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Pulmonary mycoses, mainly caused by Aspergillus, Mucorales, and other saprophytic molds are emerging diseases in the rapidly expanding population of immunocompromised patients. These opportunistic fungal pathogens cause a spectrum of pulmonary diseases depending on the severity of the underlying immunodeficiency. In particular, invasive mold infections are associated with considerable mortality despite appropriate antifungal therapy. Apart from improvements in establishment of timely diagnosis of pulmonary mycoses with establishment of non-culture-based diagnostic methods, there is a need to dissect the underlying mechanisms of immunopathogenesis in order to develop host directed therapies.


Aspergillus is a ubiquitous saprophytic mold that has a simple biologic cycle characterized by asexual reproduction and 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 may frequently inhale Aspergillus conidia, such conidia are effectively eliminated in immunocompetent individuals.3


Infections by Aspergillus species cause a wide spectrum of illnesses in humans, which reflect the immune status of the host (Table 132-1). Hence, in immunocompetent hosts, isolation of Aspergillus spp. in respiratory secretions typically reflects colonization, not infection. In normal individuals, inhalation of Aspergillus spp. does not trigger immune responses because fungal spores are covered by a hydrophobic protein layer that masks recognition of immunostimulatory fungal cell wall polysaccharides by the immune system.1–3 In atopic people, 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 (mainly as a result of prior tuberculosis), saprophytic growth of Aspergillus spp. can lead to aspergilloma formation or persistent inflammation, a disease entity called chronic pulmonary aspergillosis (CPA). Finally, in immunocompromised individuals, Aspergillus conidia may germinate in the lung to form hyphae, the invasive form of the fungus, which causes a severe, frequently fatal angioinvasive infection called invasive pulmonary aspergillosis (IPA).5–7 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 incompletely characterized, subtle immune defects, chronic forms of Aspergillus infections (CPA) in the lung have been described, which are characterized by an indolent clinical course, low-grade chronic inflammation, the development of progressive cavitary or fibrotic lesions, and minimal or no evidence of parenchymal invasion.8 A less angioinvasive form of IA, frequently called subacute IPA, has been described in patients 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 ...

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