Predicting the risk of cucurbit downy mildew in the eastern United States using an integrated aerobiological model.

Cucurbit downy mildew caused by the obligate oomycete, Pseudoperonospora cubensis, is considered one of the most economically important diseases of cucurbits worldwide. In the continental United States, the pathogen overwinters in southern Florida and along the coast of the Gulf of Mexico. Outbreaks of the disease in northern states occur annually via long-distance aerial transport of sporangia from infected source fields. An integrated aerobiological modeling system has been developed to predict the risk of disease occurrence and to facilitate timely use of fungicides for disease management. The forecasting system, which combines information on known inoculum sources, long-distance atmospheric spore transport and spore deposition modules, was tested to determine its accuracy in predicting risk of disease outbreak. Rainwater samples at disease monitoring sites in Alabama, Georgia, Louisiana, New York, North Carolina, Ohio, Pennsylvania and South Carolina were collected weekly from planting to the first appearance of symptoms at the field sites during the 2013, 2014, and 2015 growing seasons. A conventional PCR assay with primers specific to P. cubensis was used to detect the presence of sporangia in rain water samples. Disease forecasts were monitored and recorded for each site after each rain event until initial disease symptoms appeared. The pathogen was detected in 38 of the 187 rainwater samples collected during the study period. The forecasting system correctly predicted the risk of disease outbreak based on the presence of sporangia or appearance of initial disease symptoms with an overall accuracy rate of 66 and 75%, respectively. In addition, the probability that the forecasting system correctly classified the presence or absence of disease was ≥ 73%. The true skill statistic calculated based on the appearance of disease symptoms in cucurbit field plantings ranged from 0.42 to 0.58, indicating that the disease forecasting system had an acceptable to good performance in predicting the risk of cucurbit downy mildew outbreak in the eastern United States.

Five Reasons to Consider Phytophthora infestans a Reemerging Pathogen.

Phytophthora infestans has been a named pathogen for well over 150 years and yet it continues to "emerge", with thousands of articles published each year on it and the late blight disease that it causes. This review explores five attributes of this oomycete pathogen that maintain this constant attention. First, the historical tragedy associated with this disease (Irish potato famine) causes many people to be fascinated with the pathogen. Current technology now enables investigators to answer some questions of historical significance. Second, the devastation caused by the pathogen continues to appear in surprising new locations or with surprising new intensity. Third, populations of P. infestans worldwide are in flux, with changes that have major implications to disease management. Fourth, the genomics revolution has enabled investigators to make tremendous progress in terms of understanding the molecular biology (especially the pathogenicity) of P. infestans. Fifth, there remain many compelling unanswered questions.

Perchlorate content of plant foliage reflects a wide range of species-dependent accumulation but not ozone-induced biosynthesis.

Perchlorate (ClO4(-)) interferes with uptake of iodide in humans. Emission inventories do not explain observed distributions. Ozone (O3) is implicated in the natural origin of ClO4(-), and has increased since pre-industrial times. O3 produces ClO4(-)in vitro from Cl(-), and plant tissues contain Cl(-) and redox reactions. We hypothesize that O3 exposure may induce plant synthesis of ClO4(-). We exposed contrasting crop species to environmentally relevant O3 concentrations. In the absence of O3 exposure, species exhibited a large range of ClO4(-) accumulation but there was no relationship between leaf ClO4(-) and O3, whether expressed as exposure or cumulative flux (dose). Older, senescing leaves accumulated more ClO4(-) than younger leaves. O3 exposed vegetation is not a source of environmental ClO4(-). There was evidence of enhanced ClO4(-) content in the soil surface at the highest O3 exposure, which could be a significant contributor to environmental ClO4(-).

High ozone increases soil perchlorate but does not affect foliar perchlorate content.

