George Sundin, Michigan State University, presented a workshop discussion on the implications of fungicide resistance for three tree fruit pathogens of importance. Those pathogens – Blumeriella jaapii, the causal agent of cherry leaf spot; Monilinia fructicola, which results in American brown rot; and Venturia inaequalis, which causes apple scab – are controlled with fungicides, but resistance is a concern.
Preventing resistance from developing depends on proper and prudent use of chemical controls. The development of different isolates of pathogens in the fungal populations present in an MSU research orchard has caused issues with control. While the majority of the isolates in the orchard may not be resistant to fungicides, the presence of resistant strains is a significant issue.
“If there is some resistance in there, and we’re just using a single site fungicide…then we will be selecting for an increase in these resistant populations,” Sundin said, as these populations will then develop under the radar over time.
A single site fungicide attacks a pathogen by eliminating a single protein essential to the growth and life of the targeted fungus. In order to survive fungicide applications, the fungus must mutate. These mutations can result in the inability of the fungicide to bind to the fungus, rendering it ineffective. In order to be effective, a fungicide would need to target a different protein in order to eliminate the population which developed resistance.
A multiple site fungicide attacks more than one protein simultaneously, making it much less likely that resistance via mutations would occur for every site of attack. Tree fruit fungicides are often mixes of more than one fungicide, sold premixed under one brand name, providing multi-site action.
Resistance can also develop when a fungus simply increases its production of the targeted protein, so that the fungicide cannot attack the full quantity of those proteins. The target of the fungicide is the same, but without increasing application rates, some of the targeted proteins are escaping attack due to the fungus enhancing the amount of the protein it produces. “We can’t raise the rates of fungicide enough to overcome this kind of over-expression,” Sundin explained.
It isn’t true that fungi develop mutations only in response to an application of fungicide. Fungi with pre-existing mutations that would render a fungicide ineffective exist at a low rate – maybe one per 10 million or even 100 million – before they are exposed to any particular fungicide.
When using a single site fungicide, these pre-existing mutations are selected for extensively. While the number of resistant fungi are not enough to cause economic damage to an orchard immediately, over time the populations will increase until the spray program is no longer effective and disease becomes prevalent. Even if the spray program is altered, the resistant populations of fungi will not be eliminated, but will persist in the orchard over time.
Cherry leaf spot has become resistant by producing greater quantities of the protein targeted by the fungicides used for control over the years. Apple scab has had resistance develop randomly – not due to the use of fungicides – which has built up over the years so that the wild strain is less populous than the mutant strain in orchards where fungicide use has occurred over the years. Post-infection fungicide applications have led to resistance to sterol demethylation inhibitors (DMI) and to strobilurin fungicides.
Apple scab remains controlled due to the development of second generation succinate dihydrogenase inhibitors (SDHIs). These fungicides are highly effective against scab. Recent studies have compared apple scab fungal isolate growth on fungicide treated and non-treated media, using non-exposed M. fructicola pathogens as a baseline. Results show that very good control of apple scab is still occurring.
Cherry leaf spot is resistant to SDHIs, however. B. jaapii began showing resistance in 2008. Because the population of pathogens is higher in cherry leaf spot than in apple scab, the resistance developed faster, Sundin said. There are multi-site fungicides that still provide cherry leaf spot control. There are too many sites of action in these fungicides for the pathogen to mutate and evade and still remain alive.
American brown rot is the pathogen researchers are “most concerned about long-term,” Sundin said. Due to ineffective rates of DMI fungicide being utilized from 2010 – 2020, V. inaequalis has developed practical resistance to this class of fungicides.
“You always want to use the highest rate that you can,” Sundin said. “If it grows, it can mutate to resistant strains.”
Using a single site fungicide alone, at sub-optimal concentrations or where coverage is not complete, has increased resistant V. inaequalis pathogen populations. But there are still effective options for brown rot available. Disease control requires complete elimination of the pathogen in question. Problems arise as some level of pathogenic activity has been allowed to occur despite fungicide utilization.
“We really have to do a good job of protecting our fungicide modes of action,” Sundin said. “We are going to be at our limits if we lose some of these fungicides to resistance.”