Friday, May 9, 2008

Turf - Fungicide Resistance

By the early 1900’s fungicides were being used extensively on turfgrass for disease control. With widespread use has come fungicide resistance with some disease strains. The following is an article on the subject.

Early fungicides provided protection by chemically modifying basic biological processes. The deactivation of these processes resulted in the shut down of several vital cell functions and caused death to the fungus. Broad spectrum chemical modifications of this sort were usually achieved with a metal like zinc or copper and were not specific to fungi. They were also found to be phytotoxic to plant material, so they were modified to be confined to the outsides of the plants. In order for them to be effective fungicides they had to be placed on the plant before the fungus was present to prevent the establishment of an infection. There are similar materials still on the market that we refer to as contacts.

In the 1960’s materials with the capability to enter plants and theoretically cure active infections were being developed and brought to market. In order to overcome the problem of non-specific biological activity caused by the early fungicides, the toxic effects of the newer materials needed to be confined to the target fungus. Consequently, the toxic effect of these new products usually focused on a single or narrow range of metabolic processes in the fungus. This single site toxicosis is often overcome by changes in the fungus. Reports of fungicide resistance quickly followed the introduction of the new materials.

Fungicide resistance is a stable, inheritable adjustment by the fungal population to the toxic effects of the fungicide. The changes in the fungal cell that bring about resistance are sometimes regulated by a single gene. This phenomenon is called monogenic resistance. In some fungi the changes are regulated by multiple genes, which is known as polygenic resistance. Fungicides that are at the highest risk of resistance problems are those that affect a single metabolic site in the fungus and those in which the resistance factor is governed by a single gene.

It is possible that any fungus has the ability to resist two or more fungicides. This phenomenon is known as cross resistance. Cross resistance usually occurs in closely related compounds in the same chemical classes. For instance, fungal populations resistant to propiconizole are often resistant to triadimefon and fenarimol. All of these materials are found in the same chemical class (sterole demethylation inhibitors).

Fungicide resistance does not develop spontaneously. In normal fungal populations, resistant biotypes are always present. Increases in the population of these resistant biotypes are brought on by the fungicide program. If the material one uses only attacks sensitive biotypes, then over time, the resistant biotypes dominate the population and control efforts fail. This generally occurs when a single material or materials in the same chemical class are repeatedly used over a period of time. It is also not uncommon for resistance to occur if less than optimal rates of the materials are used. This allows a broader range of tolerant biotypes to survive and prosper. The point at which satisfactory disease control is no longer provided in the field by your program is called practical resistance.

Be aware that all fungicide failures are not due to practical resistance. Improper diagnosis, improper dilution rates, poor selection of materials, bad timing, tank incompatibilities, improper calibration and bad nozzle choices are just a few of the possibilities.

That being said, we have seen several cases in the Rutgers Plant Diagnostic Laboratory last summer of practical resistance to dollar spot and anthracnose. If you suspect practical resistance and have ruled out other reasons for your disease control failures, then we suggest screening for fungicides in the following chemical classes: sterole demethylation inhibitors, the strobilurins, and benzamidazoles. In order to screen for resistance, we isolate the causal agents from diseased plant material and grow them on mycological media amended with a fungicide in each of the mentioned chemical classes. We use different concentrations of the materials in each media. The concentrations range from below to well above field rates. Over a period of several days we compare the growth rates of the target fungus on the fungicide amended media to an isolate of the fungus on a non-amended media. If the growth rates are similar, we determine the sample to be insensitive or laboratory resistant to the material we are testing for. If this is the case, adjustments to your fungicide program are in order.

Adapted from "Practical Fungicide Resistance in Turf Stands, Part I" by Richard Buckley, Director, Soil Testing and Plant Diagnostic Services, Rutgers University in the April 17, 2008 edition of the Plant and Pest Advisory, Landscape, Nursery, and Turf Edition, Rutgers University Ag. Experiment Station and Cooperative Extension.

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