Project title 

Disease management strategies for controlling spring dead spot in a ‘Tifway’ bermudagrass fairway

 

Rational

Spring dead spot (SDS) is a serious root-rot disease of bermudagrass, and particularly when the grass is managed intensively in golf course settings.  Spring dead spot occurs more frequently in the states within the northern tier of the bermudagrass transition zone.  There are over 2,200 golf courses located throughout the southeastern United States (10); it is estimated that 70 to 75% of those golf courses are symptomatic for SDS (personal communication, Mr. Patrick O’Brien, USGA Green Section, Southeast Director).  The cost of applying fungicides for control of SDS is estimated to be well in excess of $3,000,000 per year. 

 Weed management and the selection of a pre-emerge for spring application is affected by SDS-diseased fairways.  Necrotic patches that result from SDS typically green up in the summer from lateral bermudagrass growth of adjacent, healthy turf.    Dinitroanilines, routinely applied as a spring pre-emerge for weed control, are mitotic inhibitors that delay lateral growth of bermudagrass into necrotic patches.  As a result, a more costly pre-emerge, Oxadiazon, which does not restrict rooting of bermudagrass stolons, must be applied for weed control.

 Spring dead spot has been a problematic disease of bermudagrass for more than a half century.  Turfgrass managers continue to develop strategies for controlling SDS in bermudagrass.  Although progress has been made to identify the causal organism(s) and define a disease profile, controlling SDS continues to require additional research.  The optimum temperatures for growth of Ophiosphaerella korrae, a causal organism of SDS, range between 77 and 86^oF (5,2).  Bermudagrass plants infected by O. korrae and exposed to cold temperatures under controlled environmental conditions have a greater degree of SDS symptom expression (2,8).  To date, however, the affects of soil temperature and soil moisture on SDS have not been examined in replicated studies in the field.

 Benefits of research to golf course superintendents

Disease management strategies for controlling spring dead spot (SDS) of bermudagrass will be enhanced based on results of this proposed research.  The precise time of year the SDS fungus is actively infecting bermudagrass roots will be identified.  The influence of soil temperature and soil moisture on occurrence of infection and disease expression of SDS in a Tifway bermudagrass fairway will be determined.  These environmental factors may be used as a tool for predicting occurrence of infection of bermudagrass roots.  This approach is a key component of disease management.  The resultant information can be applied to a specific time within the growing season for initiating aggressive disease management control measures.  Integrated with temporal data, cultural management practices will be identified that promote plant health. 

 Objectives

1.  Define environmental factors in a ‘Tifway’ bermudagrass fairway that promote infection of bermudagrass by Ophiosphaerella korrae, a causal organism of spring dead spot.

 2.  Evaluate cultural management practices for reducing the severity of spring dead spot in bermudagrass.

 Methods and materials

The study will be located at Old Waverly Golf Course (site of the 1999 U.S. Women’s Open), West Point, MS.  The number 9 fairway of ‘Tifway’ 419 bermudagrass with a history of severe spring dead spot is the site of this proposed research.  The bermudagrass is managed intensively.  Spring green-up is typically 20 days earlier than other bermudagrasses in the area and dormancy is delayed in the fall due to high management inputs.  Spring dead spot has been observed every spring on this fairway for over ten years.  Each year new necrotic patches appear and recurring necrotic patches enlarge in diameter.  Based on global positioning mapping of the fairway boundary, over two thirds of the fairway had severe symptoms of SDS.  A SDS disease severity rating of 10 (scale = 1-10, where 10 is severe) was recorded in April of 2004.  Samples were collected from the margins of necrotic patches.  Roots were washed free of soil and thatch debris, surface disinfested and plated onto 1/4 strength potato dextrose agar to recover O. korrae.  Confirmation of the SDS causal organism was obtained using polymerase chain reaction (PCR) protocol.

 In July of 2004, a study was initiated in an 84' x 69'  area within the diseased fairway.  Seven treatments were initiated in individual 12' x 15' plots, replicated four times in a randomized complete block design.  Based on soil (pH 6.9) and leaf tissue analyses and an excessive thatch layer, the following treatments were included:

 1.  Core aerification (3/4" x 4" hollow tine); 3 to 4 aerifications per growing season

2.  Chelated manganese (5 lb/acre-growing season)

3.  Verticutting; 3 to 4 verticuttings per growing season

4.  Elemental sulfur (200 lb/acre-growing season)

5.  Eagle (myclobutanil) fungicide application 30-d prior to dormancy

6.  Core aerification plus top-dressing with sand/reed sedge peat; 3 to 4 aerifications and top-dressing per growing season

7.  Untreated control

In September of 2004, a chelated manganese treatment was applied in 1 lb  applications on a bi-monthly schedule and elemental sulfur was also applied as a treatment.  Two core aerification treatments, one included top-dressing, and a verticutting treatment were initiated.  A fungicide application of Eagle will be applied 30 days prior to dormancy (1^st week of November) at a rate of 1.2 oz product per 1,000 square feet. 

 Soil temperature and soil moisture will be monitored using Spectrum’s Watchdog™ weather monitoring sensors and data loggers.  Watermark soil moisture sensors and external soil temperature sensors were placed within the root zone/soil interface of the untreated control plots.  These sensors are connected to Watchdog data loggers that record on a 120 min schedule.  All sensors will remain in place and record data throughout the duration of the study.

