The tomato late blight pandemic of 2009 made late blight into a household term in much of the eastern United States. Many home gardeners and many organic producers lost most if not all of their tomato crop, and their experiences were reported in the mainstream press. Some CSAs (Community Supported Agriculture) could not provide tomatoes to their members. In response, many questions emerged: How did it happen? What was unusual about this event compared to previous late blight epidemics? What is the current situation in 2012 and what can be done? It's easiest to answer these questions, and to understand the recent epidemics of late blight, if one knows a bit of the history of the disease and the biology of the causal agent, Phytophthora infestans.

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Isolates of Phytophthora infestans (n = 178) were collected in 2002 to 2009 from the eastern United States, Midwestern United States, and eastern Canada. Multilocus genotypes were defined using allozyme genotyping, and DNA fingerprinting with the RG-57 probe. Several previously described and three new mulitilocus genotypes were detected. The US-8 genotype was found commonly on commercial potato crops but not on tomato. US-20 was found on tomato in North Carolina from 2002 through 2007 and in Florida in 2005. US-21 was found on tomato in North Carolina in 2005 and Florida in 2006 and 2007. US-22 was detected on tomato in 2007 in Tennessee and New York and became widespread in 2009. US-22 was found in 12 states on tomato and potato and was spread on tomato transplants. This genotype accounted for about 60% of all the isolates genotyped. The US-23 genotype was found in Maryland, Virginia, Pennsylvania, and Delaware on both tomato and potato in 2009. The US-24 genotype was found only in North Dakota in 2009. A1 and A2 mating types were found in close proximity on potato and tomato crops in Pennsylvania and Virginia; therefore, the possibility of sexual reproduction should be monitored. Whereas most individuals of US-8 and US-20 were resistant to mefenoxam, US-21 appeared to be intermediately sensitive, and isolates of US-22, US-23, and US-24 were largely sensitive to mefenoxam. On the basis of sequence analysis of the ras gene, these latter three genotypes appear to have been derived from a common ancestor. Further field and laboratory studies are underway using simple sequence repeat genotyping to monitor current changes in the population structure of P. infestans causing late blight in North America.

In 2006, 2007, and 2008, we sampled 257 isolates of Phytophthora capsici from vegetables at 22 sites in four regions of New York, to determine variation in mefenoxam resistance and population genetic structure. Isolates were assayed for mefenoxam resistance and genotyped for mating type and five microsatellite loci. We found mefenoxam-resistant isolates at a high frequency in the Capital District and Long Island, but none were found in western New York or central New York. Both A1 and A2 mating types were found at 12 of the 22 sites, and we detected 126 distinct multilocus genotypes, only nine of which were found at more than one site. Significant differentiation (FST) was found in more than 98% of the pairwise comparisons between sites; approximately 24 and 16% of the variation in the population was attributed to differences among regions and sites, respectively. These results indicate that P. capsici in New York is highly diverse, but gene flow among regions and fields is restricted. Therefore, each field needs to be considered an independent population, and efforts to prevent movement of inoculum among fields need to be further emphasized to prevent the spread of this pathogen.

Petri disease of grapevine is primarily caused by Phaeomoniella chlamydospora. This pathogen affects mostly young grapevines, but is also implicated in esca disease of older grapevines. Little is known about the disease cycle of this fungus. Infected propagation material was identified as a major means of dissemination of the pathogen. Recently, the pathogen was also detected from soil in South Africa and airborne conidia have been found in vineyards. The aim of this study was to use a molecular detection technique to test different samples collected from nurseries in South Africa at different nursery stages for the presence of P. chlamydospora. A one-tube nested-PCR technique was optimised for detecting P. chlamydospora in DNA extracted from soil, water, callusing medium and grapevine wood. The one-tube nested-PCR was sensitive enough to detect as little as 1 fg of P. chlamydospora genomic DNA from water and 10 fg from wood, callusing medium and soil. PCR analyses of the different nursery samples revealed the presence of several putative 360 bp P. chlamydospora specific bands. Subsequent sequence analyses and/ or restriction enzyme digestions of all 360 bp PCR bands confirmed that all bands were P. chlamydospora specific, except for five bands obtained from callusing media and one from water. Phaeomoniella chlamydospora was positively detected in 25% of rootstock cane sections collected from mother blocks, 42% of rootstock cuttings and 16% of scion cuttings collected during grafting, 40% of water samples collected after pre-storage hydration, 67% of water samples collected during grafting, 8% of callusing medium samples and 17% of soil samples collected from mother blocks. These media can therefore be considered as possible inoculum sources of the pathogen during the nursery stages.