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

Fungicide resistance groups in Europe

FRAC is the chemical companies resistance action committee. The pages includes the latest updates on resistance development and recommendations to minimize the risk. The page also include methods for screening for resistance and links to regional FRAC groups in Europe. more..

Nordic Baltic Resistance Action Group (NORBARAG)

Resistance terminology (FRAG-UK)

Resistance occurs when a pathogen becomes so insensitive to a fungicide that the fungicide’s field performance is impaired. Resistance can arise rapidly and completely so that disease control is lost in a single step. More commonly, resistance develops gradually so that the pathogen becomes progressively less sensitive. When this happens there is usually no initial detectable loss of control.

Laboratory testing can reveal a number of things about fungal strains isolated from the field. They can tell us about the genetic make-up of the isolate and how it has changed (mutated) by comparison with sensitive “wild-type” isolates from many years ago (so called ‘base-line’ sensitivity). Growth tests on laboratory media with different doses of fungicide can show how sensitive that isolate is compared with the wild type. Where selection has taken place, it is often very difficult to find any ‘wild type’ isolates because such isolates are very sensitive to fungicides and have been removed from the population by frequent fungicide use. The isolates that remain are less sensitive than the wild type – often by a large factor – up to 1000 times less sensitive in lab tests, These isolates may only be slightly less sensitive in practical terms and still controlled in the field by robust fungicide programmes or they may be highly resistant, leading to field control failure.

IPM as part of anti resistant strategies

  • Good resistance management is based on limiting the level of exposure of the target pathogen to the fungicide.
  • Fungicide input is only one aspect of crop management and other integrated control measures should always be used, such as good hygiene through disposal of crop debris and control of volunteers which may harbour disease.
  • Always aim to select varieties exhibiting a high degree of resistance to diseases known to be prevalent in your area, in addition to the main agronomic factors you desire.
  • Avoid growing large areas of any one variety, particularly in areas of high disease risk where the variety is known to be susceptible.
Revideret 27.09.2022
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Jens Grønbech Hansen