Figure 3.

Aspergillus terreus during infection of putative host adopts a formidable means of survival.

Notes: A. terreus exploits its cytoplasmic chaperones, such as HSPs, as one of its counterresponses to adapt and mount resistance to amphotericin B (AMB), and this counterresponse could be associated with upsurge in reactive oxygen species (ROS). The interconnection between phialidic conidia (PC) and accessory conidia (AC) developmental stages on infection hyphae allows the pathogen to adapt to homeostatic changes and other adverse conditions in hosts. Production of Asp–melanin, which hijacks innate immunity, indicates that A. terreus could colonize all organs of the animal body. On the other hand, in plant host, stomata atropism (ie, inability to colonize hyphae to penetrate epidermal cells via the stomata pore) allows A. terreus to colonize superficially at a faster rate as a necrotroph while secreting metabolites that trigger necrosis and mitigate the host defense system.