surgery and reversal of immunosuppression may be the only effective therapeutic options for infections caused by S. prolificans.

Numerous studies have proven that antifungal drugs such as amphotericin B (AMB), nystatin (NYS), liposomal nystatin (L-NYS), itraconazole (ITC), flucytosine (5FC), fluconazole (FLC), terbinafine (TBF) and ketoconazole (KTC) show low in vitro activity against S. apiospermum. However, in some studies, ITC has shown some activity. Some new triazoles are promising: voriconazole (VRC) has shown MICs 90 of 0.25 mg/mL and 0.5 mg/mL and ravuconazole of 0.125 mg/mL. Posaconazole (PSC) has shown variable activity. The in vitro activity of echinocandins against S. apiospermum has generally been considered to be modest. The geometric mean MIC of caspofungin (CAS) for 6 isolates of S. apiospermum was of 1.3 mg/mL, the median MIC of anidulafungin for 5 strains was of 4 mg/mL and the geometric mean MICs against 19 strains was 39.7 mg/mL. However, it is important to exercise caution in interpreting in vitro susceptibility results, because clinical improvement of S. apiospermum infections with AMB treatment has been reported despite apparent in vitro resistance to this drug.

NOTE: The above information is educational purpose. The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition.

DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.

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