Effect of the trap crop, Solanum sisymbriifolium, on Globodera pallida, Globodera tabacum, and Globodera ellingtonae.

The effect of the nematode trap crop Solanum sisymbriifolium was assessed against three Globodera spp., the potato cyst nematode Globodera pallida (in Idaho), the recently described Globodera ellingtonae (in Oregon), and the tobacco cyst nematode Globodera tabacum (in Connecticut) in field trials. At all locations the ability of S. sisymbriifolium to reduce Globodera encysted second-stage juveniles (J2) in egg densities compared to fallow was considered. For G. ellingtonae, the impact of planting and termination dates of S. sisymbriifolium on final egg densities was also evaluated; and for G. pallida, the ability of the nematode to reproduce on potato (Solanum tuberosum) after exposure to S. sisymbriifolium was determined. Encysted J2 in egg densities of all three Globodera spp. declined from 25 to 68% after trap cropping with S. sisymbriifolium. For G. pallida, S. sisymbriifolium reduced final encysted J2 in egg density by 23 to 50% compared to the fallow treatment, and significantly decreased G. pallida reproduction on potato after exposure to S. sisymbriifolium by 99 to 100% compared to the fallow treatment (P < 0.0001). For G. ellingtonae, the planting date of S. sisymbriifolium in May or June did not impact final egg densities (P = 0.32). Rather, percentage reduction in G. ellingtonae encysted J2 in egg density was most influenced by the length of time to which nematodes were exposed to S. sisymbriifolium, with 30 and 81% reduction after 6 vs 12 wk of exposure, respectively (P < 0.0001). Similar levels of nematode reduction after S. sisymbriifolium were observed for G. tabacum after 12 to 14 wk of exposure to the trap crop; G. tabacum density changes consisted of a 114% increase after susceptible tobacco, a 65% decrease after resistant tobacco, and an 88% decrease after S. sisymbriifolium compared to bare soil. In conclusion, this research demonstrates the widespread applicability of S. sisymbriifolium in reducing a diversity of Globodera spp. present in the USA.The effect of the nematode trap crop Solanum sisymbriifolium was assessed against three Globodera spp., the potato cyst nematode Globodera pallida (in Idaho), the recently described Globodera ellingtonae (in Oregon), and the tobacco cyst nematode Globodera tabacum (in Connecticut) in field trials. At all locations the ability of S. sisymbriifolium to reduce Globodera encysted second-stage juveniles (J2) in egg densities compared to fallow was considered. For G. ellingtonae, the impact of planting and termination dates of S. sisymbriifolium on final egg densities was also evaluated; and for G. pallida, the ability of the nematode to reproduce on potato (Solanum tuberosum) after exposure to S. sisymbriifolium was determined. Encysted J2 in egg densities of all three Globodera spp. declined from 25 to 68% after trap cropping with S. sisymbriifolium. For G. pallida, S. sisymbriifolium reduced final encysted J2 in egg density by 23 to 50% compared to the fallow treatment, and significantly decreased G. pallida reproduction on potato after exposure to S. sisymbriifolium by 99 to 100% compared to the fallow treatment (P < 0.0001). For G. ellingtonae, the planting date of S. sisymbriifolium in May or June did not impact final egg densities (P = 0.32). Rather, percentage reduction in G. ellingtonae encysted J2 in egg density was most influenced by the length of time to which nematodes were exposed to S. sisymbriifolium, with 30 and 81% reduction after 6 vs 12 wk of exposure, respectively (P < 0.0001). Similar levels of nematode reduction after S. sisymbriifolium were observed for G. tabacum after 12 to 14 wk of exposure to the trap crop; G. tabacum density changes consisted of a 114% increase after susceptible tobacco, a 65% decrease after resistant tobacco, and an 88% decrease after S. sisymbriifolium compared to bare soil. In conclusion, this research demonstrates the widespread applicability of S. sisymbriifolium in reducing a diversity of Globodera spp. present in the USA.

Management of Calonectria pseudonaviculata in Boxwood with Fungicides and Less Susceptible Host Species and Varieties.

Calonectria pseudonaviculata causes leaf and stem lesions resulting in defoliation and dieback of boxwood. Trials were conducted to evaluate fungicide management of boxwood blight under greenhouse and container nursery conditions in Connecticut using fungicides previously determined to have in vitro activity against conidial germination or mycelial growth. Plants of different boxwood cultivars were inoculated 48 h after fungicide application. Disease progression was monitored over 6 weeks and progressed from leaf and stem lesions to defoliation. The level of disease control achieved by fungicides was generally good, with the most efficacious treatments averaging from 95 to nearly 100% control. Products containing propiconazole, myclobutanil, thiophanate-methyl, fludioxonil, pyraclostrobin, kresoxim-methyl, and chlorothalonil had significant efficacy. The combination of systemic plus protectant fungicides in a single application resulted in superior disease control compared to the use of a systemic fungicide. There were no differences between the fungicide treatments that included thiophanate-methyl and those that included propiconazole as the systemic fungicide. Korean and 'Winter Gem' (Buxus sinica var. insularis) were the least susceptible of the cultivars evaluated, common boxwood (B. sempervirens) and True Dwarf (B. sempervirens 'Suffruticosa') were the most susceptible, and 'Green Mountain' (B. sinica var. insularis × B. sempervirens Suffruticosa) and 'Green Velvet' (B. sinica var. insularis × B. sempervirens Suffruticosa) were intermediate. These results suggest that B. sinica var. insularis may have some level of resistance to boxwood blight. Management of boxwood blight will rely on integrated best management practices that include inspection of incoming plant material, sanitation, cultural controls including use of cultivars tolerant to infection, and fungicide application.