Ozone (O) is implicated in the natural source inventory of ClO, a hydrophilic salt that migrates to groundwater and interferes with the uptake of iodide in mammals, including humans. Tropospheric O is elevated in many urban and some rural areas in the United States and globally. We previously showed that controlled O exposure at near-ambient concentrations (up to 114 nL L, 12-h mean) did not increase foliar ClO. Under laboratory conditions, O has been shown to oxidize Cl to ClO. Plant tissues contain Cl and exhibit responses to O invoking redox reactions. As higher levels of O are associated with stratospheric incursion and with developing megacities, we have hypothesized that exposure of vegetation to such elevated O may increase foliar ClO. This would contribute to ClO in environments without obvious point sources. At these high O concentrations (up to 204 nL L, 12-h mean; 320 nL L maximum), we demonstrated an increase in the ClO concentration in surface soil that was linearly related to the O concentration. There was no relationship of foliar ClO with O exposure or dose (stomatal uptake). Accumulation of ClO varied among species at low O, but this was not related to soil surface ClO or to foliar ClO concentrations following exposure to O. These data extend our previous conclusions to the highest levels of plausible O exposure, that tropospheric O contributes to environmental ClO through interaction with the soil but not through increased foliar ClO.

The 2009 Late Blight Pandemic in the Eastern United States - Causes and Results.

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.

First Report of Phytophthora Blight Caused by Phytophthora capsici on Snap Bean in New York.

Phytophthora capsici Leonian is an important pathogen of solanaceous and cucurbit crops. Phytophthora blight was first reported on snap bean (Phaseolus vulgaris L.) in Michigan in 2003 (2) and Connecticut in 2010 (3). This report documents the discovery of P. capsici on snap bean (cv. Bronco) grown in Riverhead, NY in September 2008 and August 2010 on snap bean (cv. Valentino) in Holley, NY, more than 690 km away. Disease was favored by frequent rainfall and prolonged wet periods with air temperatures of 24 to 29°C. Both locations were commercial fields previously planted to pepper or cucurbits affected by P. capsici. In Riverhead, infected pods had characteristic yeast-like growth of P. capsici, which were predominantly sporangia. In Holley, large water-soaked lesions were observed on snap bean foliage, and as the disease progressed, leaves became necrotic and detached from the plant. Reddish brown lesions were observed on stems in advance of white areas of sporulation. Infected pods displayed white mycelial growth, were shriveled, and desiccated. P. capsici was isolated from symptomatic tissues. Stems and pods were surface disinfested for 3 min in 0.525% sodium hypochlorite solution, rinsed for 3 min in sterile distilled water, transferred to PARPH (4) media, and incubated at 22°C. After 5 days, hyphae from colony margins were excised and transferred to 15% unclarified V8 agar media. Cultures consisting of white mycelia and ovoid papillate sporangia on long pedicels were identified as P. capsici. Sporangia were 25.0 to 70.0 × 10.0 to 22.5 µm (average 42.0 × 16.25 µm). Identity was further confirmed by PCR primers specific to P. capsici (1). DNA was extracted from mycelia produced on V8 agar and amplification with the species-specific primers resulted in a PCR product of the same size as that obtained from a known isolate of P. capsici. Pathogenicity of the isolate from Holley was determined by two methods on 50-day-old snap bean plants (cv. Valentino) grown in a greenhouse. In method one, four plants were inoculated with 1-cm-diameter mycelial plugs excised from 8-day-old cultures. A single plug was placed against the stem at the soil line. Four control plants were treated similarly with noncolonized agar plugs. In method two, entire plants were atomized with 10 ml of a zoospore suspension (2.6 × 105/ml). Control plants were atomized with sterile distilled water. All plants were placed in a growth chamber with continuous mist for 24 h at 24°C. After 24 h, plants were enclosed in plastic bags and placed in a greenhouse at 27°C. Stem lesions similar to those observed in affected fields were evident on plants treated with mycelia plugs 2 days after inoculation. Plants inoculated with the zoospore suspension developed stem lesions and desiccated pods. Control plants were asymptomatic. P. capsici was successfully recovered from infected plant tissue, fulfilling Koch's postulates. The Riverhead isolate was demonstrated as pathogenic on snap bean and cucumber by placing colonized plugs on pods and fruit that were subsequently incubated in moist chambers (24°C, 90 to 100% relative humidity). P. capsici was successfully recovered from symptomatic pods and fruit. To our knowledge, this is the first report of Phytophthora blight caused by P. capsici on snap bean in New York. References: (1) A. R. Dunn et al. Plant Dis. 94:1461, 2010. (2) A. J. Gevens et al. Plant Dis. 92:201, 2008. (3) J. A. LaMondia et al. Plant Dis. 94:134, 2010. (4) G. C. Papavisas et al. Phytopathology 71:129, 1981.

