Remote Sensing for Assessing Rhizoctonia Crown and Root Rot Severity in Sugar Beet.

Rhizoctonia crown and root rot (RCRR), caused by Rhizoctonia solani AG-2-2, is an increasingly important disease of sugar beet in Minnesota and North Dakota. Disease ratings are based on subjective, visual estimates of root rot severity (0-to-7 scale, where 0 = healthy and 7 = 100% rotted, foliage dead). Remote sensing was evaluated as an alternative method to assess RCRR. Field plots of sugar beet were inoculated with R. solani AG 2-2 IIIB at different inoculum densities at the 10-leaf stage in 2008 and 2009. Data were collected for (i) hyperspectral reflectance from the sugar beet canopy and (ii) visual ratings of RCRR in 2008 at 2, 4, 6, and 8 weeks after inoculation (WAI) and in 2009 at 2, 3, 5, and 9 WAI. Green, red, and near-infrared reflectance and several calculated narrowband and wideband vegetation indices (VIs) were correlated with visual RCRR ratings, and all resulted in strong nonlinear regressions. Values of VIs were constant until at least 26 to 50% of the root surface was rotted (RCRR = 4, wilting of foliage starting to develop) and then decreased significantly as RCRR ratings increased and plants began dying. RCRR also was detected using airborne, color-infrared imagery at 0.25- and 1-m resolution. Remote sensing can detect RCRR but not before initial appearance of foliar symptoms.

Viability and maturation of Aphanomyces cochlioides oospores.

Plasmolysis, tetrazolium bromide staining and microscopic appearance were tested for their usefulness in determining viability of oospores of Aphanomyces cochlioides. For comparison, three lethal treatments were employed to contrast the reaction of dead oospores and untreated, presumably viable oospores. Few oospores stained with tetrazolium bromide, even though plasmolysis and microscopic appearance indicated that 85% were viable. Cytoplasm of viable oospores was densely organized and uniformly granular (DOUG), whereas cytoplasm of oospores exposed to lethal treatments was loosely organized and non-uniformly granular (LONG). Dose-response bioassay experiments were conducted with untreated oospores of varying inoculum densities or with mixtures of untreated DOUG and heat-treated LONG oospores in varying proportions. The number of DOUG oospores was correlated (R(2) = 0.62, P < 0.001) with severity of damping-off of sugar beet seedlings caused by A. cochlioides. Thus, the granular appearance of cytoplasm offered a fast, easy and reliable indicator of viability of A. cochlioides oospores. Tests with newly formed oospores/oogonia showed that >80% harvested at 3-4 d after inoculation of hypocotyls stained with tetrazolium, but by 8-9 d <10% stained, apparently because of declining permeability of the spore wall to tetrazolium as oospores matured.

Spatial Distribution of Aphanomyces cochlioides and Root Rot in Sugar Beet Fields.

Spatial distribution of Aphanomyces cochlioides inoculum and disease was assessed in sugar beet fields located near Moorhead, MN and Wahpeton, ND. Soil samples were collected in June and July 1994 from two main plots (60 by 60 m) in each field. Samples were evaluated for A. cochlioides using a sugar beet seedling assay in the greenhouse to determine a root rot index value (0-to-100 scale), which served as an indirect estimate of relative activity and density of inoculum. Field evaluations of Aphanomyces root rot on sugar beet (0-to-7 scale) were made at harvest in September at each soil collection site. Greenhouse root rot index values correlated positively with field disease ratings for all plots. Variance-to-mean ratios of greenhouse root rot index values and of field disease ratings among samples within each plot were calculated to compare the spatial distribution of midseason inoculum with root rot at harvest. Ratios of greenhouse root rot indices indicated that inoculum of A. cochlioides was aggregated in the field at midseason, but root rot was uniform within plots by harvest. Wet weather in July through August was conducive to infection and development of symptoms. A uniform distribution of disease at harvest likely reflects a combination of factors, including root growth into inoculum foci, redistribution of inoculum, and inoculum densities that are spatially variable but all above some minimum threshold for infection.

Variability in Sensitivity to Metalaxyl in vitro, Pathogenicity, and Control of Pythium spp. on Sugar Beet.

