▪ Abstract  Research on impacts of climate change on plant diseases has been limited, with most work concentrating on the effects of a single atmospheric constituent or meteorological variable on the host, pathogen, or the interaction of the two under controlled conditions. Results indicate that climate change could alter stages and rates of development of the pathogen, modify host resistance, and result in changes in the physiology of host-pathogen interactions. The most likely consequences are shifts in the geographical distribution of host and pathogen and altered crop losses, caused in part by changes in the efficacy of control strategies. Recent developments in experimental and modeling techniques offer considerable promise for developing an improved capability for climate change impact assessment and mitigation. Compared with major technological, environmental, and socioeconomic changes affecting agricultural production during the next century, climate change may be less important; it will, however, add another layer of complexity and uncertainty onto a system that is already exceedingly difficult to manage on a sustainable basis. Intensified research on climate change-related issues could result in improved understanding and management of plant diseases in the face of current and future climate extremes.

Sudden death syndrome of soybean, caused by Fusarium solani f. sp. glycines, is a disease of increasing economic importance in the United States. Although the ecology of sudden death syndrome has been extensively studied in relation to crop management practices such as tillage, irrigation, and cultivar selection, there is no information on the effects of herbicides on this disease. Three herbicides (lactofen, glyphosate, and imazethapyr) commonly used in soybean were evaluated for their effects on the phenology of F. solani f. sp. glycines and the development of sudden death syndrome in four soybean cultivars varying in resistance to the disease and in tolerance to glyphosate. Conidial germination, mycelial growth, and sporulation in vitro were reduced by glyphosate and lactofen. In growth-chamber and greenhouse experiments, there was a significant increase in disease severity and frequency of isolation of F. solani f. sp. glycines from roots of all cultivars after application of imazethapyr or glyphosate compared with the control treatment (no herbicide applied). Conversely, disease severity and isolation frequency of F. solani f. sp. glycines decreased after application of lactofen. Across all herbicide treatments, severity of sudden death syndrome and isolation frequency were lower in disease-resistant than in susceptible cultivars. Results suggest that glyphosate-tolerant and -nontolerant cultivars respond similarly to infection by F. solani f. sp. glycines after herbicide application.

SUMMARY A biological attack on U.S. crops, rangelands, or forests could reduce yield and quality, erode consumer confidence, affect economic health and the environment, and possibly impact human nutrition and international relations. Preparedness for a crop bioterror event requires a strong national security plan that includes steps for microbial forensics and criminal attribution. However, U.S. crop producers, consultants, and agricultural scientists have traditionally focused primarily on strategies for prevention and management of diseases introduced naturally or unintentionally rather than on responding appropriately to an intentional pathogen introduction. We assess currently available information, technologies, and resources that were developed originally to ensure plant health but also could be utilized for postintroduction plant pathogen forensics. Recommendations for prioritization of efforts and resource expenditures needed to enhance our plant pathogen forensics capabilities are presented.

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The ability to infect host flowers offers important ecological benefits to plant-parasitic fungi; not surprisingly, therefore, numerous fungal species from a wide range of taxonomic groups have adopted a life style that involves flower infection. Although flower-infecting fungi are very diverse, they can be classified readily into three major groups: opportunistic, unspecialized pathogens causing necrotic symptoms such as blossom blights (group 1), and specialist flower pathogens which infect inflorescences either through the gynoecium (group 2) or systemically through the apical meristem (group 3). This three-tier system is supported by life history attributes such as host range, mode of spore transmission, degree of host sterilization as a result of infection, and whether or not the fungus undergoes an obligate sexual cycle, produces resting spores in affected inflorescences, and is r- or K-selected. Across the three groups, the flower as an infection court poses important challenges for disease management. Ecologically and evolutionarily, terms and concepts borrowed from the study of venereal (sexually transmitted) diseases of animals do not adequately capture the range of strategies employed by fungi that infect flowers.