Population Structure and Resistance to Mefenoxam of Phytophthora capsici in New York State.

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.

First Report of the Cucurbit Powdery Mildew Fungus (Podosphaera xanthii) Resistant to Strobilurin Fungicides in the United States.

Resistance to strobilurin fungicides was documented in isolates collected from three fungicide efficacy experiments conducted in research fields in Georgia (GA), North Carolina (NC), and New York (NY). In these fields in 2002, strobilurins (fungicide group 11, quinone outside inhibitors [QoI]) when used alone on a 7-day schedule (use pattern not labeled) did not effectively control cucurbit powdery mildew. Strobilurin efficacy declined dramatically after the second application in New York (3). Efficacy also was reduced in commercial fields in Kentucky and research fields in Arizona, California, Kentucky, Illinois, Michigan, and Virginia in 2002 where strobilurins were used predominantly or exclusively. Isolates were collected on 22 July and 8 and 17 October after the last of four, five, and five applications of strobilurin (trifloxystrobin formulated as Flint or azoxystrobin formulated as Quadris) in experiments conducted by J. D. Moore in Chula, GA, M. McGrath in Riverhead, NY, and G. J. Holmes in Clayton, NC, respectively. A leaf-disk bioassay was used to determine fungicide sensitivity (2). Strobilurin sensitivity was determined using trifloxystrobin at 0, 0.5, 5, 50, and 100 µg/ml. Four of nine NY isolates, 19 of 21 GA isolates, and 13 of 15 NC isolates were resistant to strobilurins (grew well on disks treated with trifloxystrobin at 100 µg/ml). The geometric mean of the azoxystrobin baseline was 0.258 µg/ml for Podosphaera xanthii isolates collected in 1998 and 1999 in North America (4). Poor control with strobilurins under field conditions was associated with reduced sensitivity in vitro. Strobilurin sensitivity appeared to be qualitative as reported elsewhere (1). Two sensitive and three resistant isolates responded similarly when tested in another laboratory using kresoxim-methyl and pyraclostrobin (H. Ypema, personal communication). These findings and experiences elsewhere with QoI-resistant P. xanthii indicate that cross-resistance probably extends among multiple QoI's (1). Strobilurins have been available for commercial use in the United States since 1998, when azoxystrobin received Section 18 registration in some states. Federal registration was granted in March 1999. Strobilurin resistance was detected after 2 years of commercial use elsewhere in the world (1). All isolates tested in the current study were from research fields where selection pressure for resistance could have been higher than in commercial fields where strobilurins are used with demethylation inhibitors (DMIs; fungicide group 3) and contact fungicides in alternation or tank mixtures to prevent or delay resistance development. Resistance in commercial fields will reduce the utility of strobilurins, including those not yet registered, and eliminate an important tool for managing DMI resistance. Strobilurins and DMIs are the only systemic fungicides registered for cucurbit powdery mildew in the United States. Managing DMI resistance may be challenged by multiresistant strains. Strobilurin-resistant isolates also exhibited reduced sensitivity to DMIs, tolerating triadimefon at 50 to 100 µg/ml (2). One suggestion to improve resistance management is to apply a contact fungicide with strobilurins as well as DMIs. References: (1) H. Ishii et al. Phytopathology 91:1166, 2001. (2) M. T. McGrath et al. Plant Dis. 80:697, 1996. (3) M. T. McGrath and N. Shishkoff. Fungic. Nematic. Tests. (In press). (4) G. Olaya et al. Phytopathology (Abstr.) 90 (suppl):S57, 2000.

AQ10 Biofungicide Combined with Chemical Fungicides or AddQ Spray Adjuvant for Control of Cucurbit Powdery Mildew in Detached Leaf Culture.

