General information

There has been a gradual increase in the occurrence of fungicide resistance since the early 1970s. Resistance is usually first recognised when expected levels of disease control in the field are no longer achieved using commercial doses of the fungicide. Fungicide resistance can sometimes arise rapidly and disease control can be lost partially or completely. Sometimes it can be a gradual process resulting in a loss of control over many years. Examples of these types are common throughout Europe.

Many types of resistance mechanism are known. By far the commonest mechanism appears to be an alteration to the biochemical target site of the fungicide. This could explain why many of the older products, which have no specific target site, have not encountered resistance problems. In contrast, modern fungicides act primarily at single target sites, and are often referred to as single-site fungicides. In this case, a single gene mutation can cause the target site to alter, so as to become much less affected by the fungicide. Different amino acid changes can cause different levels of resistance.

Factors influencing resistance

The risk of development of resistance is linked to a number of factors including the specific mode of action (MOA) of the fungicide, the biology of the target pathogen and the level of exposure of the pathogen to the fungicide. Resistance management is vital to maintain effective control whilst minimising over-exposure of the pathogen and reducing the risk of resistance developing.

Anti-resistance strategies:

  • Make full use of disease-resistant varieties.
  • Minimise the use of fungicides by avoiding unnecessary prophylactic treatments.
  • Monitor crops regularly for disease and treat before the infection becomes well established.
  • Where possible, avoid repeated applications of fungicides of the same group, and never exceed the maximum recommended number of applications.
  • If possible, alternate applications of fungicides from different groups.
  • Use recommended formulated mixtures or tank-mixes
  • Make use of fungicides with a multi-site mode of action.

Pathogen

Benzimidazoles

Triazoles DMI

Strobilurins (QoI)

SDHIs
Carboxamides

Blumeria graminis f. sp. tritici Yes, widespread. Mutation in ß-tubulin Yes, widespread. Mutation in CYP 51 gen Yes, widespread. G143A mutation -
Zymoseptoria tritici Yes, widespread. Mutation in ß-tubulin Yes, widespread. Mutation in CYP 51 gen Yes, widespread. G143A mutation Many specific SDHI mutations have been found in Northern Europe e.g. C‐T79 N and C‐W80S
Microdochium nivale - Yes, widespread. Mutation in CYP 51 gen Yes, widespread in France. G143A mutation. Also recognized in Denmark -
Stagonospora nodorum - - Yes, found in Sweden, Denmark and Norway. G143A mutation -
Pyrenophora tritici-repentis - - Yes, widespread. G143A, F129L and G137R. Mutations found -
Puccinia striiformis - -

Specific  CYP51 mutation (Y134F) found - considered of minor importance

Puccinia triticina - - - -

Source of information: FRAC, Arvalis, FRAG UK, Norbarag. Updated May 2015, by Lise Nistrup Jørgensen