The brown rot fungus Monilinia fructicola (G. Wint.) Honey is economically the most important pathogen of peach (Prunus persica (L.) Batsch) in Georgia (30). Direct yield losses result from infection of flowers (blossom and twig blight) and from fruit rot at harvest and postharvest; indirect losses are due to the cost of fungicide application during bloom and during the pre-and postharvest periods. In most years, direct losses from M. fructicolaincited blossom blight are minor (23,32,33); however, cankers, formed on twigs as a result of blossom blight, may serve as a source of inoculum for infections that occur during the preharvest fruit ripening stage, particularly in early maturing cultivars (23,32,33). Other within-orchard inoculum sources for preharvest fruit infections include conidia produced on thinned fruit on the ground (1,9,17) and on aborted, nonabscised fruit in the tree (1,17). By contrast, conidia produced on overwintered fruit mummies in early spring do not survive long enough to cause fruit rot (24).Immature stone fruits generally do not exhibit symptoms or signs of infection by M. fructicola unless ingress and colonization are favored by prolonged rain or high humidity following injury. Even without wounding, however, immature fruit may harbor symptomless (latent) infections. Latent infections may become active as the fruit ripen, thus becoming a possible means of carryover of M. fructicola from the spring to the preharvest period. Latent infections by M. fructicola or the closely related M. laxa have been documented in apricot (25,28,29), peach (15,20,25), plum (21,25), prune (20), and cherry (8,31). Michailides et al. (19,20) reported positive relationships between the incidence of latent infection in immature French prune, nectarine, and plum and fruit rot severity at harvest and postharvest in California. Similarly, Northover and Cerkauskas (21) determined that latent infections in European plum in Ontario, Canada, occurred throughout the growing season and correlated positively with fruit rot incidence at harvest. These authors concluded that latent infections were most important in humid temperate regions, where they may readily progress to fruit rot.In peach, latent infections can occur during all stages of fruit development but their role in the epidemiology of brown rot is uncertain. Kable (13,15) concluded that only latent infections near harvest are important in the development of fruit rot in the semiarid climate of southeastern Australia. Landgraf and Zehr (17) surveyed potential inoculum sources for fruit infection by M. fructicola in South Carolina peach orchards but did not include latent infection. They did acknowledge, however, the need to evaluate the role of latent infection in the humid southeastern United States. A better understanding of the importance of latent infection in the epidemiology of brown rot could facilitate the early detection of increased fruit rot risk before harvest, thereby increasing lead time for disease management decisions (8,(18)(19)(20).The objectiv...

The regional dynamics of soybean rust, caused by Phakopsora pachyrhizi, in six southeastern states (Florida, Georgia, Alabama, South Carolina, North Carolina, and Virginia) in 2005 and 2006 were analyzed based on disease records collected as part of U.S. Department of Agriculture's soybean rust surveillance and monitoring program. The season-long rate of temporal disease progress averaged approximately 0.5 new cases day(1) and was higher in nonsentinel soybean (Glycine max) plots than in sentinel soybean plots and kudzu (Pueraria lobata) plots. Despite the early detection of rust on kudzu in January and/or February each year (representing the final phase of the previous year's epidemic), the disease developed slowly during the spring and early summer on this host species and did not enter its exponential phase until late August, more than 1 month after it did so on soybean. On soybean, cases occurred very sporadically before the beginning of July, after which their number increased rapidly. Thus, while kudzu likely provides the initial inoculum for epidemics on soybean, the rapid increase in disease prevalence on kudzu toward the end of the season appears to be driven by inoculum produced on soybean. Of 112 soybean cases with growth stage data, only one occurred during vegetative crop development while approximately 75% occurred at stage R6 (full seed) or higher. The median nearest-neighbor distance of spread among cases was approximately 70 km in both years, with 10% of the distances each being below approximately 30 km and above approximately 200 km. Considering only the epidemic on soybean, the disease expanded at an average rate of 8.8 and 10.4 km day(1) in 2005 and 2006, respectively. These rates are at the lower range of those reported for the annual spread of tobacco blue mold from the Caribbean Basin through the southeastern United States. Regional spread of soybean rust may be limited by the slow disease progress on kudzu during the first half of the year combined with the short period available for disease establishment on soybean during the vulnerable phase of host reproductive development, although low inoculum availability in 2005 and dry conditions in 2006 also may have reduced epidemic potential.