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INTRODUCTION

Aspergillosis, caused by any of several species of Aspergillus, usually manifests in immunocompromised or debilitated hosts as necrotizing cavitary pulmonary lesions or as hematogenously disseminated foci in multiple organs. Aspergillus can also cause a hypersensitivity or allergic pneumonitis in immunocompetent hosts and in patients with chronic pulmonary diseases. This is referred to as allergic bronchopulmonary aspergillosis (ABPA).

PATHOGENESIS AND EPIDEMIOLOGY

Ubiquitous in nature, Aspergillus species are commonly found in soil, in water, and on decaying vegetation. Human exposure to the spores of potentially pathogenic species, particularly Aspergillus fumigatus, is unavoidable, yet fungal disease is rare, occurring primarily in immunocompromised hosts. A fumigatus has been implicated in most of the disseminated and pulmonary infections, and less common species include Aspergillus terreus, Aspergillus nidulans, Aspergillus niger, and Aspergillus versicolor. Other pathogenic species have been described recently, such as Aspergillus lentulus, Neosartorya udagawa, and Neosartorya pseudofischeri. Transmission occurs by inhalation of airborne spores that regularly contaminate the environment; human-to-human transmission or zoonotic transmission has not been documented. Hospital-acquired infections have been described and epidemiologically linked to building demolition and construction, which release fungal spores into the environment. Outbreaks of cutaneous infection have been traced to biomedical devices, such as armboards, contaminated with fungal spores. The primary immune host defense against invasive aspergillosis is the phagocytic function of neutrophils and mononuclear cells. High-risk populations include patients with prolonged neutropenia, those receiving high-dose steroids and/or immunosuppressive agents, stem cell or solid organ transplant recipients, particularly those with graft-versus-host disease, and patients with primary immunodeficiencies and advanced acquired immunodeficiency syndrome (AIDS). There has been a significant increase in the incidence of invasive aspergillosis over the past few decades due to increasing numbers of patients undergoing transplantation, specifically for hematologic malignancies, as well as an increase in the intensity of treatment regimens. Invasive aspergillosis in a patient without underlying disease is infrequent, and an intensive investigation for a predisposing disorder, such as chronic granulomatous disease, should be undertaken.

CLINICAL MANIFESTATIONS

Infection with Aspergillus manifests as 3 distinct syndromes related to host immunocompetence. Two forms of noninvasive aspergillosis are seen in patients with normal or mildly impaired immune systems: pulmonary aspergilloma and ABPA. In contrast, invasive aspergillosis, either local or disseminated disease, affects severely immunosuppressed hosts.

Pulmonary Aspergilloma

Pulmonary aspergilloma is the most common form of aspergillosis and occurs when the fungus grows as a dense mass of hyphae and tissue debris within a preexistent cavity caused by a concomitant pulmonary disease such as tuberculosis, lung abscess, or bronchiectasis. A patient with an aspergilloma may be asymptomatic and the lesion noted on incidental radiographic examination; however, an aspergilloma may also lead to life-threatening hemoptysis as a result of invasion of local bronchial blood vessels lining the cavity.

Allergic Bronchopulmonary Aspergillosis

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