First Report of Forsythia Shoot Blight Caused by Phytophthora nicotianae in Connecticut.

Blighting of Forsythia × intermedia 'Showoff' was first observed affecting several hundred plants in a commercial nursery in Connecticut in September 2012. Symptoms included wilting, leaf and stem blight, and dieback progressing to plant death. A Phytophthora sp. was isolated from symptomatic tissues on half-strength potato dextrose agar (½PDA). Colonies were white and cottony on ½PDA, reaching 9 mm in 15 days at 25°C, but colorless and inconspicuous on pimaricin, ampicillin, rifampicin, pentachloronitrobenzene agar (PARP) with sparse and limited aerial mycelium, reaching 60 mm in 15 days at 25°C. The characteristics of the pathogen were observed and measured from a 3-month-old colony on ½PDA. Sporangia were abundant, various in shape, ovoid, ellipsoid to pyriform or limoniform, occasionally gourd shaped or irregular; (17.9) 27.2 to 41.4 (47.3) × (12.6) 19.1 to 30.5 (36.7) µm (n = 30), length/breadth ratio 1.4 ± 0.2, papillate and noncaducous. Papillae measured 2.9 ± 0.8 × 3.4 ± 0.8 µm (n = 10). Chlamydospores were present, 23.4 ± 3.1 × 22 ± 3.3 µm (n = 10). Oogonia and oospores were not observed. Arachnoid mycelia were present. These morphological characteristics are consistent with Phytophthora nicotianae Breda de Haan (1). The identity of the pathogen was confirmed as P. nicotianae by BLAST analysis of ITS, Cox II, and beta tubulin gene sequences (99% match for the three sequences, E value = 0). Pathogenicity tests were conducted four times on healthy liners of Forsythia × intermedia 'Showoff' grown in 10-cm-diameter pots. Leaves and stems were wounded by pricking with a sterile needle and six plants were inoculated with 0.25 cm2 plugs of the pathogen growing on ½PDA placed on three leaves and in three stem nodes and covered with Parafilm. Controls consisted of an equal number of plants wounded and inoculated with ½PDA alone. All plants were placed inside high humidity chambers for 24 h and then transferred to a greenhouse for up to 1 month. Typical symptoms developed within 1 week of inoculation and the pathogen was re-isolated from diseased tissue. Disease incidence was nearly 100% of inoculated leaves and stems and not observed in control plants without the pathogen. Three replicate 6-week-old broadleaf tobacco 'C9' plants were each inoculated with tobacco or forsythia isolates of P. nicotianae or sterile media alone, by wounding stems and placing colonized 0.25 cm2 ½PDA plugs into wounds and covering with Parafilm. After 1 week, stems were split and the length of internal necrosis in the stem measured. Disease resulted from inoculation with both the tobacco and forsythia isolates and stem necrosis averaged 43 and 23 mm for tobacco or forsythia isolates, respectively. No necrosis was observed in the pathogen-free controls. P. nicotianae has been reported from the basal stem and roots of F. viridissima in Italy (2) and from shoots of Forsythia × intermedia in Virginia (3). To our knowledge, this is the first report of P. nicotianae causing shoot blight on Forsythia in the northeastern United States. References: (1) J. van. Breda de Haan. Mededeelingenuit's Lands Plantentuin Batavia. 15:57, 1896. (2) S. O. Cacciola et al. Plant Dis. 78:525, 1994. (3) C. X. Hong et al. Plant Dis. 89:430, 2005.

Fungicide Efficacy Against Calonectria pseudonaviculata, Causal Agent of Boxwood Blight.

Calonectria pseudonaviculata causes leaf spot and stem lesions resulting in defoliation and dieback of boxwood. Fungicides representing 20 different active ingredients from 13 different Fungicide Resistance Action Committee groups were evaluated for their effects on conidial germination and mycelial growth using in vitro assays, and the concentration that suppressed fungal growth to 15% of that on unamended media (EC85) values were determined. A number of fungicides strongly inhibited mycelial growth of C. pseudonaviculata. Four demethylation inhibitor fungicides had EC85 values of 1.2 µg a.i./ml or less. Thiophanate-methyl, fludioxonil, pyraclostrobin, trifloxystrobin, kresoxim-methyl, mancozeb, and chlorothalonil also had activity against mycelial growth. Fludioxonil + cyprodinil had a lower EC85 than the same rate of fludioxonil alone, suggesting that cyprodinil had activity against mycelial growth. Fungicides that inhibited C. pseudonaviculata conidial germination include pyraclostrobin, trifloxystrobin, and kresoxim-methyl as well as fludioxonil, mancozeb, chlorothalonil, and boscalid. Quinoxyfen, etridiazole, fenhexamid, hymexazol, famoxadone, and cymoxanil did not inhibit either C. pseudonaviculata conidial germination or mycelial growth. In comparison with values found in the literature, EC50 values for kresoxim-methyl were up to 10 times higher than reported previously, suggesting that fungicide insensitivity may have developed. Protectant fungicides with activity against conidial germination and systemic fungicides with activity against mycelial growth, such as those identified here, may be complementary to achieve the high levels of pathogen management required for control of this disease. In addition, multiple fungicide active ingredients from different mode-of-action groups used in mixtures or over time may also act to slow selection for fungicide insensitivity.

