Fusarium is a plant pathogen and a soil saprophyte that causes a broad spectrum of infections in humans, including superficial, localized, and disseminated disease.37 Fusariosis is similar to aspergillosis in that it occurs more frequently in patients who have prolonged and profound neutropenia and in those who receive high doses of corticosteroids. Host immunity, especially T-cell defense, is important in the pathophysiology of these infections. Unlike infections in the normal host, infections with Fusarium species in immunocompromised patients are generally invasive and disseminated. The principal portals of entry for this mould are the airways followed by skin with tissue breakdown.41
Fusariosis has been widely reported in HSCT recipients. In allogeneic HSCT recipients, a trimodal distribution of infection occurs. The first peak is during the early posttransplant period (during neutropenia). The second peak is at a median 70 days after transplant (typically in patients with GVHD receiving corticosteroids). The third peak occurs more than 1 year after HSCT and is associated with treatment of chronic GVHD.41 Reports of fusariosis in SOT recipients are much less frequent than in HSCT recipients.37
The clinical manifestations of fusariosis depend on the portal of entry and the degree of immunosuppression. Endophthalmitis, sinusitis, pneumonia, and skin and soft tissue infections have been described.41 Often, the clinical presentation is indistinguishable from that seen with other invasive fungal infections. However, unlike aspergillosis, a striking characteristic of fusariosis is the high frequency of positive blood cultures. Combined with the presence of skin lesions, positive blood cultures are characteristic of disseminated disease in immunocompromised patients.
Standard blood cultures will often yield growth of Fusarium; however, fungal media is preferred in patients in whom fusariosis is suspected because the growth rate is faster than that in standard media. Positive cultures from a sinus aspirate or respiratory secretions in highly immunocompromised patients should be considered diagnostic of infection; however, this does not hold true for immunocompetent patients in whom colonization without active infection can occur.41 In tissue, Fusarium hyphae look similar to those of Aspergillus species. In the absence of microbial growth, establishing the diagnosis would be difficult.
In general, localized infections are likely to benefit from surgical debridement. Disseminated infections require treatment with systemic antifungal agents. Fusarium tends to be drug-resistant, and what constitutes optimal therapy is not clear. On the basis of in vitro susceptibility testing, Fusarium has low susceptibility to fluconazole(Drug information on fluconazole), 5-flucytosine, and amphotericin B(Drug information on amphotericin b) and variable susceptibility to itraconazole(Drug information on itraconazole), voriconazole(Drug information on voriconazole), and posaconazole. However, various species may have different patterns of susceptibility. Fusarium solani is more susceptible to amphotericin B but is less susceptible to voriconazole than is Fusarium oxysporum. Echinocandins do not have in vitro activity.41
Voriconazole is approved for the treatment of Fusarium infections in patients whose treatment with other antifungals has failed. Reports of its use for treatment of these infections are limited. When used in a compassionate- use setting, 9 of 21 patients (43%) with fusariosis had a complete or a partial response.42 Posaconazole therapy was successful in 10 of 21 patients (48%) with fusariosis who were refractory or intolerant to other antifungal agents.43 Further clinical data are needed.
Scedosporium apiospermum (and its telomorph Pseudallescheria boydii) and Scedosporium prolificans are ubiquitous filamentous fungi present in soil, sewage, and polluted waters. Infections with these organisms can be localized, can extend into the surrounding tissues, or can disseminate through hematogenous spread to distant organs.44
Patients who have advanced HIV- 1 infection, primary immunodeficiencies, or hematological malignancies and patients who are HSCT or SOT recipients are at high risk for development of Scedosporium infection. Disseminated infection is most common in immunocompromised patients. In advanced HIV-1 infection, scedosporiosis may develop during periods of neutropenia.44