The class of fungicides acting as respiration inhibitors by binding to the Qo center of cyto-chrome b (QoIs) are in wide use for the management of apple scab caused by Venturia inaequalis. In order to assess responses of V. inaequalis populations to treatments with QoIs, sensitivities of isolates were determined for germinating conidia or for mycelial colonies developing from germinating conidia. Under both test conditions, inhibitory potencies of kresoxim-methyl and trifloxystrobin were largely equivalent. V. inaequalis populations treated with QoIs in a commercial and an experimental orchard both responded with significant shifts toward declining QoI sensitivities. However, the population responses were quantitative in nature, and highly resistant isolates indicative of a cytochrome b target site mutation were not detected. V. inaequalis populations from both orchards investigated also were fully resistant to sterol de-methylation-inhibiting fungicides (DMIs) such as fenarimol and myclobutanil, but isolate sensitivities to QoIs and DMIs were largely unrelated. Performance tests with kresoxim-methyl and trifloxystrobin at the experimental orchard diagnosed as DMI-resistant revealed that the quantitative shift toward declining QoI sensitivities did not constitute the status of practical QoI resistance. In contrast to these quantitative responses, emergence of qualitative QoI resistance was documented for V. inaequalis in an orchard in North Germany, which had been treated intensively with a total of 25 QoI applications over four consecutive seasons. Isolates retrieved from the orchard were highly resistant to both kresoxim-methyl and trifloxystrobin and were characterized as G143A cytochrome b mutants. The results indicated that the paths of QoI resistance can be both quantitative and qualitative in nature. A similar phenomenon has not been described before. Circumstantial evidence suggests that the quantitative phase of V. inaequalis population responses to QoIs might be succeeded by a quantitative selection of highly resistant G143A target-site mutants.