Aspergillus fumigatus is a ubiquitous saprophytic fungus well adapted to survive a wide range of environmental conditions including that of the human host. Infection is caused by inhalation of conidia, which are usually cleared in healthy individuals but can cause chronic or invasive aspergillosis in immunocompromised individuals. Over the last 30 years, mortality rates of those with invasive aspergillosis have increased to 90-100% even with treatment due to the rapid emergence of antifungal resistant isolates. Resistance is thought to be derived in the environment from off-target exposure to agricultural fungicides, the same class of antifungals used in clinics. Therefore, it is imperative for us to understand its ecology and biology to identify novel drug targets to prevent the growth of A. fumigatus in humans. In this dissertation we first examine the population structure of environmental A. fumigatus collected in Georgia and Florida and analyzed genomes of susceptible and resistant clinical isolates to understand how resistance may be evolving. Then we tested the effect of sporulation environmental on conidial germination using a high throughput germination assay to identify conditions which resulted in fast and slow rate of germination in genetically identical spores. Finally, we performed transcriptomic analysis on conidia to better understand what regulates its development and ability to germinate. In conclusion we found that what makes A. fumigatus such a virulent pathogen is due to its basic need to reproduce and simply survive.