Sclerotinia homoeocarpa F.T. Bennett, the causal agent associated with dollar spot, is a common and economically challenging turfgrass disease in North America. Acceptable turfgrass quality requires the optimization of cultural practices and the judicious use of fungicides. Sclerotinia homoeocarpa causes significant damage to turfgrass swards from May to October annually, therefore, requiring multiple fungicide applications to maintain satisfactory turfgrass quality throughout the growing season. Sterol demethylation inhibitor (DMI) fungicides are among the most widely used in the United States and frequent use has led to the development of fungicide resistance to the DMI fungicide class. The precise mechanism of DMI fungicide resistance in S. homoeocarpa is not completely understood, however over expression of the CPY51A gene or efflux transporter genes have been reported as the molecular mechanism for other fungal systems. Fungicide resistance to the DMI class exhibits a gradual population shift towards insensitivity that can be monitored using In vitro fungicide sensitivity assays. In vitro fungicide sensitivity assays have been used to detect fungicide sensitivity differences in different S. homoeocarpa isolates and currently serve as the most accurate methodology to detect DMI insensitivity in S. homoeocarpa. Documentation of DMI field efficacy on native S. homoeocarpa populations with differing in vitro sensitivities has not been examined thoroughly and would provide critical information regarding the association between in vitro fungicide sensitivity and DMI field efficacy. The objectives of this research are (i) to determine the association between in vitro propiconazole sensitivity and reduced field efficacy for five native S. homoeocarpa populations and (ii) to develop a qualitative in vitro sensitivity assay for detection of S. homoeocarpa isolates responsible for practical field resistance.