Spring Dead Spot of Bermudagrass

Ned Tisserat   
Extension Specialist, Plant Pathology

Symptoms

Spring dead spot is a destructive disease of common bermudagrass (Cynodon dactylon) and bermudagrass hybrids throughout the northern range of its adaptation in the United States. Three different root-rotting fungi, called Ophiosphaerella herpotricha, O. korrae, and O. narmari, are responsible for the disease and all three pathogens occur in Kansas. However, O. herpotricha appears to be the most common cause of the disease in our region. Spring dead spot also infrequently occurs on buffalograss (Buchloe dactyloides). Cool-season grasses such as ryegrass (Lolium perenne, bentgrass (Agrostis), and tall fescue (Festuca arundinacea) are not susceptible to the disease. However, O. korrae causes a late spring and fall patch disease of Kentucky bluegrass (Poa pratensis) called necrotic ringspot.

Spring dead spot may occur on bermudagrass lawns of all ages, although it typically appears 3 to 4 years after the turf has been established. The disease results in the formation of circular or arc-shaped patches of dead turf in early spring as bermudagrass breaks winter dormancy. The dead patches, which are slightly depressed and straw-colored, may range in size from several inches to several feet in diameter. The patches normally are randomly distributed throughout the lawn. Roots and stolons of affected plants are dark brown to black and are severely rotted. It may be necessary to dig up a piece of sod near the margin of the dead area and wash it in water to observe this symptom. During the summer, broadleaf weeds and other weedy grasses invade and colonize the bare soil, resulting in a clumpy or patchy appearance to the lawn. Bermudagrass slowly colonizes the bare areas, and by late summer there may be little or no evidence of the disease. Dead patches reappear the following spring in the same locations. Over a number of years, the patches can become quite large, coalesce, and develop arc-like patterns in the lawn. After 7 to 10 years, disease severity may begin to decrease to the point where the disease no longer appears in the lawn.

Figure 1. Spring dead spot of bermudagrass

Figure 2. Spring dead spot of bermudagrass

Conditions

Spring dead spot fungi colonize roots, stolons, and crowns of bermudagrass plants in late summer or fall. Roots infected with the fungus turn dark brown to black as a result of extensive fungal growth in and on the roots. Although most fungal colonization occurs in autumn, foliar symptoms do not develop until late spring. During winter dormancy, infected bermudagrass roots or crowns are either killed directly by the fungus or are predisposed to desiccation or cold temperature injury. Root colonization by the pathogen decreases the cold hardiness of the bermudagrass. The disease tends to be more severe on high maintenance bermudagrass lawns. Excessive nitrogen fertilization during the summer months enhances symptom development the following spring.

Figure 4. Microscopic view of mycelium of spring dead spot fungus on bermudagrass root.

Figure 3. Root colonization of bermudagrass by fungi that
cause spring dead spot. A healthy bermudagrass root system is on
the left.

Control

Several cultural methods may limit the severity of spring dead spot. The basic philosophy is to maintain a vigorous but not excessively lush turf. Lawns should be dethatched yearly when the bermudagrass is actively growing to promote good rooting. Core aeration may also reduce spring dead spot severity. Avoid excessive nitrogen fertilization. Application of excessive amounts of nitrogen (more than 4 to 5 lb active nitrogen/1000 sq ft/year) will increase disease severity. Nitrogen applications should not be made after early August because this will increase turfgrass susceptibility to cold temperature injury. Application of ammonium sulfate from June to August at monthly intervals (1 lb N/1000 sq ft) helps acidify the soil and reduces severity of spring dead spot. Heavy applications of fast-release nitrogen fertilizers should be avoided during the summer following a severe outbreak of the disease. Application of .8 lb of potassium chloride (KCl) at monthly intervals during the summer has also been shown to reduce spring dead spot severity.

Bermudagrass cultivars vary markedly in susceptibility to spring dead spot. None are immune to the disease, but several seeded and vegetatively propagated cultivars exhibit reduced patch sizes and faster summer recovery than susceptible varieties. Resistant vegetative cultivars include Midiron and Midlawn. Another popular variety called Quickstand is moderately susceptible to SDS. The seeded cultivars Guymon, Yukon, and Reveile also show moderate resistance. Guymon has a coarse texture and is not recommended for home lawns in Kansas. Several other experimental seeded selections from Oklahoma State University also appear promising. Avoid using Arizona common bermudagrass, Cheyenne, Jackpot, Oasis, Poco Verde, Primavera, Sonesta, Tifton 10, Tifway (Tifton 419) Tropica, Vamont or Sunturf cultivars.

Several fungicides, including fenarimol (Rubigan), propiconazole (Banner) and azoxystrobin (Heritage) are labeled for control of spring dead spot. However, disease suppression with these fungicides has been erratic in Kansas trials. September applications of these fungicides have, in some years, reduced disease severity and enhanced recovery of the turf in the spring, but they did not completely control spot development. Therefore, fungicide applications are not currently recommended for control of spring dead spot in our state.

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Web updated 9/01/06
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