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Spring dead spot is a destructive disease of bermudagrass turf in climates where the host is exposed to freezing temperatures during winter dormancy. The disease is the result of a complex interaction between a dormant host plant, fungal pathogens in the genus Ophiosphaerella, and environmental conditions. Although progress has been made in our understanding of the individual factors that determine spring dead spot development, we must begin to understand how factors interact to influence the disease. This knowledge will facilitate the development of effective and integrated management plans for spring dead spot in bermudagrass turf. Introduction Bermudagrasses (Cynodon spp. and interspecific hybrids) are among the most widely cultivated grass species worldwide. They are also among the most versatile grasses on the planet, being used for a variety of purposes including erosion control, forage, landscapes, golf courses, athletic fields, and other recreational areas (Fig. 1). These warm-season (C4), perennial grasses grow vigorously in nearly all types of soil, exhibit excellent tolerance to heat and drought, and produce a dense, uniform turf that is resistant to traffic and wear (2,30,35). Today, most improved turfgrass cultivars of bermudagrass are actually hybrids of common bermudagrass [Cynodon dactylon var. dactylon (L.) Pers.] and African bermudagrass (Cynodon transvaalensis Burt-Davy) (30). These hybrids are sterile triploids (2n = 27) and typically do not produce viable seed, and therefore must be propagated vegetatively via sod or sprigs (Fig. 2). Hybrid bermudagrasses are ideal for use as a turfgrass because they combine the fine leaf texture, upright growth habit, and excellent density of C. transvaalensis with the aggressive growth habit and pest tolerance of C. dactylon (2). Fig. 1. Bermudagrasses are incredibly versatile grass species; applications include erosion control, forage, landscapes, golf courses, and athletic fields. On golf courses, cultivars of bermudagrass are available for use on tees, greens, fairways, and roughs. 10 July 2009 Plant Health Progress Compared to other turfgrass species, bermudagrasses exhibit excellent resistance or tolerance to most pest problems. In fact, there are very few fungal diseases that warrant management. One notable exception is a disease called spring dead spot, caused by fungi in the genus Ophiosphaerella. Each year, spring dead spot causes widespread damage to bermudagrass turf in regions where the turf is exposed to freezing temperatures during winter dormancy. The disease is particularly common and destructive throughout much of the turfgrass transition zone in the United States and in other countries such as Australia, New Zealand, Italy, and Argentina (14,20,26). As the name implies, symptoms of spring dead spot first appear in the spring, when bermudagrass resumes growth from its normal winter dormancy. As the stand of turf transitions from its dormant, brown appearance to one of actively growing, green plants, circular patches or rings of turf appear to remain dormant (Figs. 3 to 5). The roots, rhizomes, and stolons in affected patches are sparse and necrotic (Figs. 6 to 7). Although bermudagrass is well known for its aggressive growth habit and ability to spread quickly, recovery from spring dead spot injury is very slow. The turf in affected patches is often completely dead, so recovery occurs primarily by spread of stolons and rhizomes inward into the patch from the outside perimeter (Fig. 8). In severe cases, complete recovery may not occur in a single growing season. Fermanian et al. (12) found evidence of a toxin in methanol extracts from SDS infested soil that reduced bermudagrass seed germination, shoot growth, and root development, and Venkatasubbaiah et al. (50) identified six metabolites produced by O. herpotricha in liquid culture that caused necrosis of bermudagrass leaves. Application of dinitroanaline herbicides in the spring may also slow spring dead spot recovery due to inhibition of root growth (25). Fig. 2. Most turfgrass areas are established with hybrid bermudagrasses, which must be propagated vegetatively by sod or sprigs. Sprigs are sections of tillers, stolons, and rhizomes, which can be created by shredding pieces of sod. The sprigs are then spread uniformly, then "crimped" into the soil. Fig. 3. Symptoms of spring dead spot appear in the spring as soon as the bermudagrass begins to grow. Fig. 4. As the bermudagrass resumes growth, circular patches of turf appear to remain dormant. The dormant foliage in affected patches may persist for several weeks. 