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Pulmonary Aspergillosis

Aspergillus is a ubiquitous saprophytic mold that plays an essential role in recycling carbon and nitrogen.1 This fungus has a simple biological cycle characterized by a high sporulating capacity, which results in the release of conidia at high concentrations (1–100 conidia/m3) into the atmosphere. Aspergillus conidia have a diameter small enough (2–3 µm) to reach the pulmonary alveoli.1,2 However, while humans constantly inhale Aspergillus conidia, such conidia are effectively eliminated in immunocompetent individuals.3


Infections by Aspergillus species cause a wide spectrum of illnesses in humans depending on the immune status of the host (Table 133-1). Hence, in immunocompetent hosts, isolation of Aspergillus spp. in respiratory secretions typically reflects colonization, not infection. Under physiologic conditions, inhalation of Aspergillus spp. does not trigger immune responses because fungal spores are covered by a hydrophobin layer that masks recognition of immunostimulatory fungal cell wall molecules by host immune cells.13 In atopic individuals, the fungus triggers robust immune reactions, including allergic rhinitis, asthma, hypersensitivity pneumonitis, and allergic bronchopulmonary aspergillosis (ABPA).4 In patients with pre-existing cavitary pulmonary lesions, saprophytic growth of Aspergillus spp. can lead to aspergilloma formation. Finally, in immunocompromised individuals, some Aspergillus conidia germinate into the lung to form hyphae, the invasive form of the fungus, which causes a severe, frequently fatal angioinvasive infection called invasive pulmonary aspergillosis (IPA).57 The degree of fungal invasion, response to antifungal therapy, and outcome of invasive aspergillosis (IA) depend on the type and severity of immunosuppression. Thus, in patients with subtle or no immune defects, chronic forms of Aspergillus infections in the lung have been described, which are characterized by an indolent clinical course with the development of progressive cavitary lesions, and minimal or no evidence of parenchymal invasion.8 A less acute form of IA, frequently called subacute IPA, has been described in patients with acquired immunodeficiency syndrome (AIDS) and those with genetic defects in NADPH oxidase (chronic granulomatous disease or CGD), whereas progressive IPA is encountered in severely immunocompromised hosts.1,2,6,7 There is no doubt that since the first description in the 1940s, IA has emerged as the major problem of modern mycology. Currently, IA is a leading cause of death in severely immunocompromised individuals, with crude mortality rates approaching 50% to 70% in patients with leukemia and recipients of hematopoietic stem cell transplants (HSCTs).5,6 In addition, invasive Aspergillus has emerged as an important pathogen in an expanding spectrum of nonneutropenic patients with chronic debilitating diseases who receive corticosteroids and/or other immunosuppressive therapies. Thus, IPA is increasingly encountered in patients with inflammatory and autoimmune diseases, chronic obstructive lung disease, and prolonged ICU stays.2 At the same time, over the past two decades, we have witnessed a significant expansion in the antifungal armamentarium with the introduction of several agents with anti-Aspergillus...

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