5.5.30
PERSISTENCE AND MANAGEMENT OF STEROL DEMETHYLATION INHIBITOR RESISTANCE IN A POPULATION OF VENTURIA INAEQUALIS

PG BRAUN

Atlantic Food and Horticulture Research Centre, Agriculture and Agri-Food Canada, 32 Main St., Kentville, Nova Scotia, Canada, B4N 1J5

Background and objectives
The discovery and introduction of specific fungicides with attractive fungicidal properties and an increased risk of resistance development has heightened the need for sound anti-resistance strategies. Resistance to sterol demethylation inhibitor fungicides (DMI's) and a loss of control of apple scab, caused by V. inaequalis, occurred at Kentville after seven years of DMI efficacy testing. This provided the opportunity to determine if the repeated use of broad-spectrum fungicides would reverse the resistant population to the wild-type state and if subsequent limited use of DMI's was possible without a rapid re-selection for the DMI resistant population.

Materials and methods
An orchard block of apples, cv McIntosh and Cortland with a DMI resistant population of V. inaequalis was used in this study [1]. From 1989 to 1993 this orchard was treated only with the broad-spectrum fungicides, captan or metiram, for the control of apple scab. In 1994 and 1995 it was treated with four applications of myclobutanil (136 g ai/ha), at about 10 day intervals, beginning at tight cluster. The first two applications were myclobutanil alone and the second two were with the addition of captan (1.5 kg ai/ha). The following four and five applications of fungicide in 1994 and 1995, respectively, were captan, metiram or mancozeb at 10 to 14 day intervals. Mydobutanil sensitivity of V. inaequalis in this orchard was monitored every year except 1991. The EC50 values, of single spore isolates collected in July, were determined from the growth curve of each isolate on a series of 12 concentrations of myclobutanil in potato dextrose agar.

Results and conclusions
In 1989, there were two, normally distributed and overlapping, populations of V. inaequalis in the experimental orchard. Their mean EC50 values for myclobutanil were 0.05 and 0.83 uglmL with a range from about 0.012 to 0.263 and 0.138 to 3.25 ug/mL for the sensitive and resistant populations, respectively, and a resistance factor of 16.6. In 1992 and 1993, the fourth and fifth years of broad-spectrum fungicide use, myclobutanil EC50 values were 0.03 and 0.09 ug/mL with a range of 0.007 to 0.12 and 0.031 to 0.69 ug/mL, respectively. In 1989, the mydobutanil EC50 value of a population of V. inaequalis never exposed to DMI fungicides was 0.055 ug/mL with a range of 0.005 to 0.2 ug/mL. After four years of broad-spectrum fungicide use, the population of V. inaequalis previously resistant to myclobutanil appeared to have returned to a level of myclobutanil sensitivity similar to an unexposed population. In each of 1994 and 1995, two normally distributed populations of V. inaequalis appeared in response to the four applications of mydobutanil. The mean EC50 values were 0.075 and 0.48 ug/mL in 1994 and 0.06 and 0.50 ug/mL in 1995 for the sensitive and resistant populations, respectively. The resistance factor increased from not detectable in 1993 to 6.4 in 1994 and 8.3 in 1995. Apparently, mydobutanil resistant V. inaequalis was fit enough to compete with wild-type individuals even in the absence of any selection pressure for DMI resistance.

Therefore, in the presence of DMI insensitive individuals of V. inaequalis, even at a low frequency in the population, the current use recommendations for DMI fungicides could rapidly select for a resistant population in this multi-cydic disease. Perhaps only one application of a DMI per sexual cycle of the pathogen is a more appropriate anti-resistance strategy in areas of severe disease pressure. Such an approach is currently recommended in anti-resistance strategies for some insecticides. It would also appear that once DMI resistance in V. inaequalis has been selected it may not be possible to safely retum to DMI's for apple scab control.

References
1. Braun PG, KB McRae. 1992. Canadian Journal of Plant Pathology 14, 215-220.