Green stem disorder of soybean (Glycine max) is characterized by delayed senescence of stems with normal pod ripening and seed maturation. Three different field research approaches were designed to determine the relationship of green stem disorder to Bean pod mottle virus (BPMV) and other potential factors that may be involved in causing this disorder. The first research approach surveyed green stem disorder and BPMV in individual plants monitored in several commercial soybean fields during three growing seasons. Leaf samples from maturing plants (growth stage R6) were tested by enzyme-linked immunosorbent assay (ELISA) for BPMV. The percentage of monitored plants infected with BPMV at growth stage R6 in some fields was higher than the incidence of green stem disorder at harvest maturity. Many plants infected with BPMV did not develop green stem disorder, and conversely, many plants that had green stem disorder were not infected with BPMV. According to a chi-square test of independence, the data indicated that green stem disorder was independent of BPMV infection at growth stage R6 (P = 0.98). A second research approach compared green stem disorder incidence in an identical set of soybean entries planted in two locations with different levels of natural virus infection. Despite differences in virus infection, including BPMV incidence, 20 of 24 entries had similar green stem disorder incidence at the two locations. A third research approach completed over two growing seasons in field cages showed that green stem disorder developed without BPMV infection. BPMV infection did not increase green stem disorder incidence in comparison to controls. Bean leaf beetle, leaf hopper, or stinkbug feeding did not have an effect on the incidence of green stem disorder. The cause of the green stem disorder remains unknown.

Development of a method to identify field tolerance to bean pod mottle and soybean mosaic viruses (BPMV and SMV) in soybean [Glycine max (L.) Merr.] allowed evaluation of 33 soybean accessions for field response to BPMV and SMV. Based on measurement of parameters that included relative level of virus antigen in seed and mottling of soybean seed coats, three accessions showed tolerance to SMV and BPMV (PI 561353, M90‐18411, PI 507353), eight were tolerant to SMV (MN 1301, M92‐160047, M91‐113037, PI 423826A, A99‐216031, NE 3001, U96‐2408, Colfax), and four were tolerant to BPMV (PI 184042, M93‐326056, M95‐255017, Spansoy 201). Treatment of seed with the insecticide imidacloprid (1‐[(6‐chloro‐3‐pyridinyl)methyl]‐N‐nitro‐2‐imidazolidinimine) did not effect disease control. The relative level of virus antigen in seed harvested from experimental plots was shown to correlate significantly with virus incidence in plots. The data suggest that quantitative assay of virus seed antigen may provide a useful estimate of relative virus incidence in test plots and aid identification of field tolerance to seed‐borne viruses.

The recent introduction of the colonizing soybean aphid (Aphis glycines) to soybean in the northern United States has raised concern for potential increased disease caused by the nonpersistently aphid-transmitted Soybean mosaic virus (SMV). This study was conducted to examine the potential integration of host plant resistance and insecticide tactics for control of virus disease. Research from four location-years demonstrated that foliar application of the pyrethroid insecticide lambda-cyhalothrin (Warrior) or the organophosphate chlorpyrifos (Lorsban 4E) timed to suppress soybean aphid populations does not reduce SMV. Therefore, the introduction of a colonizing aphid to the array of migratory noncolonizing aphids that transmit SMV does not result in potential for disease control through vector suppression by foliar insecticides. Treatment also did not result in management of Bean pod mottle virus (BPMV), transmitted by the bean leaf beetle (Cerotoma trifurcata), presumably because of issues related to different phenologies of the insect vectors. Soybean cultivars with the lowest virus titer in seed produced the highest grain yield and, thus, were rated as field tolerant compared with cultivars with the highest virus titer in seed. Host plant resistance, not vector control, is the most effective tactic to control SMV.

