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Powdery mildew caused by Podosphaera cerasi is the most important fungal disease of sweet cherries in the Pacific Northwest of the United States. In this study, several factors related to disease epidemiology were evaluated. The experiments were conducted to investigate flower susceptibility to P. cerasi infection by in planta and in vitro inoculation. The susceptibility of fruit at various developmental stages was investigated using defined concentrations of P. cerasi conidia. Furthermore, the threshold of conidial concentration required for fruit infection was determined. The pathogen activity during full bloom was limited and not related to fruit disease incidence and severity at harvest. Foliar infections always preceded fruit infections by an average of 42 days during the 3 years of the study. The onset of fruit infection followed, on average, 66 days after full bloom and appeared simultaneously on all susceptible cherry cultivars in the research orchard. Disease symptoms were only observed on fruit in Biologische Bundesanstalt, Bundessortenamt, and Chemical Industry scale 8 (maturity) in all cultivars examined. During this stage, a concentration of 500 conidia/ml was sufficient to cause fruit infection at harvest. Interaction between the inoculation dates and conidial concentration revealed a dependency of disease development on the host stage at the time of inoculation; the younger the fruit, the more conidia are needed to cause disease at harvest. Molecular studies showed a rapid increase in conidia viability at the transition from asymptomatic to the symptomatic disease of fruit. No evidence of ontogenic resistance of fruit to powdery mildew infection was observed.

Host resistance, both quantitative and qualitative, is the preferred long-term approach for disease management in many pathosystems, including powdery mildew of hop (Podosphaera macularis). In 2012, an epidemic of powdery mildew occurred in Washington and Idaho on previously resistant cultivars whose resistance was putatively based on the gene designated R6. In 2013, isolates capable of causing severe disease on cultivars with R6-based resistance were confirmed in Oregon and became widespread during 2014. Surveys of commercial hop yards during 2012 to 2014 documented that powdery mildew is now widespread on cultivars possessing R6 resistance in Washington and Oregon, and the incidence of disease is progressively increasing. Pathogenic fitness, race, and mating type of R6-virulent isolates were compared with isolates of P. macularis lacking R6 virulence. All isolates were positive for the mating type idiomorph MAT1-1 and were able to overcome resistance genes Rb, R3, and R5 but not R1 or R2. In addition, R6-virulent isolates were shown to infect differential cultivars reported to possess the R6 gene and also the R4 gene, although R4 has not yet been broadly deployed in the United States. R6-virulent isolates were not detected from the eastern United States during 2012 to 2015. In growth chamber studies, R6-virulent isolates of P. macularis had a significantly longer latent period and produced fewer lesions on plants with R6 as compared with plants lacking R6, indicating a fitness cost to the fungus. R6-virulent isolates also produced fewer conidia when compared with isolates lacking R6 virulence, independent of whether the isolates were grown on a plant with or without R6. Thus, it is possible that the fitness cost of R6 virulence occurs regardless of host genotype. In field studies, powdery mildew was suppressed by at least 50% on plants possessing R6 as compared with those without R6 when coinoculated with R6-virulent and avirulent isolates. R6 virulence in P. macularis appears to be race specific and, at this time, imposes a measurable fitness penalty on the fungus. Resistance genes R1 and R2 appear to remain effective against R6-virulent isolates of P. macularis in the U.S. Pacific Northwest.

Aspergillus flavus has two morphotypes, the S strain and the L strain, that differ in aflatoxin-producing ability and other characteristics. Fungal communities on maize dominated by the S strain of A. flavus have repeatedly been associated with acute aflatoxin poisonings in Kenya, where management tools to reduce aflatoxin levels in maize are needed urgently. A. flavus isolates (n = 290) originating from maize produced in Kenya and belonging to the L strain morphotype were tested for aflatoxin-producing potential. A total of 96 atoxigenic isolates was identified from four provinces sampled. The 96 atoxigenic isolates were placed into 53 vegetative compatibility groups (VCGs) through complementation of nitrate non-utilizing mutants. Isolates from each of 11 VCGs were obtained from more than one maize sample, isolates from 10 of the VCGs were detected in multiple districts, and isolates of four VCGs were found in multiple provinces. Atoxigenic isolates were tested for potential to reduce aflatoxin concentrations in viable maize kernels that were co-inoculated with highly toxigenic S strain isolates. The 12 most effective isolates reduced aflatoxin levels by >80%. Reductions in aflatoxin levels caused by the most effective Kenyan isolates were comparable with those achieved with a United States isolate (NRRL-21882) used commercially for aflatoxin management. This study identified atoxigenic isolates of A. flavus with potential value for biological control within highly toxic Aspergillus communities associated with maize production in Kenya. These atoxigenic isolates have potential value in mitigating aflatoxin outbreaks in Kenya, and should be evaluated under field conditions.