Sudden Vegetation Dieback in Atlantic and Gulf Coast Salt Marshes.

Salt marshes rank as the most productive ecosystems on the planet. Biomass production can be greater than 3 kg dry matter/m2/year, which is 40% more biomass than tropical rainforests produce. Salt marshes provide multiple benefits to mankind. For example, coastal communities receive protection from storm surges and wave erosion. Salt marshes absorb excess nitrogen and phosphorus from sewage and fertilizer run-off into rivers, which, in turn, prevents algal blooms and hypoxia in coastal waters. In addition, these unique ecosystems provide habitat and shelter for many hundreds of species of shellfish, finfish, migratory and sedentary birds, and other marine animals. Despite the richness in animal species, the intertidal marshes of the salt marsh ecosystem are dominated by only a few plant species. Of these, the most prevalent plant species in a marsh are the tall and short forms of smooth cordgrass (Spartina alterniflora). The first recorded account of a dieback in a U.S. salt marsh was in the early 1990s in the Florida panhandle where patches of Sp. alterniflora as large as 1 ha died. This article explores possible causes of Sudden Vegetation Dieback.

First Report of Target Spot of Broadleaf Tobacco Caused by Rhizoctonia solani (AG-3) in Connecticut.

In June 2011, 15 transplant beds of broadleaf cigar wrapper tobacco (Nicotiana tabacum L., cv. C9) plants in Hartford County, Connecticut, were observed with almost every plant diseased. Leaf lesion symptoms ranged from small (2 to 3 mm) water-soaked spots to larger (2 to 3 cm) lesions. Disease was subsequently observed, also at nearly 100% incidence in a 10-hectare field on that farm and at additional broadleaf tobacco farms from two other towns in Hartford County and one town in Tolland County. Lesions exhibited a pattern of concentric rings, necrotic centers and tears in the centers, and margins that often resulted in a shot-hole appearance. Some lesions had chlorotic halos. Rhizoctonia solani Kuhn (Thanatephorus cucumeris A. B. Frank) was isolated from the margins of lesions that had been surface sterilized in 0.5% NaOCl for 30 s and then rinsed in sterile distilled water and placed on the surface of half-strength potato dextrose agar (PDA). Multiple isolations were made and the pathogen was identified on the basis of mycelial characteristics including multinucleate cells, septate hyphae wider than 7 µm, and hyphal branches occurring at approximately right angles, constricted at the base (4). Eight-week-old potted tobacco plants were each inoculated by spraying with a mycelial suspension (1 × 105 CFU) of an isolate of R. solani recovered from tobacco onto leaves, or with water alone (five plants each). The plants were placed in plastic bags in a 24°C growth chamber and misted. After 2 days, the bags were removed and the potted plants placed in trays filled to a depth of 1 cm with water in the growth chamber. After 8 days, the pathogen was reisolated from all inoculated plants exhibiting water-soaked spots as disease symptoms. Leaves inoculated with water or half-strength PDA plugs alone were asymptomatic. DNA was liberated from hyphae of the R. solani isolate by bead beating in STE buffer using 0.15 mm zirconium beads. Two microliters of the eluate was used to amplify the ITS region. Amplified DNA was purified in a Qiagen QIAquick PCR purification kit and submitted to the Yale science hill genomic facility for standard Sanger dideoxy sequencing. The sequence was exactly the same as an isolate from Massachusetts that we sequenced in 2010 (GenBank Accession No. HQ241274). The ITS sequence confirmed our identification of this new isolate as R. solani anastomosis group (AG) 3. This disease has been previously reported on tobacco from South America, South Africa, and the southern United States (1), Canada (3), and Massachusetts (2). Conditions were very conducive for disease because 2011 was a very wet year in Connecticut. To our knowledge, this is the first report of this disease in broadleaf cigar wrapper tobacco in Connecticut. The sequence data suggested that it may have been introduced to Connecticut from Massachusetts. We have found the target spot pathogen distributed across the tobacco producing area of Connecticut. This constitutes a serious threat as there are no systemic fungicides currently registered for control of this disease in broadleaf tobacco. References: (1) J. S. Johnk et al. Phytopathology 83:854, 1993. (2) J. A. LaMondia and C. R. Vossbrinck, Plant Dis. 95:496, 2010. (3) R. D. Reeleder et al., Plant Dis., 80:712. (4) B. Sneh et al. Identification of Rhizoctonia species. The American Phytopathological Society, St. Paul, MN, 1991.

First Report of Boxwood Blight Caused by Cylindrocladium pseudonaviculatum in the United States.

