Annual decreases in soybean (Glycine max L. Merrill) yield caused by diseases were estimated by surveying university-affiliated plant pathologists in 28 soybean-producing states in the United States and in Ontario, Canada, from 2010 through 2014. Estimated yield losses from each disease varied greatly by state or province and year. Over the duration of this survey, soybean cyst nematode (SCN) (Heterodera glycines Ichinohe) was estimated to have caused more than twice as much yield loss than any other disease. Seedling diseases (caused by various pathogens), charcoal rot (caused by Macrophomina phaseolina (Tassi) Goid), and sudden death syndrome (SDS) (caused by Fusarium virguliforme O’Donnell & T. Aoki) caused the next greatest estimated yield losses, in descending order. The estimated mean economic loss due to all soybean diseases, averaged across U.S. states and Ontario from 2010 to 2014, was $60.66 USD per acre. Results from this survey will provide scientists, breeders, governments, and educators with soybean yield-loss estimates to help inform and prioritize research, policy, and educational efforts in soybean pathology and disease management.

Soybean (Glycine max [L.] Merrill) yield losses as a result of plant diseases were estimated by university and government plant pathologists in 29 soybean producing states in the United States and in Ontario, Canada, from 2015 through 2019. In general, the estimated losses that resulted from each of 28 plant diseases or pathogens varied by state or province as well as year. Soybean cyst nematode (SCN) (Heterodera glycines Ichinohe) caused more than twice as much loss as any other disease during the survey period. Seedling diseases (caused by various pathogens), Sclerotinia stem rot (white mold) (caused by Sclerotinia sclerotiorum [Lib.] de Bary), and sudden death syndrome (caused by Fusarium virguliforme O’Donnell & T. Aoki) caused the next greatest yield losses, in descending order. Following SCN, the most damaging diseases in the northern United States and Ontario differed from those in the southern United States. The estimated mean economic loss from all soybean diseases, averaged across the United States and Ontario, Canada was US$45 per acre (US$111 per hectare). The outcome from the current survey will provide pertinent information regarding the important soybean diseases and their overall severity in the soybean crop and help guide future research and Extension efforts on managing soybean diseases.

Annual reductions in corn (Zea mays L.) yield caused by diseases were estimated by university Extension-affiliated plant pathologists in 26 corn-producing states in the United States and in Ontario, Canada, from 2016 through 2019. Estimated loss from each disease varied greatly by state or province and year. Gray leaf spot (caused by Cercospora zeae-maydis Tehon & E.Y. Daniels) caused the greatest estimated yield loss in parts of the northern United States and Ontario in all years except 2019, and Fusarium stalk rot (caused by Fusarium spp.) also greatly reduced yield. Tar spot (caused by Phyllachora maydis Maubl.), a relatively new disease in the United States, was estimated to cause substantial yield loss in 2018 and 2019 in several northern states. Gray leaf spot and southern rust (caused by Puccinia polysora Underw.) caused the most estimated yield losses in the southern United States. Unfavorable wet and delayed harvest conditions in 2018 resulted in an estimated 2.5 billion bushels (63.5 million metric tons) of grain contaminated with mycotoxins. The estimated mean economic loss due to reduced yield caused by corn diseases in the United States and Ontario from 2016 to 2019 was US$55.90 per acre (US$138.13 per hectare). Results from this survey provide scientists, corn breeders, government agencies, and educators with data to help inform and prioritize research, policy, and educational efforts in corn pathology and disease management.

Aspergillus flavus, the primary causal agent of aflatoxin contamination, includes many genetically diverse vegetative compatibility groups (VCGs). Competitive ability during infection of living maize kernels was quantified for isolates from 38 VCGs. Kernels were inoculated with both a common VCG, CG136, and another VCG; after 7 days (31°C), conidia were washed from kernels, and aflatoxins and DNA were extracted from kernels and conidia separately. CG136-specific single-nucleotide polymorphisms were quantified by pyrosequencing; VCGs co-inoculated with CG136 produced 46 to 85 and 51 to 84% of A. flavus DNA from kernels and conidia, respectively. Co-inoculation with atoxigenic isolates reduced aflatoxin up to 90% and, in some cases, more than predicted by competitive exclusion alone. Conidia contained up to 42 ppm aflatoxin B₁, indicating airborne conidia as potentially important sources of environmental exposure. Aflatoxin-producing potential and sporulation were negatively correlated. For some VCGs, sporulation during co-infection was greater than that predicted by kernel infection, suggesting that some VCGs increase dispersal while sacrificing competitive ability during host tissue colonization. The results indicate both life strategy and adaptive differences among A. flavus isolates and provide a basis for selection of biocontrol strains with improved competitive ability, sporulation, and aflatoxin reduction on target hosts.

Aflatoxins are potent Aspergillus mycotoxins that contaminate food and feed, thereby impacting health and trade. Biopesticides with atoxigenic Aspergillus flavus isolates as active ingredients are used to reduce aflatoxin contamination in crops. The mechanism of aflatoxin biocontrol is primarily attributed to competitive exclusion but, sometimes, aflatoxin is reduced by greater amounts than can be explained by displacement of aflatoxin-producing fungi on the crop. Objectives of this study were to (i) evaluate the ability of atoxigenic A. flavus genotypes to degrade aflatoxin B₁ (AFB1) and (ii) characterize impacts of temperature, time, and nutrient availability on AFB1 degradation by atoxigenic A. flavus. Aflatoxin-contaminated maize was inoculated with atoxigenic isolates in three separate experiments that included different atoxigenic genotypes, temperature, and time as variables. Atoxigenic genotypes varied in aflatoxin degradation but all degraded AFB1 >44% after 7 days at 30°C. The optimum temperature for AFB1 degradation was 25 to 30°C, which is similar to the optimum range for AFB1 production. In a time-course experiment, atoxigenics degraded 40% of AFB1 within 3 days, and 80% of aflatoxin was degraded by day 21. Atoxigenic isolates were able to degrade and utilize AFB1 as a sole carbon source in a chemically defined medium but quantities of AFB1 degraded declined as glucose concentrations increased. Degradation may be an additional mechanism through which atoxigenic A. flavus biocontrol products reduce aflatoxin contamination pre- or postharvest. Thus, selection of optimal atoxigenic active ingredients can include assessment of both competitive ability in agricultural fields and their ability to degrade aflatoxins.