Off the Record: The long and complicated history of spring dead spot research

The symptoms of spring dead spot (SDS) were first described in a publication from Oklahoma in the 1950s, although information indicates that the disease was present in Oklahoma as early as 1936.

Photo: Mike Kenna, Ph. D.

The cause of the disease was unclear, but certain fungi seem to be involved. At the time, pathologists in Australia and California believed the causal pathogen to be Leptosphaeria namari and Leptosphaeria korrae; however, there were doubts that this was true.

Leon Lucas, Ph.D., North Carolina State University, and postdoctoral research associate Bert McCarty, Ph.D., received funding from the USGA for SDS research. In 1986, they coordinated fall fungicide trials in Alabama, North Carolina and Virginia on fairways with SDS in the spring.

Rubigan (fenarimol) and Tersan (benomyl) provided the best control. Also, avoiding late fall nitrogen fertilization and preventing excessive thatch accumulation were thought to decrease disease occurrence.

During the 1990s, the USGA supported research to evaluate alternative disease control methods in response to environmental concerns and increasing restrictions on chemical pesticides.

A new theory

In 1991, William Casale, Ph.D., and Howard Ohr, Ph.D., University of California, Riverside, sampled sites where the disease declined naturally. They thought the decline may be due to the increased activity of indigenous microorganisms One hundred forty-seven microbial organisms were isolated from a UCR bermudagrass plot showing a decline of SDS caused by Leptosphaeria korrae. The disease had spread sufficiently so that green, symptomless patches were evident in the center of brown, diseased areas. They performed a comparison of microbial profiles from each of these areas.

Among this collection were 41 bacteria and 19 fungi that inhibited Sclerotium rolfsii growth (cause of southern blight) by antibiosis and six fungi that parasitized S. rolfsii in petri-dish experiments. Growth of Rhizoctonia solani (cause of brown patch) was inhibited by 25 bacteria and 26 fungi from the collection in the lab. Greenhouse studies narrowed the biocontrol candidates to one bacterial and one fungal isolate for field testing on SDS.

In a 1993 field experiment, the researchers compared bacterial and fungal isolates to fungicide treatments (e.g., Rubigan, Lynx and Bayleton). Unfortunately, there was no significant control compared to the untreated using the biocontrol agents.

GOTCHA!

It was not until 1989 that Ophiosphaerella species were discovered as the causal agent of SDS in bermudagrass. Research by Ned Tisserat, Ph.D., Kansas State University, identified this fungus as the primary pathogen causing SDS symptoms in bermudagrass. Identifying Ophiosphaerella as a causal agent marked a significant step in understanding the disease and developing effective management strategies for controlling SDS.

We now know that three closely related root-rotting fungi called Ophiosphaerella korrae (previously called Leptosphaeria korrae), O. herpotricha and O. narmari cause SDS. It’s essential to determine which Ophiosphaerella species is the cause of SDS at a specific location because these pathogens may differ in seasonal development, sensitivity to fungicides and aggressiveness to individual bermudagrass cultivars.

Research in the early and mid-2000s by Nathan Walker, Ph.D., Oklahoma State University, showed that the fungus was able to colonize roots without causing cell death (necrosis) in the early stages of infection of Midlawn and all stages of C. transvaalensis.

However, infection of Tifway 419 roots almost always resulted in necrosis. Thus, bermudagrass susceptibility may result from its cell death response, while C. transvaalensis tolerance could stem from nonrecognition to a fungus presence.

Selecting cold-tolerant cultivars, mapping spring disease outbreaks for fall fungicide treatments, managing thatch and reducing fall nitrogen applications can significantly reduce SDS.