Development of Strategies to Reduce the Risk of Fungicide Resistance in the Cranberry Cottonball Pathogen

Control of cranberry cottonball disease has relied on the sterol demethylation inhibitor (DMI) fungicides Funginex® (triforine) and Orbit® (propiconazole) since 1982. In other crop systems, some pathogens, including species related to Monilinia oxycocci (the cottonball fungus), have become resistant to DMI fungicides after several years of use. Cottonball management strategies are being developed to reduce the risk of fungicide-resistant M. oxycocci evolving in Wisconsin. Field studies in 1996 and 1997 showed that budbreak sprays had little or no impact on the percent cottonball infected fruit at harvest. Skipping budbreak sprays, and just spraying during bloom, was as effective in reducing the percentage of cottonball infected fruit as spraying during both budbreak and bloom. Non-DMI fungicides were effective in controlling cottonball when used alone or mixed with Orbit®. In the 1996 study, cottonball incidence was lower in a portion of a bed that had been sanded than in an unsanded portion. However, in 1997 disease incidence was too low at the field site to evaluate the effect of sanding. Further work will focus on developing a laboratory test to monitor populations of M. oxycocci for shifts toward fungicide resistance.

Cottonball, caused by the fungus Monilinia oxycocci, is the most important disease of cranberry occurring during the growing season in Wisconsin. Losses of 27-48% can occur if the disease is left unchecked. When disease levels are high, it is not profitable for growers to deliver fruit to the receiving stations, resulting in 100% loss of the crop.

Cottonball can be controlled by applying a sterol demethylation inhibitor (DMI) fungicide such as triforine (Funginex®) or propiconazole (Orbit®) twice during primary infection which coincides with budbreak and twice during secondary infection which coincides with bloom. However, the sensitivity to DMI fungicides of some fungal pathogens, including species related to M. oxycocci, has decreased after continuous and exclusive use over periods of about 10 years. Optimizing the timing of applications so that the total number of sprays can be reduced will delay the emergence of propiconazole-resistant populations of M. oxycocci and will be cost-effective for growers. The proposed research compares the efficacy of spray regimes differing in the total number and timing of fungicide applications.

The baseline sensitivity to propiconazole (sensitivity before propiconazole use becomes frequent and widespread) of populations of M. oxycocci will serve as a standard for future resistance monitoring. Developing anti-resistance strategies will prolong the usefulness of propiconazole; registration of new materials is a lengthy process with no guarantees for success.

Objective 1, fungicide efficacy and timing. The following six treatments were applied to 1.5 m² plots (8 repetitions; randomized block design) in beds of the cultivars ‘Ben Lear’ and ‘Searles’ in central and northern Wisconsin, respectively. Treatments varied in the fungicides used and the timing (budbreak, bloom, or both) of application.

Budbreak application dates at the central site (Jackson Co.) were 30-May and 11-June; bloom application dates were 1-July and 11-July. Budbreak application dates at the northern site (Rusk Co.) were 4-June and 13-June; bloom application dates were 9-July and 18-July. Sprays were applied at 30 psi and the equivalent of 50 gallons/acre.

Primary infection was rated by counting the number of symptomatic uprights per total uprights in three 113 cm² (18 in²) randomly selected areas in each plot on 3-July at the central site and 9-July at the northern site. Counts from the three samples were pooled into one larger sample (339 cm²) for further analyses. Secondary infection was rated by determining pecent infected berries in two 1,000 cm² (155 in²) randomly selected areas in each plot on 10-September at the central site, and in three 1,000 cm² areas in each plot on 25-September at the northern site. The two or three samples collected from each plot were pooled into larger samples (2,000 cm² or 3,000 cm²) for further analyses.

Primary infection data were transformed by calculating ln(X+1), where X is the percent infected shoots. Secondary infection data were transformed by the arcsin-square root transformation. Analysis of variance and means separation were performed on the transformed data, but the data presented are the means of original data. Evaluation of secondary infection in the sanded portion of the bed at the northern site revealed data points in one block that were statistical outliers. Thus, this block was eliminated from the analysis.

Objective 2, baseline sensitivity. This objective is currently being addressed.

Objective 1, fungicide efficacy and timing. Objective 1 was expanded to include an experimental compound (CGA219) that has a mode of action different from that of Orbit®. All fungicide treatments resulted in a significantly lower incidence of cottonball-infected fruit at harvest than the untreated control. CGA219 alone (Treatment 4) or mixed with Orbit® (Treatments 5) was as effective as Orbit® (Treatment 2) at both the central and northern locations (Figures 1 and 2). In general, treatments in which fungicides were applied during both budbreak and bloom (Treatments 2, 4, and 5) only slightly reduced primary infection, and did not reduce secondary infection compared to treatments in which fungicides were applied only during bloom (1, 3, and 6). Secondary infection in the sanded portion of the bed at the northern site was greater than in the unsanded portion, but we can not rule out the possibility that a pre-existing disease gradient was responsible for this result. Yield did not differ among treatments.

Baseline sensitivity. We have collected approximately 300 isolates from five marshes in Wisconsin. We are currently determining the ED₅₀s for isolates from sites in which DMI fungicides have never been used.

The field experiments will be repeated with the following modifications. At least one more non-DMI fungicide will be tested. Additional sites will be sought to further test the impact of sanding on cottonball incidence. The field experiments will be repeated for at least one more season.

ED₅₀ values will be determined for approximately 50 isolates from two sites in which DMI fungicides have never been used and one site where DMI fungicides have been used extensively. Frequency distributions for ED₅₀ values for each of the three populations will be constructed to determine if the population exposed to DMIs has shifted toward resistance. If no shift is apparent, and growers do not detect a breakdown in control, then it is likely that pathogen populations are still sensitive to DMIs.

I do/do not (circle choice) authorize Wisconsin Cranberry Board, Inc. to include this report in "Cranberry Agricultural Research 1996 Progress Reports", a collection of preliminary results to be distributed to cranberry scientists with abstracts for distribution to growers.

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Figure 1. Cottonball incidence at the central site in Wisconsin, 1996. Bars marked with the same letter within a graph indicate that differences are not significant according to the Least Significant Difference test (P=0.05).

Figure 2. Cottonball incidence at the northern site in Wisconsin, 1996. Bars of the same color (gray for sanded plots; black for unsanded plots) marked with the same letter within a graph indicate that differences are not significant according to the Least Significant Difference test (P=0.05).