NECROTIZING GRANULOMATOUS DERMATITIS, SECONDARY TO SCEDOSPORIUM APIOSPERMUM
Scedosporium apiospermum is the anamorphic or asexual form of Pseudallescheria boydii, which was first described as a human pathogen in 1911 by Saccardo in an Italian patient with mycetoma (1). Either form can be isolated from cultures. When baglike structures, called cleistothecia, containing sexually derived (telomorphic) spores (ascospores) are observed then the isolate is P. boydii. If the characteristic asexual oval or club shaped conidia are seen, then it is S. apiospermum.
Scedosporium apiospermum is a ubiquitous saprophytic ascomycete isolated from a myriad of natural sites including plant residues, soil, sewage, waterlogged pastures, and poultry and cattle manure (1,4,5). It has, in recent years, been shown to be pathogenic in both immunocompetent as well as immunosuppressed patients (2-5,7). The latter group includes patients post-transplantation, those neutropenic from hematologic malignancies, or on corticosteroids or cytotoxic drugs. In these patients hematogenous dissemination with endophthalmitis, endocarditis, and metastatic abscesses have been described (1,2,5,7).
Human infection has been most commonly reported following subcutaneous traumatic or surgical implantation (2,3,6). In our patient the portal of entry can be speculated to be the dialysis access site, similar to that reported at the site of catheter insertion used for chemotherapy (7). Clinically, cutaneous infections may present as solitary ulcers, infiltrative erythematous plaques and nodules, or suppurative nodules and ulcers in a sporotrichoid (lymphangitic) pattern (2-5). This latter clinical presentation, and the typical histomorphology is similar to that seen in our case, with necrotizing granulomas and a mixed dermal infiltrate. However, the presence of epidermal acanthosis and thrombosis of superficial and deep dermal vessels have also been described (5,7).
The second most common route of infection is inhalation (1,7). In addition, bronchopulmonary colonization or invasive pulmonary disease is not uncommon following cutaneous infection. Our patient, one month after initial presentation, was admitted to the cardiothoracic intensive care unit with mental status changes secondary to uremic encephalopathy, dyspnea, volume overload and congestive cardiac failure. During his hospitalization, repeated tracheal cultures isolated S. apiospermum, with subsequent development of a left upper lobe infiltrate.
Although the organism is often resistent to amphotericin B, several reports have shown Itraconazole, an imidazole derivative, to be effective in the treatment (3,4,5,7). The latter is currently the drug of choice agaist this organism.
In conclusion, in recent years, an increasing number of cutaneous infections by S. apiospermum are being encountered (2). These are seen predominantly in immunocompromised patients. In tissue sections the organism is morphologically similar to Aspergillus species with branching septate hyphae. However the presence of conidia which are characteristically tadpole or sperm-shaped should alert the pathologist to the possibility of infection by S. apiospermum. This will facilitate prompt therapeutic intervention in an attempt to prevent disseminated infection in a susceptible patient.
Contributed by Shashi Ariyanayagam-Baksh MB,BS and John Abernethy MD, PhD