Brown Stem Rot

Overview: Brown stem rot, first reported in Illinois in 1944, is widespread in Canada and in the midwestern and some southeastern states of the United States. The host range is limited to adzuki bean, mung bean, which, develops a vascular disease similar to brown stem rot in field plots in Illinois and Wisconsin, and soybean. Yield losses up to 25% may occur primarily through the reduction in number and size of seeds. Yield losses are greatest when wet cool weather during the plant pod-fill stage is followed by hot, dry weather.

Symptoms: Infected plants normally do not exhibit external symptoms before early pod set and leaf symptoms generally become apparent at the R3 to R4 growth stages. The tissue between the leaf veins turn yellow and brown, and a narrow green border may outline the veins. A dark brown discoloration of the vascular elements and pith, extending up from the roots or crown is evident in longitudinally split stems. As plants mature, the vascular browning becomes continuous throughout the stems of susceptible cultivars.

Causal Organisms: Brown stem rot is caused by Phialophora gregata. The fungus grows slowly on soybean stem extract agar. Radial growth rate is a good initial diagnostic test to distinguish the pathogen from other fungi it resembles. Isolates of Acremonium and Plectosporium spp. that can be confused with P. gregata grow much faster and sporulate sooner on both soybean stem extract and bean pod agar. Isolates vary in cultural characteristics, growth rate in culture, sporulation, virulence, and the severity of symptoms they produce. Highly virulent isolates can cause premature death of plants, while less virulent isolates can cause either internal stem vascular browning or mild leaf symptoms.

Disease Cycle: P. gregata survives in soybean stem residue and in soil. Survival of P. gregata is associated closely with speed of residue decomposition. Mycelium of P. gregata enters plants through main and lateral roots and slowly grows upward in the xylem vessels. The spread of conidia from the xylem stream to other plant parts has been postulated as the primary means of spread within diseased plants. Mycelium within xylem vessels varies from a few strands to a solid mass of hyphae occupying the entire lumen. The fungus readily colonizes the leaf vascular system and the pathogen can be isolated from leaf tissue.

Management: Resistance has been reported in the following soybean plant introductions (PIs): Rbs1 gene, L78-4094, 84946-2 and 90138; Rbs2 gene, 423930A, 437490A, 4377685D, 437883 and 90138; and Rsb3 gene, 437685D, 437970, 86150, and 90138. Other PIs that show resistance are: 424285A, 424353, 424611A, 437327, 437366, 437475, 437497, 437685D, 437934A, 437970, 86150, L84-5873, L84-5932, and LL-89-605. In addition, soybean germplasm lines with the Rbs1 gene, L845932, LN-7579 and LN80-9789, Rbs2 gene, LN86-1505 and LN86-1947, or Rbs3 gene, L84-5873 have been released for use in cultivar development. Cultivars with resistance, A20, Archer, Asgrow 3733, Bell, BSR101, BSR201, BSR301, BSR302, Chamberlain, Fayette, and Jack also are available.

Researchers: At the Laboratory for Soybean Disease Research, Dr. Monte Miles is conducting research on this disease.