Empirical and mechanistic modeling indicate that pathogens transmitted via aerially dispersed inoculum follow a power law, resulting in dispersive epidemic waves. The spread parameter (b) of the power law model, which is an indicator of the distance of the epidemic wave front from an initial focus per unit time, has been found to be approximately 2 for several animal and plant diseases over a wide range of spatial scales under conditions favorable for disease spread. Although disease spread and epidemic expansion can be influenced by several factors, the stability of the parameter b over multiple epidemic years has not been determined. Additionally, the size of the initial epidemic area is expected to be strongly related to the final epidemic extent for epidemics, but the stability of this relationship is also not well established. Here, empirical data of cucurbit downy mildew epidemics collected from 2008 to 2014 were analyzed using a spatio-temporal model of disease spread that incorporates logistic growth in time with a power law function for dispersal. Final epidemic extent ranged from 4.16 ×108 km2 in 2012 to 6.44 ×108 km2 in 2009. Current epidemic extent became significantly associated (P < 0.0332; 0.56 < R2 < 0.99) with final epidemic area beginning near the end of April, with the association increasing monotonically to 1.0 by the end of the epidemic season in July. The position of the epidemic wave-front became exponentially more distant with time, and epidemic velocity increased linearly with distance. Slopes from the temporal and spatial regression models varied with about a 2.5-fold range across epidemic years. Estimates of b varied substantially ranging from 1.51 to 4.16 across epidemic years. We observed a significant b ×time (or distance) interaction (P < 0.05) for epidemic years where data were well described by the power law model. These results suggest that the spread parameter b may not be stable over multiple epidemic years. However, b ≈ 2 may be considered the lower limit of the distance traveled by epidemic wave-fronts for aerially transmitted pathogens that follow a power law dispersal function.

Wheat powdery mildew is a disease of global importance that occurs across a wide geographic area in the United States. A virulence survey of Blumeria graminis f. sp. tritici, the causal agent, was conducted by sampling 36 wheat fields in 15 U.S. states in the years 2013 and 2014. Using a hierarchical sampling protocol, isolates were derived from three separated plants at each of five separated sites within each field in order to assess the spatial distribution of pathotypes. In total, 1,017 isolates from those fields were tested individually on single-gene differential cultivars containing a total of 21 powdery mildew resistance (Pm) genes. Several recently introgressed mildew resistance genes from wild wheat relatives (Pm37, Pm53, MlAG12, NCAG13, and MlUM15) exhibited complete or nearly complete resistance to all local B. graminis f. sp. tritici populations from across the sampled area. One older gene, Pm4b, also retained at least some efficacy across the sampled area. The B. graminis f. sp. tritici population sampled from Arkansas and Missouri, on the western edge of the eastern soft red winter wheat region, had virulence profiles more similar to other soft wheat mildew populations than to the geographically closer population from hard wheat fields in the Plains states of Oklahoma, Nebraska, and Kansas. The Plains population differed in that it was avirulent to several Pm genes long defeated in the soft-wheat-growing areas. Virulence complexity was greatest east of the Mississippi River, and diminished toward the west. Several recently introgressed Pm genes (Pm25, Pm34, Pm35, and NCA6) that are highly effective against mildew in the field in North Carolina were unexpectedly susceptible to eastern-U.S. B. graminis f. sp. tritici populations in detached-leaf tests. Sampled fields displayed a wide range of pathotype diversity and spatial distribution, suggesting that epidemics are caused by varying numbers of pathotypes in all regions. The research confirmed that most long-used Pm genes are defeated in the eastern United States, and the U.S. B. graminis f. sp. tritici population has different virulence profiles in the hard- and soft-wheat regions, which are likely maintained by host selection, isolation by distance, and west-to-east gene flow.

Mehra, L. K., MacLean, D. D., Savelle, A. T., and Scherm, H. 2013. Postharvest disease development on southern highbush blueberry fruit in relation to berry flesh type and harvest method. Plant Dis. 97:213-221.Postharvest decay, incited by various fungal pathogens, is a major concern in most blueberry production areas of the United States. Because the risk of infection is increased by fruit bruising, which in turn is increased by machine-harvesting, it has been difficult to harvest fruit from the early-maturing but soft-textured southern highbush blueberries (SHB) mechanically for the fresh market. This could change fundamentally with the recent development of SHB genotypes with crisp-textured ("crispy") berries, i.e., fruit with qualitatively firmer flesh and/or more resistant skin. Four replicate row sections of two or three SHB genotypes having crispy fruit and three with conventional fruit were either hand-or machine-harvested at a commercial blueberry farm in northern Florida in April 2009 and May 2010. Harvested fruit were sorted, packed, and placed in cold storage (2°C) for up to 3 weeks. Average counts of aerobic bacteria, total yeasts and molds, coliforms, and Escherichia coli on fruit samples before the cold storage period were below commercial tolerance levels in most cases. In both years, natural disease incidence after cold storage was lowest for hand-harvested crispy fruit and highest for machine-harvested conventional fruit. Interestingly, machine-harvested crispy fruit had the same or lower disease incidence as hand-harvested conventional fruit. Across all treatments, natural postharvest disease incidence was inversely related to fruit firmness, with firmness values >220 g/mm associated with low disease. In separate experiments, samples from the 0-day cold storage period were inoculated at the stem end with Altemaria alternata, Botrytis cinérea, or Colletotrichum acutatum, and disease incidence was assessed after 7 days in a cold room followed by 60 to 72 h at room temperature. In response to artificial inoculation, less disease developed on crispy berries. No significant effect of harvest method was observed, except for A. alternata inoculation in 2009, when hand-harvested fruit developed a lower level of disease than machine-harvested fruit. Taken together, this study suggests that mechanical harvesting of SHB cultivars with crisp-textured berries is feasible from a postharvest pathology perspective.