Chronic granulomatous disease (CGD) is a rare in-herited disorder of the NADPH oxidase complex in which phagocytes fail to generate reactive oxidants such as superoxide, hydrogen peroxide, and hy-droxyl radical, which are key elements in host de-fense against a variety of pathogens (14). Patients with CGD are therefore susceptible to recurrent, severe, life-threatening bacterial and fungal infections (14). Infection with Aspergillus species is commonly encountered in patients with CGD, is frequently as-sociated with pneumonia and disseminated disease, and is a major source of mortality (9, 28, 29, 30, 35). Aspergillus species are ubiquitous environmental molds that cause invasive disease primarily in pa-tients with quantitative or qualitative neutrophil defects (11, 15). Aspergillus fumigatus is by far the most frequent pathogen. Aspergillus nidulans has been recognized as a human pathogen since the late nineteenth century, when it was identified in a case of otomycosis (cited in reference 22). In contrast to A. fumigatus, A. nidulans is rarely encountered in patient populations at risk for aspergillosis (for ex-ample, those with prolonged neutropenia from intensive myeloablative chemotherapy). A. nidulans has been reported in patients with CGD or with histories suggestive of CGD (2, 6, 7, 16, 19, 20, 31, 32, 36, 42, 46), and White et al (46) have suggested that CGD patients are at greater risk for A. nidulans than are other immunocompromised patient populations. Characteristic morphologic features of A. nidulans are shown in Figure 1.