In September and October 2011, a new disease was observed on Buxus spp. in North Carolina and Connecticut, respectively. In North Carolina, over 10,000 containerized Buxus sempervirens (American boxwood) were affected at one location. A few weeks later, the disease was found in Connecticut on entire plantings of B. sempervirens 'Suffruticosa' (English boxwood) at two residential properties, and shortly thereafter on over 150,000 plants at two production nurseries. Initial foliar symptoms appeared as light to dark brown spots, often with dark borders. Spots enlarged and coalesced, often with a concentric pattern, and black streaks or cankers developed on stems. Infected leaves became brown or straw colored and dropped quickly after foliar symptoms were visible. Branch dieback and plant death were also observed in Connecticut. Cultures were isolated from symptomatic leaves and stems and identified as Cylindrocladium pseudonaviculatum Crous, Groenewald & Hill 2002 (1) (syn. Cylindrocladium buxicola Henricot 2002 [2]) on the basis of morphological characteristics. Macroconidiophores were single or in groups of up to three and comprised a stipe, stipe extension, and a penicillate arrangement of fertile branches. The stipe extension was septate, hyaline (89 to 170 × 2 to 4.5 µm), and terminated in an ellipsoidal vesicle (6 to 11 µm diameter) with a papillate or pointed apex. Conidia were cylindrical, straight, hyaline, and one septate (48 to 62 × 4 to 6 µm), occurring in slimy clusters. No microconidiophores were observed. Chlamydospores were medium to dark brown, thick walled, and smooth to rough. Microsclerotia were observed on PDA (1). A portion of ß-tubulin gene sequence from two Connecticut (Genbank Accession Nos. JQ866628 and JQ866629) and two North Carolina isolates showed 100% similarity with only C. pseudonaviculatum strains. USDA-APHIS-PPQ confirmed this new United States record on October 24, 2011. Pathogenicity was confirmed by inoculating three 1-gallon container plants of B. sempervirens 'Suffruticosa' in North Carolina and four liners of B. sinica var. insularis × B. sempervirens 'Green Velvet' in Connecticut with a spore suspension of approximately 5.0 × 106 conidia (North Carolina) or 1.0 × 106 conidia (Connecticut) on the foliage of each plant; untreated control plants were sprayed with water. After incubation at ambient temperature, all inoculated plants developed foliar and stem lesions within 3 to 4 days and blighting occurred within 2 weeks; control plants remained asymptomatic. C. pseudonaviculatum was reisolated from inoculated plants. To our knowledge, this is the first report of C. pseudonaviculatum in the United States. C. pseudonaviculatum causes a serious disease of Buxus spp. in the United Kingdom and several other European countries as well as New Zealand (1). Confirmation of boxwood blight in the United States is significant because of the popularity of boxwood as a landscape plant, and because of the potential economic impact this disease may have on commercial growers; boxwood production in the United States has an annual wholesale market value of approximately $103 million (3). References: (1) P. Crous, et al. Sydowia 54:23, 2002. (2) B. Henricot and A. Culham Mycologia 94: 980, 2002. (3) USDA-NASS, Census of Horticulture, 2010.

First Report of Cylindrocladium pseudonaviculatum Causing Leaf Spot of Pachysandra terminalis.

Cylindrocladium pseudonaviculatum Crous, J.Z., Groenew. & C.F. Hill 2002 was recently reported infecting common boxwood, Buxus sempervirens L., in Connecticut (2). We isolated the pathogen from leaf and stem lesions of B. sempervirens and obtained single-spored cultures on half-strength potato dextrose agar (½PDA). The pathogen was identified as C. pseudonaviculatum by morphological characteristics (1). Colony size reached 71 mm in diameter after 14 days at room temperature on ½PDA, and was fluffy with white aerial hyphae, mars brown, and reverse color chestnut brown at the center fading to pale brown forming concentric bands. Macroconidiophores were solitary or in a group of up to three, comprised a stipe, a sterile elongation, and one to three penicillate fertile branches. The stipe was up to nine septate, 90 to 250 µm long, colorless, smooth, terminating in a naviculate or broadly ellipsoidal vesicle with a pointed or papillate apex, and 27 to 50 × 6.5 to 9 µm. Primary branches were zero- to one-septate, 20 to 36 × 4 to 5 µm; secondary branches were aseptate and 11 to 20 × 3 to 4.5 µm; tertiary branches were rare, each terminal branch producing two to five phialides; phialides were doliiform or reniform, colorless, 12 to 18 µm. Conidia were cylindrical, rounded at both ends, straight, smooth, colorless, two-celled, 48 to 55 × 4.5 to 5.5 µm, and in colorless slimy cylindrical clusters. Microconidiophores were not observed. Chlamydospores were golden to dark brown, thick-walled, and smooth or rough. Microsclerotia were present on ½PDA. Primers T1 and T22 (3) were used to amplify a portion of the ß-tubulin gene from isolates Cps-CT-L1 and Cps-CT-S1. Amplified sequences were used in a BLAST search against the GenBank database to demonstrate 100% sequence identity only with other C. pseudonaviculatum strains. Both sequences were deposited in GenBank (Accession Nos. JQ866628 and JQ866629), using corresponding gene data from C. pseudonaviculatum strain STE-U 3399 (GenBank Accession No. AF449455) to distinguish coding from noncoding regions. Healthy plants of Japanese spurge, Pachysandra terminalis, with three plants per 10 cm diameter pot, were inoculated with water alone or a conidial suspension of C. pseudonaviculatum isolate Cps-CT-L1 (ATCC MYA-4891) (1.0 × 106 conidia/plant) with a handheld sprayer until runoff. Plants were kept moist in a plastic bag for 48 h at laboratory temperature and then transferred to the greenhouse. Circular lesions (1- to 4-mm diameter) were evident on leaves after 10 days. All 12 inoculated plants developed lesions, and no lesions were observed on noninoculated plants. Leaves with lesions were surface sterilized in 0.5% NaOCl for 30 s, rinsed twice in sterile water, and lesion margins plated onto water agar or ½PDA. The pathogen was reisolated from at least one leaf per plant. Koch's postulates were performed again with isolate Cps-CT-S1 (ATCC MYA-4890). After 3 weeks, many of the leaves with lesions yellowed and dropped to the soil surface and heavy sporulation of C. pseudonaviculatum and microsclerotia were observed. To our knowledge, this is the first report of C. pseudonaviculatum causing a leaf spot disease on P. terminalis. Pachysandra is a widely grown ground cover suitable for shady, humid environmental conditions that may be conducive for the development of disease. References: (1) P. Crous, et al. Sydowia 54:23, 2002. (2) K. Ivors et al. Plant Disease. 96:X, 2012. (3) K. O'Donnell and E. Cigelnik Mol. Phylogenet. Evol. 7:103, 1997.

