Ophiosphaerella spp. (spring dead spot on bermudagrass)

Taxonomy

Domain	Eukarya
Kingdom	Fungi
Phylum	Ascomycota
Subphylum	Pezizomycotina
Class	Dothideomycetes
Subclass	Pleosporomycetidae
Order	Pleosporales
Family	Phaeosphaeriaceae
Genus	Ophiosphaerella

Scientific Name

Ophiosphaerella herpotricha

Scientific Name Synonyms

Ophiobolus herpotrichus

Common Name

Ophiosphaerella fungus

Author: Lee Miller, University of Missouri

Reviewed by:Name, Organization

Pathogen

Spring dead spot is caused by three different species in the genus Ophiosphaerella, which are primarily soil inhabitants. These fungi produce asci and ascospores in erumpent pseudothecia, which are rarely observed in nature (9). Pseudothecia are black, produced on stolons and roots, and are usually closely packed with a globose body and a thick neck. Ascospores are 35-180 μm long (depending on species), filiform, slightly twisted in a bundle, and parallel to each other (2). Dark, flat brown infection mats of aggregated hyphae, approximately 60-400 μm in diameter, are more often observed in nature, along with a mycelial network of dark hyphae surrounding infested plant tissue (4). Due to the difficulty in observing the required morphological characters, molecular techniques are often relied upon for identifying spring dead spot pathogens to the species level (5).

Symptoms and Signs

Spring dead spot symptoms are first evident in the spring as uninfected turfgrass breaks dormancy and greens up. The disease appears as randomly distributed, straw-colored, mostly circular patches ranging from a few inches to several feet in diameter. The turfgrass in these patches is often completely dead, with infested roots, stolons, and rhizomes appearing black, brittle and severely rotted. Dense dark-brown to black networks of hyphae are observed on infected plant parts.

Ecology and Spread

Ophiosphaerella spp. are known as ectotrophic root-infecting fungi, indicating superficial growth and colonization of these pathogens along the surface of below-ground plant tissues before infection. Hyphae directly infect root cortical tissue, stolons or rhizomes resulting in localized necrosis (9). After infection, freezing temperatures and resultant bermudagrass dormancy are required for symptom occurrence and plant death. The role of ascospores in pathogen dissemination is not fully understood. Long distance dissemination may be facilitated by ascospore transport in wind or water, or through the transport and establishment of infested vegetative plant parts. Pathogen dissemination over shorter distances may occur as healthy roots, rhizomes or stolons come into contact with infected plant tissues, or through pathogen growth over small distances in the soil. Ophiosphaerella spp. also cause disease on alternative hosts, such as necrotic ring spot caused by O. korrae on Kentucky bluegrass and fescues.

Geographic Distribution

Spring dead spot is most prevalent and damaging on Cynodon dactylon (bermudagrass) and its hybrids, but has also been documented on Buchloë dactyloides (buffalograss) (6) and some cultivars of Zoysia japonica (zoysiagrass) in North America and Japan (1, 7). The disease is common throughout the United States, Australia, Japan, and New Zealand in regions where low temperatures induce dormancy of warm-season turfgrasses. For reasons that are unclear, Ophiosphaerella spp. are not evenly distributed, with O. narmari commonly found in Australia and New Zealand, O. herpotricha most prominent in the Midwestern U.S., and O. korrae most prevalent in California and the Southeastern U.S. (9).

Management

Spring dead spot control with fungicides is erratic, and few control options are available that are both effective and economically feasible. Management of the disease with cultural practices centers on proper nitrogen fertility, regular cultivation practices and soil pH modification.

Cultural Control

Due to the link between freezing temperatures and disease incidence, management practices that increase bermudagrass cold tolerance generally reduce disease. Increasing mowing height prior to winter dormancy may reduce spring dead spot severity in some vegetative cultivars. Fertilizing late in the fall may prolong shoot growth, predispose the plant to freezing damage, and result in higher spring dead spot severity. Heavy fall applications of potassium have produced varying effects on spring dead spot severity, and use of any nutrient beyond what is required for optimum growth is not recommended. The use of acidifying fertilizer sources, such as ammonium sulfate, has reduced spring dead spot incidence caused by O. herpotricha. Conversely, spring dead spot caused by O. korrae may be reduced with calcium nitrate applications (8). Cultivation practices, such as routine hollow-tine aerification and verticutting, that improve drainage and cause rhizome and stolon regrowth have also been demonstrated to reduce spring dead spot incidence.

Host Resistance

Although there are no truly resistant cultivars, bermudagrass cultivars with improved cold tolerance have been shown to exhibit less spring dead spot severity than cold sensitive cultivars. Some of the cold tolerant cultivars that have demonstrated partial spring dead spot resistance include ‘Midfield’, ‘Midlawn’, and ‘Tifsport’ (3).

Diagnostic procedures

Spring dead spot is most often diagnosed based on symptom timing combined with the observation of black brittle roots, rhizomes, and stolons surrounded by a dark network of hyphae. Ophiosphaerella spp. grow slowly in culture and are difficult to isolate. Due to the difficulty in obtaining morphological characters required for identifying Ophiosphaerella to the species level, sequencing the ITS region or utilizing species-specific primers is most often used for this purpose (5, 9).

Resources and References

• Beard, J. B., and Tani, T. 1997. Color Atlas of Turfgrass Diseases. Ann Arbor Press, Chelsea, Michigan.
• Couch, H. B. 1995. Diseases of Turfgrasses. Krieger Publishing, Malabar, FL.
• Martin, D., Walker, N., Taliaferro, C., Bell, G., Wetzel, H., III, and Tisserat, N. 2006. Evaluation of NTEP bermudagrass trial entries for spring dead spot resistance. in ASA-CSSA-SSSA International Meetings, Indianapolis, IN.
• Smiley, R. M., Dernoeden, P. H., and Clarke, B. B. 2005. Compendium of Turfgrass Diseases. APS Press, St. Paul, MN.
• Tisserat, N., Hulbert, S. H., and Sauer, K. M. 1994. Selective amplification of rDNA internal transcribed spacer regions to detect Ophiosphaerella korrae and O. herpotricha. Phytopathology 84:478-482.
• Tisserat, N., Wetzel, H., III, Fry, J., and Martin, D. L. 1999. Spring dead spot of buffalograss caused by Ophiospharella herpotricha in Kansas and Oklahoma. Plant Disease 83 (2):199.
• Tredway, L. P., and Butler, E. L. 2007. First report of spring dead spot of zoysiagrass caused by Ophiosphaerella korrae in the United States. Plant Disease 91 (12):1684.
• Tredway, L. P., Soika, M. D., and Butler, E. L. 2009. Response of spring dead spot caused by Ophiosphaerella korrae and O. herpotricha to fertilization programs and preventive fungicide applications. Phytopathology 99 (6):S129.
• Tredway, L. P., Tomaso-Peterson, M., Perry, H., and Walker, N. R. 2009. Spring Dead Spot of Bermudagrass: A Challenge for Researchers and Turfgrass Managers. Plant Health Progress:1-18.

Acknowledgment

• National Institute of Food and Agriculture, U.S. Department of Agriculture, under Agreement No. 2011-41530-30818 as part of "Diagnostic Image Series Development for Supporting IPM in the North Central Region" (USDA-NIFA-RIPM-003349)