Case Presentation:
A 5 year‐old previously healthy boy presents following traumatic amputation of his left four digits in an accident involving a plane hanger doorway system. He required multiple operative procedures, including digital re‐implantation and a pedicle flap procedure to increase wound vascularity. His early post‐operative course was complicated by wound necrosis and local Aspergillus flavus wound infection, which was initially treated with voriconazole and micafungin. Later in his hospitalization, he returned to the operating room (OR) for wound debridement and irrigation. Wound culture at that time grew Scedosporium prolificans. Fungal blood cultures were negative, thereby suggesting localized infection. Standard sensitivity testing for S. prolificans demonstrated high minimum inhibitory concentrations (MIC) to all classes of antifungals. In an attempt to achieve synergistic effects, he was initially treated with micafungin and voriconazole, and ultimately discharged home on terbinafine and posaconazole. Definitive treatment for the local S. prolificans infection required multiple operative debridements and irrigation with polyhexamethylene biguanide (PHMB). Two months post‐discharge, theScedosporiuminfection was clinically resolved. This sustained clinical improvement was primarily attributed to aggressive surgical intervention and PHMB irrigations rather than antifungal therapy.
Discussion:
Scedosporium prolificans is an emerging fungal pathogen first documented as a cause of human disease in 1984. Although the majority of case reports are in immunocompromised patients, it is increasingly recognized as a cause of bone and soft tissue infections in healthy hosts. Penetrating trauma represents a common risk factor for deep local S. prolificans infections in immunocompetent patients. The majority of cases of S. prolificansin the United States have been described in southern states and California.
Scedosporium species are difficult to treat due to resistance to typical antifungals. S. prolificans demonstrates high in‐vitro resistance to amphotericin B, nystatin, several azoles, and the echinacandins. Of the newer generation triazoles, voriconazole exhibits the best activity, and the addition of terbinafine may offer synergistic benefit. In all case reports of locally invasive disease, in addition to antifungal therapy, surgical intervention was performed. Local tissue debridement was often sufficient to cure the infection; however, more extensive limb amputation may be necessary. In addition to antifungals and surgical debridement, the synthetic biocide PHMB, has been successfully used to treat S. prolificans.
Mortality rates may be as high as 55‐70%, particularly in neutropenic patients and in disseminated disease. There have been no reported fatalities from local bone, joint, or soft tissue infections in healthy hosts. Due to the increasing incidence of this invasive fungal infection and its high associated morbidity and mortality, hospitalists should be familiar with S. prolificans and the available treatment options.
Conclusions:
S. prolificans is an emerging fungal pathogen that causes disseminated disease in immunocompromised patients and local joint, bone, and soft tissue disease in healthy hosts, particularly after penetrating trauma.
S. prolificans has high MIC to most available antifungals and treatment of local disease often requires extensive debridement and in some cases amputation