In August of 2006, soybean (Glycine max (L.) Merr.) plants collected from Columbia, Dane, Green Lake, Walworth, Jefferson, and Waushara counties in southern Wisconsin exhibited symptoms typical of sudden death syndrome (SDS) caused by Fusarium virguliforme O'Donnell & Aoki [synonym F. solani (Mart.) Sacc. f. sp. glycines] (1). Foliar symptoms ranged from chlorotic spots to severe interveinal chlorosis and necrosis. Taproots of symptomatic plants were necrotic and stunted and stems exhibited a light tan discoloration, but never the dark brown discoloration typical for brown stem rot, a disease with similar foliar symptoms. Isolations from root and crown tissue of symptomatic plants were made using one-quarter-strength potato dextrose agar (PDA) amended with 100 ppm of streptomycin. Slow-growing, white-to-cream fungal colonies with blue and turquoise sporodochia were observed. Spores produced in sporodochia grown on PDA ranged in size from 32.5 to 70 μm long (average 53.1 μm) and 3 to 6 μm wide (average 4.4 μm) and with 3-5 septa (mode of 3). Isolates were characteristic of F. virguliforme based on colony morphology, spore morphology and size, and the absence of microconidia (3). The identity of F. virguliforme was confirmed by PCR amplification and DNA sequencing of the ITS, BT1, Act, and EF1B regions. All isolate sequences exhibited single nucleotide polymorphisms that matched the sequences of these regions of F. virguliforme. Koch's postulates were conducted to confirm that the causal agent of the observed symptoms was F. virguliforme. Inoculum of single-spore isolates was produced on sterilized sorghum seed. After 14 days of incubation at 20 to 22°C and a 12-h photoperiod, the sorghum seed was assayed to determine colonization incidence by transferring seeds to PDA. In all trials, sorghum seed was 100% infested. Infested sorghum seeds (35) were placed in potting soil at 2 cm beneath each seed of the susceptible soybean cv. Williams 82 (4). Noninfested sorghum seed was used for a noninoculated control. Three trials were performed, each using 15 replicates of several fungal isolates and 15 replicates of the noninoculated control. Plants were grown in water baths located in a greenhouse (trial 1) and in a growth chamber (trial 2) and both maintained at an average temperature of 25°C with a 14-h photoperiod (2). The third trial was conducted in the growth chamber without a water bath with the same temperature and light regimen. In all environments, inoculated plants developed chlorotic spots 14 days after planting. After 21 days, symptoms progressed to a range of chlorotic mottling to interveinal chlorosis and necrosis. Foliar and root symptoms that resembled those on the original plant samples infected with F. virguliforme appeared on 88% of inoculated plants. Isolates that resembled the original F. virguliforme were recovered from 75% of inoculated plants and from 88% of plants showing symptoms. No symptoms were observed and no isolates were recovered from noninoculated plants. There was a statistically significant difference between inoculated and control plants (P < 0.001) based on the presence of symptoms and isolation success using the Goodman χ2 analysis. The confirmation of the presence of SDS in five counties suggests that the disease is widespread in Wisconsin and could become a serious threat to soybean production in the future. References: (1) T. Akoi et al. Mycoscience 46:162, 2005. (2) R. Y. Hashmi et al. Online publication. doi:10.1094/PHP-2005-0906-01-RS. Plant Health Progress, 2005. (3) K. W. Roy et al. Plant Dis. 81:259, 1997. (4) J. C. Rupe et al. Can. J. Bot. 79:829, 2001.

Soybean cyst nematode (Heterodera glycines Ichinohe) is the most damaging pathogen of soybean [Glycine max (L.) Merr.] in the United States. Observations in fields suggest that high H. glycines population densities are associated with high soil pH, but H. glycines and soil pH have not been linked to soybean yield. The objective of our study was to assess the relationship between soil pH and H. glycines population densities and subsequent effect on yield. Experiments were conducted in Wisconsin from 1997 to 2000 and in Iowa from 1996 to 1998. Results were consistent among the experiments and showed a positive correlation between soil pH and H. glycines population densities and a negative correlation between yield and both soil pH and H. glycines population densities in both states. In the Wisconsin experiment, yield of both H. glycines–resistant and H. glycines–susceptible cultivars decreased as pH increased, but the decrease was less with H. glycines–resistant cultivars. Overall, results indicate that H. glycines population densities and the impact of nematode population densities on soybean yield are related to soil pH; however, the mechanism of these interactions is unknown.