Aspergillus crown rot, caused by Aspergillus niger, a member of the dark spore producing aspergilli, Aspergillus section Nigri, is an important disease of peanut, Arachis hypogaea L. Crown rot often affects germinating seed and seedlings, and can cause plant death. Control of Aspergillus crown rot is heavily dependent on chemical seed treatment. Until recently, azoxystrobin, a quinone outside inhibitor (QoI) was the primary component of the predominant seed treatment that targeted crown rot. Recent reduction in efficacy of azoxystrobin applied as a seed treatment or as an in-furrow spray has led to concerns of potential resistance to this fungicide in A. niger, field and microplot studies were conducted to compare efficacy of current peanut seed treatments, and to determine effects of foliar application of QoI, SDHI, and DMI fungicides on sensitivity of A. niger. A collection of 248 isolates of Aspergillus section Nigri were used to examine genetic diversity and determine frequency of mutations at cytochrome b, the target site of QoI fungicides, associated with resistance to this group of fungicide. The isolates were also characterized for relative in vitro sensitivity to azoxystrobin, and the relationship between mutations in the cytochrome b gene and EC50 values for the isolates for combination with phenotyping isolates of Aspergillus section Nigri. There was little difference among seed treatments in field trials to evaluate efficacy of seed treatment in 2018 and 2019. However, seed treatment effects were significant in 2017, with Rancona outperforming Dynasty and Vitavax. Microplot trials to evaluate foliar applications of QoI, DMI, and SDHI fungicides were found to be inconclusive for driving QoI resistance. However, the number of isolates with > 50% germination on 0.1 µg/ml concentration of azoxystrobin amended plates increased from 14.7% in 2017 to 94.2% in 2018, regardless of the foliar fungicides applied. In the genetic diversity trial, the Aspergillus section Nigri isolates were genetically diverse, as indicated by DAPC and clone correct analysis. Sensitivity to azoxystrobin varied widely among the isolated examined with 18.5% of the isolates having EC50 values >30 µg/ml. Although84.7% of the isolates had the F129L mutation in the cytochrome b gene only two isolates had the G143A mutation typically associated with severe reductions in sensitivity. These results showed that reduced sensitivity to the QoI fungicide azoxystrobin is present in the Aspergillus section Nigri isolates. The sensitivity from the fungicide amended spore germination assay shown was not explained by high frequency of mutation at the G143A location. There was a wide range of EC50 values among isolated with the F129L mutation, indicating other factors, and possible additional mutations may be responsible for high levels of resistance to azoxystrobin. The results from these investigations conducted at the University of Georgia and the USDA-ARS indicate that resistance to the QoI fungicide, azoxystrobin is present in isolates of Aspergillus section Nigri from peanut in Georgia.