[5] Aspergillus terreus also produces aspterric acid and 6-hydroxymellein, inhibitors of pollen development in Arabidopsis thaliana.
[3][8] On Czapek or malt extract agar (MEA) medium at 25 °C (77 °F), colonies have the conditions to grow rapidly and have smooth-like walls.
[8] Aspergillus terreus has conidial heads that are compact, biseriate, and densely columnar, reaching 500 × 30–50 μm in diameter.
The conidia of A. terreus are small, about 2 μm in diameter, globose-shaped, smooth-walled, and can vary from light yellow to hyaline.
[10] Unique to this species is the production of aleurioconidia, asexual spores produced directly on the hyphae that are larger than the phialoconidia (e.g. 6–7 μm in diameter).
[16] Elevation of the sporulating head atop a long stalk above the growing surface may facilitate spore dispersal through the air.
[18] In turn, A. terreus has a better chance to disperse its spores amongst a vast geography which subsequently explains for the worldwide prevalence of the fungus.
[4] Tolerance of relatively low Aw conditions may explain, in part, the ubiquitous nature of this species given its ability to grow is a wide array of places.
[4] The Broad Fungal Genome Initiative funded by the National Institute of Allergy and Infectious Disease carried out the sequencing A. terreus in 2006.
[12][20] Identification of virulence determinants within the genome of A. terreus may facilitate the development of new approaches to the treatment of A. terreus-related diseases.
[17][24] Aspergillus terreus has no adaptation in terms of changing its physical structure when infecting a human or animal host.
[28] Aspergillus terreus has also been shown to disrupt the male sexual reproductive cycle in the plant model organism Arabidopsis thaliana.
Its secondary metabolites, aspterric acid and 6-hydroxymellein, released from the fungus inhibit the production of pollen, the male gamete in plants.
[24][26] Although less frequently seen in clinical samples, A. terreus displays evidence of amphotericin B resistance which correlates to a high rate of dissemination and an overall poor prognosis.
In addition, A. terreus releases toxic metabolites that attack immune cells like neutrophils which provide the suitable conditions for the fungus to thrive.
[12] Epidemiology studies have shown the incidence of A. terreus in causing invasive aspergillosis has increased relative to other species in the genus.
In fact, invasive aspergillosis has been named as the leading cause of death in leukemia and stem cell transplantation patients.
[12] Treatment of A. terreus is clinically challenging due to its nearly complete resistance to amphotericin B, the fallback drug for serious fungal infections.
A. terreus strains have a tendency to mutate while in the animal host, resulting in a substantial reduction or loss of characteristic spore heads in primary culture.
[33] A simple way to take preventive action is to provide good air filtration and ventilation throughout the hospital rooms.
[12][35] The fungus also produces a secondary metabolite called lovastatin, a potent drug for lowering blood cholesterol levels in humans and animals.
In this case, carbon and nitrogen are very important in fermentation productivity which in turn also increases the biomass of the metabolite lovastatin.