First described in Europe in 1777, stripe rust (SR) caused by Puccinia striiformis Westend. f. sp. tritici Erikss (Pst) is one of the most important and destructive diseases of wheat worldwide. Until 2000, SR was mainly endemic to cooler regions, but since then, new aggressive strains have emerged, spread intercontinentally, and caused severe epidemics in warmer regions across the world. This has put SR as a disease that poses a threat to the world food security. At present, the preferred strategy for control of SR is the access to wheat cultivars with adequate levels of SR resistance. However, wheat breeding programs are not sufficiently advanced to cope with the recently emerged Pst strains. Under this scenario, foliar fungicide applications have become an important component of SR management, but information on the effects of fungicide applications on SR control and wheat cultivar yield response is scarce. This review seeks to provide an overview of the impact and role of fungicides on SR management. With focus on wheat management in the major wheat-growing regions of the world, the review addresses: (a) the efficacy of different fungicide active ingredients, optimal fungicide timing and number of applications in controlling SR, and (b) the impact of fungicide on wheat grain yield response. Inclusion of fungicides in an integrated crop management approach is discussed.

Two new penta-and tetrasubstituted cyclopentenones, named phaseocyclopentenones A and B (1 and 2), together with guignardone A (3), were isolated from Macrophomina phaseolina cultures. The phytopathogenic fungus was isolated from infected soybean tissues showing charcoal rot symptoms in Argentina. Charcoal rot is a devastating disease considering that soybean is one of the main legumes cultivated in the world. Phaseocyclopentenones A and B were characterized by 1D and 2D 1 H and 13 C NMR spectroscopic and HRESIMS spectrometric data and chemical methods as 4-benzoyl-3,4,5-trihydroxy-2-phenylcyclopent-2enone and 3,5-dihydroxy-2,4-diphenylcyclopent-2-enone, respectively. The relative configuration of phaseocyclopentenones A and B was assigned by 1 H and NOESY NMR methods, while their absolute configurations were assigned by electronic circular dichroism methods. When assayed on a nonhost plant (Solanum lycopersicum L.) by the leaf puncture assay, phaseocyclopentenones A and B and guignardone A showed phytotoxic activity, while only 1 and 2 were toxic when tested on cuttings of the same plant. No phytotoxicity or antifungal activity was detected for the three compounds on the host plant soybean (Glycine max L.) and against some of its fungal pathogens, namely, Cercospora nicotianae and Colletotrichum truncatum, also isolated from infected soybean plants in Argentina.

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Cercospora species cause cercospora leaf blight (CLB) and purple seed stain (PSS) on soybean. Because there are few resistant soybean varieties available, CLB/PSS management relies heavily upon fungicide applications. Sensitivity of 62 Argentinian Cercospora isolates to demethylation inhibitor (DMI), methyl benzimidazole carbamate (MBC), quinone outside inhibitor (QoI), succinate dehydrogenase inhibitor (SDHI) fungicides, and mancozeb was determined in this study. All isolates were sensitive to difenoconazole, epoxiconazole, prothioconazole, tebuconazole, and cyproconazole (EC50 values ranged from 0.006 to 2.4 µg/ml). In contrast, 51% of the tested isolates were sensitive (EC50 values ranged from 0.003 to 0.2 µg/ml), and 49% were highly resistant (EC50 > 100 µg/ml) to carbendazim. Interestingly, all isolates were completely resistant to azoxystrobin, trifloxystrobin, and pyraclostrobin, and insensitive to boscalid, fluxapyroxad, and pydiflumetofen (EC50 > 100 µg/ml). The G143A mutation was detected in 82% (53) of the QoI‐resistant isolates and the E198A mutation in 97% (31) of the carbendazim‐resistant isolates. No apparent resistance mutations were detected in the succinate dehydrogenase genes (subunits sdhB, sdhC, and sdhD). Mancozeb completely inhibited mycelial growth of the isolates evaluated at a concentration of 100 µg/ml. All Argentinian Cercospora isolates were sensitive to the DMI fungicides tested, but we report for the first time resistance to QoI and MBC fungicides. Mechanism(s) other than fungicide target‐site modification may be responsible for resistance of Cercospora to QoI and MBC fungicides. Moreover, based on our results and on the recent introduction of SDHI fungicides on soybean in Argentina, Cercospora species causing CLB/PSS are insensitive (naturally resistant) to SDHI fungicides. Insensitivity must be confirmed under field conditions.