Abstract

Blast disease (gray leaf spot) of perennial ryegrass (Lolium perenne L.), caused by Pyricularia grisea (Cooke) Sacc., in golf course fairways in Pennsylvania, was first reported in 1991 (1). The disease was primarily confined to the southeastern region of the state. In August and September 1998, severe outbreaks of blast disease occurred in perennial ryegrass fairways in numerous golf courses in the same region in Pennsylvania. Additionally, in 1998, the disease was diagnosed in ryegrass fairways for the first time in the western region of the state, where serious disease outbreaks occurred. The disease develops on leaf blades as small, watersoaked lesions that become necrotic spots. The spots expand rapidly, and develop into gray, grayish-brown, or light brown, circular spots with purple to dark brown borders often surrounded by a yellow halo on the leaf blades. As the disease progresses, the circular necrotic spots coalesce, become irregular in shape, and cause partial (tip blight) or complete blighting of the leaf blades. The blighted blades may often appear twisted. Turfgrass loss due to the disease was over 90% in several golf courses. During the 1998 epidemics, a survey was conducted in the affected regions, which included three golf courses in western Pennsylvania and 15 golf courses in southeastern Pennsylvania. P. grisea was consistently isolated from the symptomatic ryegrass leaf blades of turf samples (12 to 28 samples per location) collected from the blighted fairways. Of the 122 isolates of P. grisea collected from the 18 golf courses, seven isolates (two from western Pennsylvania and five from southeastern Pennsylvania) were selected for pathogenicity assays. Five Pennfine perennial ryegrass plants were grown in each Cone-Tainer (4 mm in diameter) that was filled to 1 cm below the rim with granular calcine clay medium (Turface MVP; Allied Industrial Material, Buffalo Grove, IL). Three weeks after seeding, grasses were fertilized with water-soluble 20-20-20 fertilizer (1.3 g per liter of water) once a week to field capacity of the growing medium. Treatments (the isolates) were arranged as a randomized complete block with four replications (a Cone-Tainer per replication). Six-week-old ryegrass plants were atomized with an aqueous suspension of P. grisea conidia (approximately 8 × 104 conidia per ml of sterilized, distilled water) until the leaves were completely wet. Individual Cone-Tainers were placed in clear polyethylene bags, enclosed, and were placed in an incubator that was maintained at continuous 28°C and 12-h-day fluorescent light (72 μE s-1 m-2). Three days after inoculation, water-soaked lesions (<2 mm in diameter) developed on leaves of the ryegrass inoculated with each isolate of P. grisea. No lesions developed on leaves of the control plants. Seven days after inoculation, the polyethylene bags were removed, and disease incidence (percent infected leaves) was assessed. P. grisea was isolated from the necrotic lesions or the blighted leaf blades of every plant inoculated with the fungus. This is the first report of blast disease outbreak in golf course fairways in western Pennsylvania. The impact of blast disease epidemics on golf courses in the northeastern United States in 1998 was significant, and caused serious concern to turf managers. The survey indicates that blast disease of perennial ryegrass may be emerging as a new problem for the turfgrass industry in the northeastern United States. Reference: (1) P. J. Landschoot and B. F. Hoyland. Plant Dis. 76:1280, 1992.

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