First Report of Target Spot of Tobacco Caused by Rhizoctonia solani (AG-3) in Massachusetts.

In June 2010, shade-grown cigar wrapper tobacco (Nicotiana tabacum L.) plants in Hampshire County, Massachusetts were observed with leaf lesion symptoms that ranged from small (2 to 3 mm) water-soaked spots to larger (2 to 3 cm) lesions. Lesions had a pattern of concentric rings, necrotic centers and tears in the centers, and margins that often resulted in a shot-hole appearance. Some lesions had chlorotic halos. Rhizoctonia solani Kuhn (Thanatephorus cucumeris A.B. Frank) was isolated from lesions and identified on the basis of mycelial characteristics including multinucleate cells, septate hyphae wider than 7 µm and hyphal branches occurring at approximately right angles, and constricted at the base (3). Eight-week-old, potted tobacco plants were each inoculated either by spraying with a mycelial suspension (1 × 105 CFU) (five plants) or by placing colonized half-strength potato dextrose agar (PDA) plugs (0.2 cm) of an isolate of R. solani recovered from tobacco onto leaves (five plants) or with water or half-strength PDA plugs alone (five plants each). The plants were placed in plastic bags in a 24°C growth chamber and misted. After 2 days, the bags were removed and the potted plants were placed in trays filled with water to a depth of 1 cm in the growth chamber. After 8 days, the pathogen was reisolated from inoculated plants exhibiting water-soaked spots as disease symptoms. Leaves inoculated with water or half-strength PDA plugs alone were not diseased. DNA was extracted from the R. solani isolate and the nuclear ribosomal internal transcribed spacer (ITS) region was amplified and sequenced (GenBank Accession No. HQ241274). The ITS sequence confirmed our identification of this new isolate as R. solani anastomosis group (AG) 3. This disease had been previously reported on tobacco from South America, South Africa, the southern United States (1), and Canada (2). To our knowledge, this is the first report of this disease in cigar wrapper tobacco in New England. The humid environmental conditions under which shade tobacco is grown make this new disease a significant threat for the Massachusetts and Connecticut growing area. References: (1) J. S. Johnk et al. Phytopathology 83:854, 1993 (2) R. D. Reeleder et al. Plant Dis. 80:712, 1996. (3) B. Sneh et al. Identification of Rhizoctonia species. The American Phytopathological Society, St. Paul, MN, 1991.

January Temperatures Predict Tobacco Blue Mold Severity: Evidence for Local Source and Long-Distance Transport of Inoculum in Connecticut.

The tobacco blue mold pathogen, Peronospora tabacina, has been periodically reintroduced to the Connecticut River Valley cigar wrapper tobacco (Nicotiana tabacum) area of Connecticut and Massachusetts. Once introduced, there is a greater likelihood of disease in following years. Blue mold occurred from 1937 to 1956, 1979 to 1981, and most recently from 1996 to 2008. Disease severity was evaluated and rated annually from 1979 to 2008, and was correlated (r = 0.84; P = 0.002) with January temperatures when the pathogen was present in moderate amounts the previous year (severity rating >1). The date of the first report of disease was negatively correlated with disease severity the previous year (r = -0.63) and February temperatures (r = -0.83). Blue mold severity was not correlated with the date of the first disease, the previous year's disease severity, or rainfall amount or frequency after introduction of the pathogen. January temperatures may be used to predict the need for early-season fungicide applications to control disease from local overwintering inoculum following moderate to high blue mold severity. In years following little or no disease, forecasts of long-distance transport will continue to be a valuable tool to predict the risk of long-distance reintroduction and the need for fungicide application based on exposure.

First Report of Blight of Common Bean Caused by Phytophthora capsici in Connecticut.

