Managing fungicide resistance in Irish crops

Over the past 50 years, the use of fungicides has become an integral part of crop production across north-western Europe. The climatic conditions that prevail across the region are highly favourable to the development and spread of fungal diseases.

To safeguard crop yields, fungicides are used in combination with a range of cultural measures to prevent these diseases from inflicting crop damage. As the most western nation in Europe, Ireland is at the forefront of this battle.

Our mild winters, and typically wet springs and summers are ideal for diseases such as septoria in winter wheat, ramularia in barley and late blight in potatoes to thrive.

As most crop diseases are fungal in nature, they often complete multiple lifecycles during the growing season and are easily spread through either rain splash or simply in the wind.

The combination of these factors means they are often highly adaptable, with the evidence of this unfortunately often manifesting in the form of fungicide resistance.

What causes fungicide resistance?

Simply put, it is the ability of a fungus to resist the toxic effects of a fungicide – a fungicide no longer kills the fungus. It should be noted, that fungicide resistance is not just unique to crop protection.

Any fungus, irrespective of its environment or host, and irrespective as to how the fungicide may be applied, has the potential to become resistant to fungicides.

As fungal pathogens are the main causes of diseases in cropping systems, it makes sense that it is in those crops – and related diseases that are most widely treated with fungicides – that resistance develops.

The consequences are loss of efficacy of the fungicide applied and failure to prevent, control or manage the disease targeted.

Since the 1970s, there have, unfortunately, been multiple examples of this occurring, with devastating consequences for the management of the disease and crop in question.

The most notable cases include the development of metalaxyl resistance in late blight in the early 1980s, resistance in septoria to the strobilurins or QoIs in 2002, and most recently the emergence and spread of CAA (Revus) and OSBPI (Zorvec) resistance across northern Europe, again in late blight, in 2023.

While not a new phenomenon, our understanding of the causes or mechanisms of fungicide resistance have greatly increased in recent decades. This has allowed us to better predict and subsequently map its potential emergence and spread. In doing so, it allows us to better manage and mitigate the consequences.

At its most basic, a fungicide interferes with the day-to-day functioning of the disease. This is where the concept of single site or multi-site fungicides come into play and how susceptible a fungicide may be to the development of resistance.

What we refer to as multi-sites (folpet, for example) likely interfere with a multitude of functions in the disease. This doesn’t make it impossible for the disease to adapt or become resistant, it just makes it that bit more difficult.

If the disease is required to adapt across a range of functions all at once, it can often impact its fitness to survive. When a fungicide is applied, such fitness impacts may not have an overly negative impact, the benefit provided by resistance is vastly of more value.

However, as fungicides are often only applied during a certain period of the year, these diseases must survive between cropping seasons. Such fitness penalties may leave the disease vulnerable to be easily out competed in the battle of survival that is the natural environment.

For these reasons, multi-sites are often referred to as low-resistance risk fungicides, which makes them a good mix partner from the aspect of resistance management – of course assuming they provide adequate control of the disease in question.

As the name suggests, single site fungicides target specific protein(s) in the fungal disease.

Unlike multi-sites, this level of specificity often allows them to be more versatile, effective and to some extent more environmentally favourable and easier to get through the strict regulatory hurdles that now exist.

Unfortunately, this level of specificity does come with a compromise. Simple changes in the disease, typically in the protein targeted by the fungicides, referred to as the fungicide target site, can completely render the fungicide ineffective.

The classical example of this is the development of the mutation G143A in septoria that rendered the QoIs ineffective against the disease. Often these changes are as simple as a single change in the disease’s DNA.

In the case of septoria, as each individual strain contains approximately 40 million pieces of DNA, crudely put, the chance of resistance emerging is therefore a one in 40 million chance, the wrong change in one of these pieces results in resistance. This seems like a crazy low chance.

However, a typical hectare of winter wheat with a moderate level of septoria is estimated to have anything up 10 trillion spores of the fungus present.

