Aspergillus fumigatus and related species

Abstract

The genus Aspergillus contains etiologic agents of aspergillosis. The clinical manifestations of the disease range from allergic reaction to invasive pulmonary infection. Among the pathogenic aspergilli, Aspergillus fumigatus is most ubiquitous in the environment and is the major cause of the disease, followed by Aspergillus flavus, Aspergillus niger, Aspergillus terreus, Aspergillus nidulans, and several species in the section Fumigati that morphologically resemble A. fumigatus. Patients that are at risk for acquiring aspergillosis are those with an altered immune system. Early diagnosis, species identification, and adequate antifungal therapy are key elements for treatment of the disease, especially in cases of pulmonary invasive aspergillosis that often advance very rapidly. Incorporating knowledge of the basic biology of Aspergillus species to that of the diseases that they cause is fundamental for further progress in the field.

Figure 1.

Saprophytic and pathogenic cycles of A. fumigatus. Saprophytic cycle: (1) A. fumigatus conidial head bearing conidia (spores). (2) Mature conidia are highly hydrophobic and readily dispersed. (3) On germination, conidia swell and germinate into hyphal filaments. (4) Extension of hyphal filaments forms an interwoven net called mycelia. Pathogenic cycle: (5) and (6) Airborne conidia are constantly inhaled by humans. (7) In severely immunosuppressed patients, conidia may escape from host defenses and grow invasively. (8) Extensive hyphal growth in the lungs of an immunocompromised patient. (9) Colony growth.

Figure 2.

Major pathogenic species of Aspergillus. A. fumigatus, A. terreus, A. nidulans, A. flavus, and A. niger were inoculated on Czapek-Dox agar and grown at 37°C.

Figure 3.

Select genes associated with A. fumigatus virulence. The listed genes interfere with various aspects of A. fumigatus survival, growth, and response to host defenses. Growth stages of A. fumigatus inside of lungs of mice immunosuppressed with hydrocortisone are represented. Fungal cells were stained with Grocott’s methenamine silver stain. This list includes: genes controlling the cell wall (Mellado et al. 1996; Langfelder et al. 1998; Tsai et al. 1998; Mouyna et al. 2005; Maubon et al. 2006; Romano et al. 2006; Li et al. 2007; Schmalhorst et al. 2008), signaling and metabolism regulation (Panepinto et al. 2003; Krappmann et al. 2004; Liebmann et al. 2004; Fortwendel et al. 2005, 2012; Steinbach et al. 2006; Zhao et al. 2006; da Silva Ferreira et al. 2007; Cramer et al. 2008; Ibrahim-Granet et al. 2008; Soriani et al. 2008; Ejzykowicz et al. 2009, 2010; Gravelat et al. 2010), thermotolerance (Bhabhra et al. 2004; Wagener et al. 2008), nutrition (Hensel et al. 1998; Schrettl et al. 2004, 2007; Hissen et al. 2005; Moreno et al. 2007; Liu et al. 2010), toxin genes (Bok et al. 2005; Sugui et al. 2007; Spikes et al. 2008), and response to stress (Paris et al. 2003; Tsitsigiannis et al. 2005; Reeves et al. 2006; Willger et al. 2008; Feng et al. 2011; Dinamarco et al. 2012; Grahl et al. 2012).