Phytophthora capsici Leonion was first identified on pepper (Capsicum annuum L.) and is widespread on solanaceous and cucurbitaceous crops. It was first documented on Phaseolus lunatus L. in Delaware in 2002 (1), followed by reports on snap beans (Phaseolus vulgaris L.) in Michigan in 2003 (2), and on Long Island, NY in 2008 ( http://vegetablemdonline.ppath.cornell.edu/ NewsArticles/Bean_phytoJune09.html ). In 2009, we observed snap and wax beans in commercial production with water-soaked lesions on foliage, stems, and pods. Twelve to sixteen hectares were affected in the flood plain of the Connecticut River in central Connecticut. Weather conditions had been warm and very wet. Lesions displayed white mycelia and sporangia. P. capsici was isolated from surface-sterilized tissue on potato dextrose agar (PDA) and malt extract agar. Hyphal tips were subcultured onto V8 media for further analysis. To confirm Koch's postulates, two isolates were tested for pathogenicity against bean (cv. Valentino) and pepper (cv. Cayenne) by placing colonized PDA plugs or PDA alone next to the crown or in stem branches. Symptoms similar to those observed in the field on bean and pepper developed on inoculated plants and the pathogen was reisolated. Controls did not develop disease. Sporangia of P. capsici growing on V8 medium were ellipsoid, ovoid, pyriform, but occasionally irregular, papillate, and 54.0 ± 5.7 × 31.1 ± 4.7 µm (n = 31) with a length/width (L/W) ratio of 1.8 ± 0.3. The papillae were 5.4 ± 0.9 µm (n = 31) and the pedicels were 24.5 ± 12.6 × 3.0 ± 1.0 µm. Sporangia collected from bean plants were smaller with longer pedicels; the sporangia were 44.9 ± 9.1 × 26.0 ± 2.8 µm with a L/W ratio of 1.7 ± 0.2; papillae were 4.6 ± 1.0 µm; and the pedicels were 49 ± 20.0 × 2.8 ± 0.9 µm (n = 20). To confirm the identity of our isolate genetically, DNA was extracted from one P. capsici isolate and the nuclear ribosomal internal transcribed spacer (ITS) region was amplified and sequenced (GenBank Accession No. GU011684). The ITS sequence was identical to sequences of P. capsisci in GenBank and confirmed our identification of this new isolate as P. capsici. To our knowledge, this is the first report of P. capsici infecting Phaseolus vulgaris in Connecticut and New England. References: (1) C. R. Davidson et al. Plant Dis. 85:886, 2002. (2) A. J. Gevens et al. Plant Dis. 92:201, 2008.

Effect of a Chromosome Segment Marked by the Php Gene for Resistance to Phytophthora nicotianae on Reproduction of Tobacco Cyst Nematodes.

Host resistance is an important strategy for managing Globodera tabacum subsp. solanacearum and G. tabacum subsp. tabacum, important nematode pests of flue-cured tobacco (Nicotiana tabacum) in Virginia, and cigar wrapper tobacco (N. tabacum) in Connecticut and Massachusetts, respectively. Field research from 1992 to 2005 evaluated reproduction of G. tabacum subsp. solanacearum on genotypes with and without a chromosome segment from N. plumbaginifolia containing a gene (Php) that conferred resistance to race 0 of Phytophthora nicotianae (causal agent of tobacco black shank). Ratios of G. tabacum subsp. solanacearum eggs/500 cm3 soil at the end versus the beginning of experiments (Pf/Pi) were significantly lower in cultivars and breeding lines possessing the Php-containing chromosome segment from N. plumbaginifolia compared with genotypes without the segment. Numbers of vermiform G. tabacum subsp. solanacearum juveniles in roots were similar among genotypes but numbers of swollen and pyriform nematodes were significantly lower for the known G. tabacum subsp. solanacearum resistant cv. NC 567 and in genotypes possessing the Php gene compared with genotypes and cultivars without the gene. In a 2003 greenhouse test, the percentage of plants with visible G. tabacum subsp. tabacum cysts was also significantly lower for parental and progeny genotypes homozygous and heterozygous, respectively, for Php compared with similar lines without the gene. These results indicate a close linkage or association between a likely single, dominant gene (Php) for resistance to P. nicotianae and suppressed reproduction by G. tabacum subsp. solanacearum and G. tabacum subsp. tabacum. Further research to accurately elucidate the relationships among these genes could lead to significant improvements in tobacco disease control.

Early crop root destruction for management of tobacco cyst nematodes.

Prompt tillage after crop harvest was investigated as a cultural control for the tobacco cyst nematode, Globodera tabacum tabacum, on stalk-cut broadleaf cigar wrapper tobacco. Stalk stumps and roots remaining after harvest were destroyed by tilling immediately or from 2 to 6 wk after harvest in field experiments over 4 yr. Cyst nematode Pf/Pi ratios ranged from 0.65 to 1.62 when plants were tilled immediately after harvest and 1.13 to 5.88 when tillage was delayed. Nematode population development was monitored by inoculating plants in pots placed in fields with J2 in eggs and sampling over time (8 to 18 wk). Three generations per year were observed, and G. t. tabacum generation time was as short as 6 wk for each generation. Destroying stalks and root systems remaining after harvesting stalk-cut broadleaf cigar wrapper tobacco removes the host to preclude development of nematodes at the end of the second and entire third generation. Early tillage resulted in consistently lower tobacco cyst nematode populations than allowing viable roots to remain in fields for an additional 8 to 18 wk. This management tactic reduces the need for nematicide application to slow nematode population increases over time and can reduce losses due to infection by G. t. tabacum.