Of course, not all spores will have a mutation or change in DNA, and the vast majority of spores will actually land on a leaf and go on to cause disease, but when we look across all thousands of hectares of wheat, it becomes a lot easier to understand that the development of resistance resulting from such a change in the DNA of septoria is purely a numbers game.

While the numbers may be stacked against us, it doesn’t mean that we can’t manipulate them. As mentioned above, for most crop-disease interactions, fungicides are only applied for a relatively short period of their overall lifecycle.

It is only during the period where the disease is exposed to the fungicide that selection for that resistant mutation occurs, outside of this, the resistance strain has no advantage over a sensitive strain and competes for survival like any other strain.

There are always, unfortunately, exceptions to the rule, with some crops requiring fungicide applications for a large proportion of the lifespan. Potatoes and late blight is the most obvious.

For control of late blight, fungicides are typically applied from crop emergence to desiccation to protect against late blight. This is why late blight is often regarded among one of the highest diseases at risk of developing fungicide resistance and requires even greater attention when managing.

So how can we manage?

Fungicide usage drives resistance. It was previously believed that the excessive use of low rates of fungicides aided the development and spread of fungicide resistance.

This perception was in part driven by the grouping of all herbicides, fungicides and insecticides as one.

However, we must remember while they all may target and control pests, the specific pests they control differ and what might be the cause for one may not be for the other.

In the case of fungicides, the predominant mechanism of resistance are target site mutations as described above.

The levels of resistance conferred are extremely clear, they either work or they don’t.

Combined with the fact that most fungal diseases can complete their lifecycle and reproduce and spread onwards well beyond where they originated within a matter of days to weeks, mean that the more a fungicide is applied, whether by increased doses or numbers of applications, the longer a resistant strain has to develop and spread.

All other fungicide sensitive strains are kept under check by the fungicide. Therefore, from the aspect of fungicide resistance, emergence and selection and managing this, the lower the dose of fungicide used or the number of times it is applied to an individual crop, the better.

As mentioned above, this is not always the case for other pesticides, in particular herbicides where different mechanisms of resistance may operate, and the life cycle of the pest is annual and localised.

While lower fungicide doses and/or lower application frequencies will help reduce the emergence and selection for resistance, we must not lose sight of the fact that we are applying fungicides to control diseases and protect crop yields, be it quantity or quality. Undoubtedly, this is the key consideration when a fungicide control programme is being devised, and rightly so. But we must also recognise that how the programme is developed can, and does, impact resistance emergence and spread. So, what can we do to reduce fungicide resistance?

1. It seems strange to say it, but fungicides should only be added when they are needed. There must be a measurable risk to the crop from fungal diseases.

2. The choice and dose of the fungicide used must equally reflect the disease risk. In any given season, crops will be attacked by a plethora of different diseases. It might be possible to observe what disease(s) are present in the crop prior to application and to select accordingly. However, disease resistance ratings should also be consulted to provide an indication as to the risk any given crop variety may have. And of course, the weather is a critical factor in disease development and any fungicide application must take account of the past weather, with an eye on what may be forecast in the short term.

3. As resistance is related to the exposure of the disease to a specific fungicide, they should be mixed with different modes of action. Fungicides with different modes of action mean the two fungicides target different targets in the disease. In the perfect world, it means that if resistance were to develop to one of the partners, then the other partner would not be affected and would be able to control the disease and hence prevent selection for resistant strains.

4. It is important to note that there are lots of products with the same mode of action so, when selecting fungicides to partner that mode of action, that the active is looked at. Often on the label a FRAC (Fungicide Resistance Action Committee) number is provided. Different numbers indicate different modes of action – mix different numbers or ensure the product applied has at least two numbers in it.

5. Following on from mixing, if possible where sequential applications of fungicides are required they should be of different fungicide groups than those used in the previous application. Unfortunately, this may not always be possible given fungicide availability and/or efficacy. However, it should be considered when devising fungicide programmes.

6. Finally, all other available measures for disease control must equally be implemented. It is essential to remember that only by reducing the risks of disease will it be possible to reduce the risks of fungicide resistance – genetics protects chemistry, while chemistry protects genetics.