Pythium ultimum var. sporangiiferum (76 isolates) and P. aphanidermatum (21 isolates) cultured from diseased sugar beet seedlings in Minnesota and North Dakota were tested for sensitivity to metalaxyl, pathogenicity on sugar beet, and disease control by metalaxyl seed treatment. Sensitivity to metalaxyl (effective concentration causing 50% growth inhibition [EC50]) was determined by linear growth on corn meal agar amended with 0, 0.01, 0.1, 1, 10, and 100 µg a.i. metalaxyl ml-1 after 48 h in the dark at 21 ± 1°C. Variation among isolates was significant (P = 0.05) within and between species, and EC50 values averaged 0.16 (range: 0.05 to 1.30 µg ml-1) for P. ultimum var. sporangiiferum and 2.06 (range: 1.19 to 3.12 µg ml-1) for P. aphanidermatum. In pathogenicity tests on sugar beet, most isolates of P. ultimum var. sporangiiferum (72 of 76) and all of P. aphanidermatum significantly (P = 0.05) decreased final stands compared to the noninoculated control. There was no correlation between aggressiveness in the absence of metalaxyl and in vitro sensitivity to metalaxyl. When Pythium-infested soil was planted with seed treated with metalaxyl at the standard (0.625 g a.i. kg-1) or half rate, some isolates that were least sensitive to metalaxyl in vitro resulted in a significant (P = 0.05) reduction in disease control. These results may explain, at least in part, why producers do not attain expected stands when they plant metalaxyl-treated sugar beet seed.

Characterization and Pathogenicity of Thanatephorus cucumeris from Sugar Beet in Minnesota.

In 1993, hymenia of Thanatephorus cucumeris occurred on petioles of sugar beet leaves, but disease was not observed on leaves, crowns, or roots. Of 33 cultures isolated from sugar beet, 28 were identified as Rhizoctonia solani AG-3 (from four fields planted to potatoes in 1992) and five isolates were AG-5 (from one field planted to wheat in 1992). These isolates of R. solani AG-3 and AG-5 were nonpathogenic to moderately pathogenic on sugar beet seedlings (stands ranged from 49 to 95%). The same isolates were nonpathogenic when inoculated on 8-week-old sugar beet roots (root rot indices were ≤1 [0 to 7 scale]). All isolates of R. solani AG-3 (but none of AG-5) formed sclerotia on roots. Disease indices (0 to 4 scale) on potato sprouts at 10°C were low, did not differ significantly (P = 0.05) among isolates and the control in either of two experiments, and averaged 0.9 for 14 isolates of AG-3, 0.5 for three isolates of AG-5, and 0.5 in the control. All isolates of AG-3 (but none of AG-5) formed sclerotia on potato seed pieces. When potato sprouts were grown at 25°C, disease indices were low (averaged 0.4 in each of two experiments), but four isolates of AG-3 and three of AG-5 had disease indices significantly (P = 0.05) higher than those of the uninoculated control. Sclerotia were not observed. The presence of hymenia of T. cucumeris is significant in that sexual reproduction and inoculum production occurred on a nonhost crop and were related to AGs of R. solani associated with the previous crop (AG-3 for potato and AG-5 for wheat).

Reaction of Soybean Cultivars to Isolates of Fusarium solani from the Red River Valley.

Five isolates of Fusarium solani, originally isolated from diseased soybean roots in the Red River Valley (RRV) of Minnesota and North Dakota, were evaluated for their ability to cause symptoms on 10 genetically diverse soybean cultivars. Taproots of 2-week-old plants were inoculated with F. solani-infested oat kernels, and 3 and 10 weeks later, plants were evaluated for root rot and foliar symptoms. At 3 weeks after inoculation, taproots of all cultivars had extensive reddish brown to black lesions; root rot severity (1-6 scale) ranged from 4.8 to 5.1, and 3.5% of the plants had died. Foliar symptoms were not observed. At 10 weeks after inoculation, all cultivars showed extensive decay of taproots and >50% of lateral roots were necrotic; root rot severity (1-4 scale) ranged from 2.7 to 3.7, and 42.5% of the plants had died. Foliar symptoms were first observed between the R-1 to R-6 growth stages (about 5 weeks after inoculation) on the lower leaves and consisted of chlorosis at the margins that progressed inward. Veins initially were green, but leaves eventually became chlorotic, then necrotic, and fell with petioles still attached to the stem. In some cases, all of the foliage died. There was no significant (P = 0.05) isolate × cultivar interaction for root rot at 3 or 10 weeks after inoculation or for severity of foliar symptoms. Thirty-three cultivars commonly grown in southern Minnesota and the RRV were evaluated for reaction to one isolate of F. solani. Root rot severity ranged from 4.2 to 5.7 (1-6 scale) and 3.5 to 4.0 (1-4 scale), at 3 and 9 weeks after inoculation, respectively, and >50% of the plants died by 9 weeks after inoculation. Severity of foliar symptoms was low. These results indicate that isolates of F. solani from the RRV cause root rot and foliar symptoms on soybean and that cultivars grown in the region lack resistance to this pathogen. Foliar symptoms were not identical to those associated with sudden death syndrome.