10 July 2009 Plant Health Progress Fig. 5. Eventually, the dormant foliage in spring dead spot patches collapses, leaving sunken depressions in the turf stand that may persist for several months. Fig. 6. Necrosis of roots, rhizomes, and stolons is evident upon the appearance of spring dead spot symptoms. The majority of pathogen activity is thought to occur in the fall, winter, and spring prior to the onset of disease symptoms. Fig. 7. A significant reduction in root depth is noted in spring dead spot patches (left) as compared to healthy turf (right) (Photo courtesy E. L. Butler). Fig. 8. Recovery from spring dead spot injury is very slow, and may take the entire growing season in severe situations. Although some bermudagrass tillers within the patch may survive, most recovery occurs via spread of stolons into the patch from the outer perimeter. 10 July 2009 Plant Health Progress Although spring dead spot is a severe and persistent problem in the turfgrass industry, relatively little is known about its biology, epidemiology, and management. The slow progress hasn't been for a lack of effort. Many researchers across the world have devoted their careers, or a significant portion of them, to the study of spring dead spot and its causal agents. Rather, the complexity of the spring dead spot pathosystem has hindered research progress. Many factors interact to facilitate spring dead spot occurrence, including multiple pathogen species, a host that undergoes a dormant state during winter, freezing temperatures, soil types, thatch accumulation, cultivar susceptibility, and cultural management practices. Historical Perspective Spring dead spot was first observed in Oklahoma by a golf course superintendent in 1936 (53), during a time in which the game of golf was becoming a popular meeting place for the nouveau riche of America (21). Dead, circular areas were repeatedly observed in bermudagrass swards as they were greening up from dormancy following the harsh Oklahoma winter months. Symptoms of this springtime disease became so prevalent in bermudagrass lawns, parks, and golf courses that in the 1950s, D. F. Wadsworth and H. C. Young, of the Department of Botany and Plant Pathology, Oklahoma State University, referred to the disease as spring dead spot (53). At this time, the causal agent was unknown. Wadsworth and Young speculated that the disease was caused by an unidentified Helminthosporium species isolated from rotted roots. With raised awareness, reports of spring dead spot came from Pennsylvania, Arkansas, Missouri, and Nebraska (21). Wadsworth and Young observed that spring dead spot was most prevalent on well-fertilized, high quality bermudagrass turfs, which led to the first investigations of the relationship between fertilization practices and spring dead spot development. Following three years of study, however, the results were inconclusive (21,53). By the mid-1960s, spring dead spot had become a widespread problem in the suburbs of Atlanta on lawns that were sodded with 'Tifway' hybrid bermudagrass (21). Although the disease had also been observed on bermudagrass golf courses in Georgia, the demands of homeowners provided incentive to develop a spring dead spot research program at the University of Georgia (21). The emphasis of this research was placed on chemical control, which included multiple fungicide applications throughout the growing season. Following three years of research, it was determined that chemical control results were too inconsistent to make definitive recommendations (21). Cultural practices were also evaluated, with the only successful approach resulting from tilling deep into the root zone to stimulate new sod growth. The causal organism was not yet identified at this time. Kozelnicky (21) and others isolated species of Helminthosporium, Pythium, Fusarium, and Curvularia from rotted bermudagrass roots. However, the disease was not reproducible in greenhouse or field inoculations with these fungi. A similar patch disease of common bermudagrass (Cynodon dactylon), also known as "couch grass," was being investigated in Australia in the 1960s. Ophiobolus herpotrichus (Fr:Fr) Sacc. & Roum., a dark-mycelium producing root-rot fungus was identified by A.M. Smith as the causal organism (54). Subsequently, Smith (33) identified a second root-rot fungus, Leptosphaeria narmari J.C. Walker and A.M. Smith, and determined that it was more prevalent in Australia. In the meantime, a taxonomic review conducted by Walker and Smith determined that the fungus originally identified as O. herpotrichus more closely resembled a Leptosphaeria, and thereby renamed the fungus Leptosphaeria korrae J.C. Walker and A.M. Smith (54). Smith determined the optimum temperature for growth of L. narmari and evaluated fungicides for controlling spring dead spot in couch grass that included mercuric chloride, phenyl mercury acetate, methyl arsine oxide, thiram, and nabam (41). Of these, thiram and nabam provided control throughout the season. 10 July 2009 Plant Health Progress Spring dead spot research in the United States was gaining momentum in the 1980s. Researchers in California and Maryland independently isolated and identified L. korrae as the causal organism of spring dead spot (6,11). Attempts to isolate L. narmari and L. korrae from bermudagrass exhibiting spring dead spot sympt

Spring Dead Spot of Bermudagrass: A Challenge for Researchers and Turfgrass Managers