Ecological Relationships between Meloidogyne spartinae and Salt Marsh Grasses in Connecticut.

Healthy specimens of selected grasses were collected from salt marshes and grown in the greenhouse. Plants were inoculated with Meloidogyne spartinae to determine the host range of this nematode. After 12 weeks, Spartina alterniflora plants formed root galls in response to infection and increased M. spartinae populations. Spartina patens, Spartina cynosuroides, Juncus gerardii and Distichlis spicata were non-hosts. In order to determine the natural distribution of M. spartinae in dieback areas, S. alterniflora plants were sampled from transects adjacent to dieback areas in Madison, CT, at low tide. Plants were sampled at the top or the creek and at 1-m intervals to the lowest area of plant growth at the low tide water's edge. Five samples were taken over an elevation drop of 90 cm. Two transects were taken each day on 21 June and 5 July 2007, and one transect was taken on 31 October 2007. Meloidogyne spartinae galls per gram root were higher at the higher elevations. In late June and early July 2007, M. spartinae developed more quickly in the higher elevations, perhaps because peat and sediments were drier and warmer away from low tide water levels. The effects of M. spartinae on S. alterniflora and the role of the nematode in marsh decline and dieback in the northeast United States remain to be determined.

Actigard Increases Fungicide Efficacy Against Tobacco Blue Mold.

Blue mold, caused by Peronospora tabacina, can be economically damaging to cigar wrapper tobacco (Nicotiana tabacum). We evaluated acibenzolar-S-methyl (ASM) as Actigard 50WG alone and in combination with a standard fungicide program for efficacy against blue mold on shade-grown cigar wrapper tobacco in Windsor, CT. The standard fungicide program consisted of dimethomorph (Acrobat MZ or Forum) plus mancozeb (Dithane), alternated with azoxystrobin (Quadris), and applied at label rates on six occasions at 14-day intervals. Treated and untreated 5-by-5-m plots were replicated four times in 2003, 2004, 2005, 2006, and 2007. ASM treatments were applied alone or in combination with fungicides at the third, fourth, and fifth spray dates at rates ranging from 1.1 to 17.5 g a.i./ha. Disease was greatest in nontreated plots and reduced in all fungicide, Actigard, or combination treatments. The combination of three ASM applications at rates of 17.5 g a.i./ha down to 4.4 g a.i./ha with the standard fungicide program was more efficacious than either fungicides or ASM alone (P < 0.001) in reducing the number of blue mold lesions per plot or number of diseased leaves harvested. The combination of fungicides and low rates of ASM (2.2 or 1.1 g a.i./ha) was similar to either fungicides or ASM (17.5 g a.i./ha) applied alone. Combining low rates of ASM with fungicide applications greatly increased efficacy and marketable yield.

The Association of Tobacco mosaic virus with Green Spot of Cured Wrapper Tobacco Leaves.

Near-isogenic lines of cigar wrapper tobacco resistant or susceptible to Tobacco mosaic virus (TMV) were used to evaluate the association of TMV infection with green spot symptoms in cured leaves. TMV infection, as determined by double-antibody sandwich enzyme-linked immunosorbent assay (ELISA), was detected on susceptible but not resistant plants in field experiments. Green spot severity on cured leaves was greater for susceptible than resistant plants, even when symptoms of TMV were not evident in the field. Some green spots were present on resistant leaves despite the fact that the virus was not detected by ELISA. Resistant and susceptible plants had similar responses to virus infection and similar ELISA detection of TMV when plants were held at continuous temperatures over 28°C in growth chambers. Plant resistance was not compromised in the field in cloth-covered shade tents even when 33.5 of the 96 h immediately following inoculation were above 28°C. Green spot of cured leaves was strongly associated with TMV infection in susceptible plants, even when plants were infected after leaf expansion and mosaic symptoms were not present. Green spot also occurred to a lesser extent and for a limited time in inoculated resistant plants. The development of green spot symptoms on cured leaves may be the result of either systemic infection of TMV-susceptible plants or associated with the systemic resistance response to TMV inoculation of resistant plants.

Occurrence of Meloidogyne spartinae on Spartina alterniflora in Connecticut and Massachusetts.

