June 2003

2.

3.

4.

Diagnosis: Cutaneous Fusariosis

Histopathology: A biopsy for H + E (Figure 2) revealed a granulomatous dermatitis with septate fungal organisms demonstrating a "ribbon-like" appearance in the mid-reticular dermis. GMS weakly stained the fungal forms (Figure 3). Staining for acid-fast bacilli and tissue gram stains were negative. Histologically, Fusarium is often difficult to distinguish from Aspergillus.1 Both demonstrate septate hyphae with acute-angled branching, and they both invade the dermal vasculature, causing thrombosis and tissue infarction.2 Fungal cultures stained with lactophenol cotton blue (Figure 4) demonstrated clusters of multiseptate, "canoe-shaped" macroconidia which are characteristic of Fusarium (1,2).

Course: The patient was initially treated with an intravenous amphotericin B lipid complex and subsequently switched to Voriconazole 200 mg twice daily. He also underwent debridement of the lesion. Upon follow-up, the patient's wound was healing well via second intention, and healthy granulation tissue covered the base of the wound. There were no signs of wound infection. He denied fever and chills, and no further skin findings were noted upon physical exam. His wound care regimen included dressing changes bid, Keflex, and topical polysporin ointment. He may require a skin graft in the future for complete wound healing.

Discussion: Fusarium, a ubiquitous, saprophytic fungus, is a known human pathogen. In the immunocompetent host, it is generally localized to the skin or nail plate, though it has been known to superinfect wounds and ulcers, particularly in burn patients (3). In immunocompromised patients, primary cutaneous fusariosis similarly occurs at sites where the skin barrier has been disrupted (such as surgical wounds, IV catheter sites, or arthropod bites), and is most commonly seen on the distal extremities. In such cases, focal excision of the infection in addition to antifungal treatment and resolution of neutropenia may prevent or delay progression to disseminated infection (4 ).

Disseminated fusariosis almost exclusively affects immunocompromised patients, especially in the setting of hematological malignancies, chemotherapy, or a BMT with prolonged or severe neutropenia (i.e. an absolute neutrophil count <500/ul) (5 ). Disseminated fusariosis may be marked by fever, myalgias, and fungemia, with cutaneous involvement in occurring in over 70% of patients. The cutaneous lesions of disseminated Fusarium infection typically begin as erythematous or gray macules which evolve into an erythematous plaque containing a central ulceration or black eschar (6). The severity of the infection generally correlates with the degree and duration of neutropenia (7 ). However, it has been documented that bone marrow transplant patients or those who experience GVHD, even after resolution of neutropenia, are at increased risk for disseminated Fusarium infection. This may be due to the finding that lymphocyte function is impaired for up to one year following a BMT.

In summary, it is vital to biopsy and culture skin lesions that are characteristic for Fusarium in neutropenic patients. For in this subset of patients: 1) early treatment of localized cutaneous disease may prevent dissemination, and 2) disseminated fusariosis carries a mortality rate of up to 90% despite aggressive antifungal treatment and efforts to reverse profound neutropenia, such as with GM-CSF therapy (6,8,9).

References:

1. Bushelman SJ, Callen JP, Roth DN, Cohen LM. Disseminated Fusarium solani
infection. J Am Acad Dermatol. 1995;32:346-351.
2. Veglia KS, Marks VJ. Fusarium as a pathogen: a case report of Fusarium sepsis and
review of the literature. J Am Acad Dermatol 1987;16:260-263.
3. Antony SJ. Disseminated Fusarium in an immunocompromised host. Int J Dermatol.
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over 10 years. Br J Haematol. 2000;108:544-548.
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Fusarium solani cutaneous infection in a neutropenic patient. Dermatology.
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infection with cutaneous nodules in a bone marrow transplant patient. Int J Dermatol.
1988;10:698-702.
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disseminated Fusarium infection in the neutropenic patient. Clinical and Experimental
Dermatology. 1995;20:428-430.