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About 60 scientists representing all the major agrochemical companies as well as government and independent organisations from the UK and other European countries attended this conference. Edinburgh produced splendid weather, which encouraged delegates outside at breaks and lunchtimes. A few energetic souls, including two of our Queen’s University Belfast (QUB) postgrads, Cliodhna McCartney and Steven Kildea, even used the afternoon after the end of the conference to climb Arthur’s Seat: I didn’t supervise this!
In the opening session, Karl-Heinz Kuck (FRAC/Bayer) gave a thought-provoking paper on risk assessment. He pointed out the difficulty of extrapolating risk assessments between fungicides of different mode of action (MOA) groups. However, he suggested that by looking at the rate of development of resistance over time by a specific pathogen to new MOAs, it is possible to get a better measure of pathogen risk. On this bas is , my favour i te pathogen Phytophthora infestans is re-classified as medium rather than high risk. Agronomic risk should also be considered, taking into account the conditions of fungicide use. However, I was left unclear what classifying a pathogen as medium rather than high resistance risk will mean and also felt that the practical consequences for growers of the occasional rapid development of resistance by “medium risk” pathogens need to be considered.
Many speakers focussed on resistance to the DMI and QoI fungicides. The mechanisms conferring resistance to both these groups are becoming clearer and we are beginning to understand why resistance fails to develop in some cases and what happens where multiple mechanisms are involved. Helge Sierotski (Syngenta) considered the cytochrome b gene and QoI resistance: so far none of the pathogens which have type I introns have developed resistance associated with the G143A mutation, the combination of this mutation and the intron appears to interfere lethally with cytochrome b function. This may allow better prediction of the risk of QoI resistance. For the DMIs, Hans Cools (Rothamsted Research) discussed how combinations of different mutations act in concert to confer resistance and how some mutations reduce sensitivity to certain DMIs, but not to others.
The widespread distribution in Europe of resistance to the QoI fungicides in Mycosphaerella graminicola, the cause of septoria tritici blotch of wheat, was shown by papers and posters from Denmark, Belgium and France. Cliodhna McCartney (QUB) demonstrated that when QoI fungicides were added to epoxiconazole in field trials in Northern Ireland, selection for G143A resistance occurred and disease control, green leaf area and yield were generally not improved.
Despite the dawning understanding of DMI resistance mechanisms, there is far from a consensus on their practical consequences for the control of septoriatritici blotch. Gerd Stammler (BASF) stated that the performance of epoxiconazole has been consistent over the past 12 years and does not correlate with sensitivity, while Andreas Mehl (Bayer) reported shifts in sensitivity of M. graminicola to tebuconazole in the UK and northern Germany, but not in France and Ireland. However, Steven Kildea (Teagasc/QUB) found that over the period 2004-2006 in Ireland, sensitivity to tebuconazole and metconazole of M. graminicola from commercial crops declined, but sensitivity to epoxiconazole and prothioconazole remained constant. In Denmark, Lise JÃ¸rgensen (Danish Institute of Agricultural Sciences) reported a decline in performance of propiconazole, but epoxiconazole was only registered in 2004 and so far performance has been good. Bill Clark (ADAS) presented a scary poster showing UK performance at four sites in 2006 of 12 DMIs currently marketed for the control of M. graminicola: striking pictures showed the severity of septoria in most treated plots and only epoxiconazole and prothioconazole gave better than 80% control. Clearly DMIs behave very differently from one another, but can the molecular biologists tells us if there are some DMIs where mutations conferring reduced sensitivity are unlikely to accumulate?
Perhaps the most provocative paper was “Is there such a thing as a fungicide resistance strategy? A modeller’s perspective” given by Mike Shaw (Reading University). In this, he argued that reducing the fungicide dose inevitably reduces selection for resistance, de-bunking the idea that repeated low doses are more risky. At last, with Mike’s clear presentation, we seem to have reached a consensus that high doses encourage fungicide resistance. This should help us to give clearer messages to growers and advisers in future. More controversially, Mike stated that mixtures of fungicides with different modes of action aren’t an anti-resistance strategy at all since they do not reduce selection for resistance, only the size of the population on which selection occurs. However, they may be a useful tactic to reduce the consequences of resistance and are very effective in avoiding lawsuits. I am still pondering on this!
Finally, Bill Clark’s concluding paper highlighted the worrying reliance of the agricultural industry on old fungicides as mixture partners for new single-site fungicides and the limitations of existing strategies. His conclusion was that the war is against crop diseases, rather than fungicide resistance, and can only be won by improving crop plant resistance, most effectively through the use of genetic modification. I found this a most useful conference and am very grateful to the BSPP for their travel grant. For anyone who wants to find out more about the current status of fungicide resistance research, most of the papers presented at this conference have been published in Aspects of Applied Biology 78, available from the AAB.
Louise Cooke, Agri-Food & Biosciences Institute, Belfast