Meloidogyne spartinae (Rau & Fassuliotis, 1965) was described from roots of smooth cordgrass (Spartina alterniflora Loisel) in Florida, Georgia, North and South Carolina, New Jersey, and New York (1,2). Affected plants were sampled in declining saltwater marshes at the Cape Cod National Seashore in Wellfleet, MA in May 2006 and Hammonassett State Park in Madison, CT in August 2006. Plants in adjacent, healthy stands were also sampled. Females, males, juveniles, and eggs of nematodes identified as M. spartinae were visible in roots stained with acid fuschin or were dissected from terminal galls at the root apex and from pockets in the root cortex where no galling was evident. The circular to ovoid terminal galls typically stopped root elongation. Morphological characteristics were used to identify this nematode as M. spartinae. Mature females in the root cortex were visible under a discolored lesion that appeared to result from a split in the cortex, probably from female expansion during development. Females were oval to lemon shaped with the neck protruding markedly to one side. Females also exhibited protruding perineal regions. In terminal galls, females were oriented toward the root tip; however, in the root cortex they were oriented either toward the root tip or toward the crown, with no obvious pattern. Egg masses were not observed and the eggs were deposited freely inside the gall or root cortex. Second-stage juveniles were long (730.3 µm, n = 60) with an elongate tail terminus. Males (2,203 µm, n = 40) were present in galls containing females. No morphological differences were observed between nematodes from the terminal galls or root cortex. M. spartinae was widespread in declining and adjacent healthy S. alterniflora. To our knowledge, this is the first report of M. spartinae from Connecticut and Massachusetts and the first report of M. spartinae development within root cortical tissues without gall formation. The role of this nematode in the sudden wetland dieback phenomenon (3) is being investigated. References: (1) J. D. Eisenback and H. Hirschmann. Nematology 3:303, 2001. (2) G. J. Rau and G. Fassuliotis. Proc. Helminthol. Soc. Wash. 32:159, 1965. (3) E. C. Webb and I. A Mendelssohn. Am. J. Bot. 83:1429, 1996.

Management of lesion nematodes and potato early dying with rotation crops.

Soil-incorporated rotation/green manure crops were evaluated for management of potato early dying caused by Verticillium dahliae and Pratylenchus penetrans. After two years of rotation/green manure and a subsequent potato crop, P. penetrans numbers were less after 'Saia' oat/'Polynema' marigold, 'Triple S' sorghum-sudangrass, or 'Garry' oat than 'Superior' potato or 'Humus' rapeseed. The area under the disease progress curve (AUDPC) for early dying was lowest after Saia oat/marigold, and tuber yields were greater than continuous potato after all crops except sorghum-sudangrass. Saia oat/marigold crops resulted in the greatest tuber yields. After one year of rotation/green manure, a marigold crop increased tuber yields and reduced AUDPC and P. penetrans. In the second potato crop after a single year of rotation, plots previously planted to marigolds had reduced P. penetrans densities and AUDPC and increased tuber yield. Rapeseed supported more P. penetrans than potato, but had greater yields. After two years of rotation/green manure crops and a subsequent potato crop, continuous potato had the highest AUDPC and lowest tuber weight. Rotation with Saia oats (2 yr) and Rudbeckia hirta (1 yr) reduced P. penetrans and increased tuber yields. AUDPC was lowest after R. hirta. Two years of sorghum-sudangrass did not affect P. penetrans, tuber yield or AUDPC. These results demonstrate that P. penetrans may be reduced by one or two years of rotation to non-host or antagonistic plants such as Saia oat, Polynema marigold, or R. hirta and that nematode control may reduce the severity of potato early dying.

Comparison of Pratylenchus penetrans Infection and Maladera castanea Feeding on Strawberry Root Rot.

The interaction of lesion nematodes, black root rot disease caused by Rhizoctonia fragariae, and root damage caused by feeding of the scarab larva, Maladera castanea, was determined in greenhouse studies. Averaged over all experiments after 12 weeks, root weight was reduced 13% by R. fragariae and 20% by M. castanea. The percentage of the root system affected by root rot was increased by inoculation with either R. fragariae (35% more disease) or P. penetrans (50% more disease) but was unaffected by M. castanea. Rhizoctonia fragariae was isolated from 9.2% of the root segments from plants not inoculated with R. fragariae. The percentage of R. fragariae-infected root segments was increased 3.6-fold by inoculation with R. fragariae on rye seeds. The presence of P. penetrans also increased R. fragariae root infection. The type of injury to root systems was important in determining whether roots were invaded by R. fragariae and increased the severity of black root rot. Pratylenchus penetrans increased R. fragariae infection and the severity of black root rot. Traumatic cutting action by Asiatic garden beetle did not increase root infection or root disease by R. fragariae. Both insects and diseases need to be managed to extend the productive life of perennial strawberry plantings.

Interaction of Pratylenchus penetrans and Rhizoctonia fragariae in Strawberry Black Root Rot.

A split-root technique was used to examine the interaction between Pratylenchus penetrans and the cortical root-rotting pathogen Rhizoctonia fragariae in strawberry black root rot. Plants inoculated with both pathogens on the same half of a split-root crown had greater levels of root rot than plants inoculated separately or with either pathogen alone. Isolation of R. fragariae from field-grown roots differed with root type and time of sampling. Fungal infection of structural roots was low until fruiting, whereas perennial root colonization was high. Isolation of R. fragariae from feeder roots was variable, but was greater from feeder roots on perennial than from structural roots. Isolation of the fungus was greater from structural roots with nematode lesions than from non-symptomatic roots. Rhizoctonia fragariae was a common resident on the sloughed cortex of healthy perennial roots. From this source, the fungus may infect additional roots. The direct effects of lesion nematode feeding and movement are cortical cell damage and death. Indirect effects include discoloration of the endodermis and early polyderm formation. Perhaps weakened or dying cells caused directly or indirectly by P. penetrans are more susceptible to R. fragariae, leading to increased disease.