Potato growers face an annual battle against the devastating pathogen “Phytophthora infestans,” which causes potato late blight. Regular fungicide sprayings are used to control the disease, but the current EU Farm-to-Fork strategy aims to reduce the use and risk of fungicides by 50% by 2030. However, only a few new active ingredients are expected to be approved during this period. Therefore, the emergence of fungicide-insensitive variants of the pathogen poses a significant threat to the fight against late blight. Research conducted by a team of scientists from Aarhus University (Denmark) and the James Hutton Institute (Scotland) revealed, for the first time, the existence of a new genotype of P. infestans that is resistant to a key fungicide active ingredient, mandipropamid, which belongs to the carboxylic acid amide (CAA) group of fungicides. This resistance poses a serious threat to the efficacy of mandipropamid and potentially other CAA fungicides, which are a key component of potato late blight management in Europe and beyond.
Late blight, caused by Phytophthora infestans, is a major threat to potato production and can lead to significant yield losses, as witnessed during the Great Irish Famine (1845-1852). Fungicides have played a crucial role in managing late blight as currently grown potato varieties are susceptible to this disease. However, just like antibiotic resistance in humans and animals, if the pathogen causing the crop disease becomes resistant to a specific active ingredient in a fungicide, the fungicide becomes ineffective at controlling the disease.
Mandipropamid is a carboxylic acid amide (CAA) and is an active ingredient in fungicides, used worldwide for controlling potato late blight. Since its introduction, mandipropamid has provided excellent control of late blight in potatoes. However, from 2019 to 2022 reduced mandipropamid effectiveness was observed in Danish potato fields. Subsequent analysis revealed a novel P. infestans genotype called EU43, first found in Denmark in 2018.
To investigate the true cause of the reduced efficacy, scientists from Aarhus University (Denmark) and the James Hutton Institute (Scotland) studied the sensitivity of isolates collected from fields where mandipropamid had been reported to be ineffective. Due to the apparent correlation between decreased efficacy of mandipropamid and the emergence of the EU43 genotype, it was hypothesized that resistance in the EU43 P. infestans genotype to mandipropamid was responsible for this reduced effectiveness.
The scientists employed microsatellite markers to genotype P. infestans isolates from Danish potato fields, revealing a high prevalence of the EU43 genotype. Mandipropamid sensitivity was assessed in the laboratory on isolates belonging to the genetic groups EU43, EU41, EU36, and EU37. Of these, only EU43 showed insensitivity to all tested fungicide concentrations. Field experiments confirmed EU43’s resistance to mandipropamid. Consequently, the study concluded that EU43 genotype resistance to mandipropamid was the underlying cause of reduced effectiveness of the fungicide.
While this finding is the first documented resistance of P. infestans to a CAA fungicide, previous studies have identified resistance in the grape pathogen Plasmopara viticola and an artificially-mutated P. infestans strain to mandipropamid (Gisi et al., 2007, Blum et al., 2010a, Blum et al., 2010b). In both cases, the resistance was caused by a mutation in a cellulase synthase gene, resulting in the substitution of glycine with other amino acids at position 1105. A similar mutation might be responsible for the EU43 P. infestans genotype’s resistance to mandipropamid.
Previous research has shown that resistance to mandipropamid in the grape pathogen Plasmopara viticola leads to resistance to other CAA fungicides. Therefore, it would be of critical concern if this is the case in P. infestans as other CAA fungicides (e.g. benthiavalicarb, dimethomorph, and valifenalate) are crucial for managing late blight in Europe and beyond.
While the EU43 genotype is widely distributed across Denmark, it has been found in other countries such as the Netherlands, Belgium, Germany, Sweden, Norway, and Portugal. Further monitoring of this resistance in a pan-European context is vital to minimizing its spread. Moreover, emphasis must be placed on adopting other elements of integrated pest management, including resistant varieties, disease forecasting, and fungicide anti-resistance strategies (e.g. the mixing and alternation of active ingredients), to optimize late blight management while protecting the lifespan of the current active plant protection ingredients.
Isaac K. Abuley, James S. Lynott, Jens G. Hansen, David E. L. Cooke and Alison K. Lees published this study in Plant Pathology:
TITLE IMAGE: A destruction of potato plants (Cultivar: Kuras) by late blight in plots sprayed twelve times with mandipropamid (left) and untreated (right) (i.e. no fungicide application to control late blight), both inoculated with EU43 Phytophthora infestans genotype All images used with permission of the author.