The biofungicide AQ10, a pelleted formulation of conidia of Ampelomyces quisqualis, did not significantly reduce the size of colonies of the cucurbit powdery mildew (Podosphaera xanthii) in detached squash leaf culture but did reduce the amount of inoculum produced by each colony. No significant reduction in colonization of powdery mildew colonies by AQ10 was observed when it was sprayed in conjunction with the fungicides myclobutanil at 10 µg/ml or triadimefon at 100 µg/ml, suggesting that it is not sensitive to the fungicides at these concentrations. The spray adjuvant AddQ did not increase percent colonization by A. quisqualis but reduced the size of mildew colonies when used alone or with AQ10.

First Occurrence of Powdery Mildew Caused by Leveillula taurica on Pepper in New York.

Powdery mildew was observed for the first time on pepper (Capsicum annuum L.) in western New York in August 1999 and on Long Island, NY, in August 2000. Infected plants were found in commercial fields planted with transplants from Georgia and Florida. Powdery mildew was not found in nearby commercial fields in either year, and it was not found in 2000 in western New York. Symptoms included white sporulation on the undersurfaces of leaves, causing yellow lesions on upper surfaces that turned necrotic and led to premature defoliation. The pathogen was confirmed to be Leveillula taurica (Lév.) G. Arnaud, a species complex that infects more than 1,000 plant species in 74 families, including pepper, tomato and eggplant. Only the Oidiopsis stage was found. Conidia were 47.3 to 74.3 µm × 10.5 to 20.3 µm (average 64.0 × 16.8 µm (N = 71). Symptoms were observed on all cultivars of bell and chili pepper in the Long Island field but not on tomato (Lycopersicon esculentum) and eggplant (Solanum melongena var. esculentum) in adjacent rows. Powdery mildew of pepper was first observed in North America in 1971 in southwest Florida (1). Symptoms were found on field-grown peppers in Florida in April 2001 at the time that transplants were being produced for New York. Considering the latent period is 18 to 21 days and symptoms tend to be initially subtle, diseased seedlings could easily go undetected. This disease is a problem on tomatoes and peppers in California (2), Arizona, Utah, and Nevada. Powdery mildew of pepper was reported in Puerto Rico in 1992, in Idaho on greenhouse-grown pepper in 1998, in north-central Mexico in 1998, and in both Canada and Oklahoma on greenhouse-grown pepper in 1999. Powdery mildew of peppers has not been seen in Connecticut, Massachusetts, New Jersey, North Carolina, or Ohio. References: (1) C. H. Blazquez. Phytopathology 66:1155, 1976. (2) R. F. Smith et al. Calif. Agric. 53:40, 1999.

Control of Cucurbit Powdery Mildew with JMS Stylet-Oil.

Laboratory and greenhouse studies were conducted to determine the effect of JMS Stylet-Oil on cucurbit powdery mildew. In laboratory studies, JMS Stylet-Oil (1.5%) applied with a low-pressure sprayer (138 kPa) significantly reduced colony size, but did not eradicate pre-existing mildew colonies. Applying oil every 4 days was more effective than a single application. Oil did not significantly reduce spore viability, since spores taken from sprayed colonies readily formed new colonies. Although oil appeared to cause abnormalities of conidiophores and spores immediately after application, this effect was temporary. Tween 20 had an inhibitory effect on mildew growth and increased the effectiveness of oil when the two were applied together. Efficacy of oil was increased by using a high-pressure sprayer (1380 kPa). In the greenhouse experiment, JMS Stylet-Oil (0.75%) applied once to summer squash either 4 h before transfer of conidia to inoculation sites or 5 days after inoculation suppressed the size of the area infected by 48 to 60%. A single application of oil 5 days before inoculation was not effective. A 4-day spray program beginning 5 days after inoculation was effective. Compared with nontreated plants, oil-treated plants had fewer symptomatic leaves (71 vs. 34%, excluding leaf 1 and inoculated leaves) and fewer colonies (244 vs. 26) 20 days after inoculation.