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What would you do if you had only 6 days to live?

How would you spend it? Would you still be working overtime? Would you be wondering who to catch up with on the weekend? Would you be here right now reading this blog? Hell no!

The lifespan of powdery mildew is only six days long, and they are certainly making the most of it. They’re not just releasing spores close by, they’re spreading them across huge distances – sometimes crossing continents. They’re not just releasing a small handful either – in fact, each mature pustule is popping out 10,000 spores per day. Living life indeed!

Could this short life cycle be a reason why we’re seeing pathogens such as powdery mildew as trailblazers of Australia’s fungicide resistance list?

Researchers from the UK’s ADAS and Rothamsted studied 61 global cases of fungicide resistance in the past, and from doing so, were able to build a model for determining the time a product takes to develop resistance from when it has been released to market.

Interestingly, they found that it’s the number of lifecycles per year (and with six days to live, powdery mildew has many) that’s one of the more important determinants for a fungicide’s shelf life, along with three other variables:

  1. Fungicide molecular complexity
  2. Number of crop hosts
  3. The agronomic system

    PMW 2
    Powdery mildew has only 6 days to live

The research nutted out

Some pathogens evolve resistance to fungicides within as little as two years from release to market. The researchers thought if they could predict how many years it takes for resistance to develop in any pathogen after a fungicide has been released, they could help with future regulatory decisions.

They started with a list of 61 cases of fungicide resistance against single-site-acting fungicides. Each case took between 2 and 24 years for the first signs of resistance to be detected. They called this the First Detection of Resistance (FDR) time.

Taking a list of 43 traits relating to the pathogen, fungicide and agronomic system (such as spore type, chemical group, whether it’s outdoors or indoors etc.), they used statistical analysis to pick out the traits that were more statistically related with FDR time.

These were:

  1. Number of lifecycles per year: The shorter the life cycle and the more generations they can fit in per year, the higher the risk of resistance
  2. Fungicide molecular complexity: The less complex, the higher the risk of resistance
  3. Number of crop hosts: The fewer crop hosts, the higher the risk of resistance
  4. The agronomic system – outside or protected: Protected systems have a higher risk of resistance

Interestingly, the first one, the number of lifecycles per year, came out the strongest.

By combining these four traits into the final model, the researchers were able to give improved predictions (explaining 61% of the variation) on when resistance may appear in any pathogen once a fungicide is released.

 

In summary what does this mean for Australia’s diseases?

Six out of nine diseases on Australia’s fungicide resistance list have short lifecycles of around six days. These are powdery mildew (the different species that cause disease in wheat, barley and grapes) botrytis (one species in both legumes and grapes) and downy mildew in grapes.

Putting two and two together, short lifecycles of diseases could help us think about what the next fungicide resistant disease will be.

Could it be rust, I hear you say?

Rust has a short life cycle. Like powdery mildew and other diseases with a proven track record for developing resistance, rust’s thousands of spores can spread far and wide.

But up until now, it has been considered a low-risk disease for developing resistance. There have been no detected cases of resistance in Australia, which is great news as fungicides were estimated in 2009 to be saving Australian wheat farmers more than $400m per year in losses to rusts.

rust-vs-powdery-mildew-fw

 

Should we be worried about rust?

In a recent review, CCDM’s Richard Oliver explores why rust has been such a steady pathogen so far, and why we should reconsider its current low risk for developing resistance.

Of the nine classes of fungicides in which resistance has developed, six don’t work against rust. Of the three left over classes, Richard goes through each:

“Strobilurins or ’strobes’ are protected, for the time being, by a genetic mutation which makes resistance much less likely – we call this mutation the ‘blessed intron’,” Richard said.

“With triazoles, resistance develops slowly and has recently been found in Asian Soybean Rust in South America. We are currently looking out for early signs of resistance.

“Succinate dehydrogenase inhibitors (SDHIs) are not very active against rust, but we have no reason for complacency – it could just be a matter of time for this class.”

Richard said resistance to SDHIs has already been seen in septoria, fusarium and botrytis in other countries, only three years after the fungicide was released.

Because of this, the fungicide industry has taken a cautious approach and released products for rust control as mixtures with other fungicides with different modes of action.

“Such mixtures have only been on the Australian market since 2003 – I’m thinking not enough time has elapsed for resistance issues to emerge, and we should remain vigilant.”


What’s the best way forward?

To ensure rust keeps up its non-mutated self, Richard said fungicide use should be one part of a wider disease management strategy, involving resistant crop varieties, crop rotations, stubble management and green bridge control.


The papers

For research on the fungicide resistance risk assessment method: Michael K Grimmer, Frank van den Bosch, Stephen J Powers and Neil D Paveley (2014). Fungicide resistance risk assessment based on traits associated with the rate of pathogen evolution. http://onlinelibrary.wiley.com/doi/10.1002/ps.3781/abstract

For Richard Oliver’s review on rust’s resistance risk: Richard P Oliver (2014). A reassessment of the risk of rust fungi developing resistance to fungicides. https://www.ncbi.nlm.nih.gov/pubmed/24616024

 

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