ABSTRACT

Aspergillus fumigatus is a saprophytic fungus that plays an essential role in recycling environmental carbon and nitrogen. It grows naturally on decaying organic material in the soil and sporulates abundantly. The conidia are present in all environments, indoors and outdoors, with a range of concentration between 0 to 100 conidialm3• They have a diameter small enough (2-3 ILm) to reach all lung compartments. Inhalation of conidia by the immunocompetent host rarely has any adverse affect since they are eliminated relatively efficiently by innate immune mechanisms. Thus, until recently, A. fumigatus was viewed as a rather weak and infrequent pathogen responsible for aspergilloma, an overgrowth of the fungus in preexisting lung cavities, and allergic bronchopulmonary aspergillosis, a complication occurring in patients suffering from atopic asthma or cystic fibrosis [1,2]. Because of the increase in the number of immunocompromised patients and the degree of severity of modern immunosuppressive therapies, the situation has changed dramatically in recent years. Over the past 10 years, A. fumigatus has become the most prevalent airborne fungal pathogen, causing severe and usually fatal invasive infections mainly among hematology patients. This situation mainly results from (I) a difficult clinical and laboratory diagnosis; (2) a relatively ineffective antifungal therapy, mainly based on the use of amphotericin-B, which has severe secondary toxic effects for humans; and (3) a poor understanding of the physiopathology of invasive aspergillosis (lA).