 Turfgrass samples (2" x 4") will be collected on a monthly basis beginning September 2004 and continue throughout the study.  Characteristics to be determined and  recorded from these turf samples will include depth of thatch layer, root health, shoot and root dry weights, and frequency of O. korrae isolation.

 1.  The depth of the thatch layer will be determined by measuring the thatch/mat zone.

 2.  Root health will be determined using a visual rating that is based on a scale of 0-5 where 0 = no discoloration and 5 = greater than 76% root discoloration.

 3.  Shoot and root dry weights will be determined by thoroughly washing and separating shoots and roots, drying them at 149^o F for 24 hours, then recording sample weights.

 4.  Frequency of O. korrae occurrence in bermudagrass roots will be determined by first washing roots in tap water to remove debris.  Root surface disinfestation will be carried out on root segments (0.5 in) by washing the roots in a 0.6% sodium hypochlorite solution and triple-rinsing in sterile distilled water.  Dried roots will be placed onto 1/4 strength potato dextrose agar supplemented with streptomycin sulfate and chloramphenical antibiotics.  Frequency will be based on the number of O. korrae isolates recovered from the total number of roots.

 5.  Confirmation of O. korrae will be achieved through PCR techniques described by Tisserat et al. (12).  DNA amplification of unknown isolates will be accomplished using specific O. korrae primers, OKITS1 and OKITS2.  The first phase includes extracting DNA from the unknown isolates using a Dneasy Plant Mini Kit for isolation of cellular fungal DNA.  PCR protocol of Tisserat et al. (12) will be followed.  Confirmation will be achieved when OK-primers amplify a 454-bp fragment from DNA of O. korrae isolates.

 Turfgrass quality (visual rating on a scale of 0 to 9 where 9 = best) will be recorded for all treatments in the fall (October) and spring (April).  Disease ratings (visual rating on a scale of 0 to 10 where 10 = severe) will be recorded in April.

 Expected results

This project will define the relationships between soil temperature and soil moisture and the frequency of O. korrae in bermudagrass roots maintained under fairway conditions over the course of a calendar year.  The resultant data will identify the time of the year O. korrae is actively infecting bermudagrass roots, as well as what influence soil temperature and soil moisture have on fungal activity, plant resistance, and symptom expression.

 Cultural management practices will be employed as treatments on the Tifway bermudagrass fairway to determine influences on plant health and effects on disease severity.  It will be determined whether an aggressive core aerification program can promote the development of healthy bermudagrass plants and the overall relationship to infection by O. korrae.  The benefits of top-dressing with a sand:reed sedge peat mix will be identified.  Reed sedge peat has a neutral pH that promotes beneficial bacteria and actinomycetes.  These beneficial microorganisms may have antagonistic affects on O. korrae, thereby reducing or inhibiting O. korrae activity.  Reed sedge incorporated into the root zone may promote the development of a healthy root system, thereby reducing fungal infection and/or SDS symptom expression.  Composts of this nature have been successful for controlling take-all root rot of St. Augustinegrass (personal communication, Dr. Phil Colbaugh, Plant Pathologist, Texas A&M Research Center, Dallas, TX).  Take-all root rot is caused by the ectotrophic root-infecting fungus, Gaeumannomyces graminis var. graminis.

 Applications of sulfur or manganese to bermudagrass plots will stimulate a more acidic soil solution over time.  The effect of acidic soil conditions on SDS development will be determined.  The efficacy of myclobutanil fungicide for controlling SDS will be determined.  Fungicide applications have not been a reliable single-component disease management tool for controlling SDS as compared to other turfgrass diseases.

 This project will define parameters that will lead to a better understanding of the implementation of successful disease management strategies for controlling SDS of bermudagrass.

 A graduate student (master’s level) will have extensive research responsibilities in this proposed project.  Mr. Hunter Perry will receive his Bachelor’s of Science degree Spring 2005 in Golf and Sports Turf Management from Mississippi State University.  As part of the required co-op, Mr. Perry spent eight months of 2004 at Farm Links Golf Club, Sylacauga, AL.  In addition, during  the eight month co-op, Mr. Perry was selected to serve as one of two United State Golf Association Green Section Interns for the Southeast region.  With his experience in turfgrass management, impressive academic standing, and his desire to solve problems associated with turfgrass management, Mr. Perry has the potential to become a highly motivated graduate student that can bring much success to this turfgrass pathology research program, as well as gain professional training in the area of turfgrass pathology.

 Literature review

Spring dead spot (SDS) is a serious disease of bermudagrass (Cynodon dactylon [L.] Pers.), particularly the hybrid bermudagrasses (Cynodon dactylon x Cynodon transvaalensis Burtt- Davy).  Spring dead spot has been researched for more than a half century, and there are still many ‘unknowns’ yet to be defined.  To date, three fungi from the same genus, Ophiosphaerella, have been identified as causal organisms of SDS of bermudagrass.  In the spring of 2004, Ophiospaerella. korrae was isolated from roots of a Tifway bermudagrass fairway displaying severe symptoms of SDS in Mississippi.  Polymerase chain reaction (PCR) as described by Tisserat et al. (12) was used to confirm the identification of O. korrae (unpublished).

 Spring dead spot symptoms first appear during spring green-up of bermudagrass.  This disease occurs in bermudagrasses in home lawns, sports fields, putting greens, fairways, tees, and roughs.  Necrotic patches of dead grass ranging from a few inches to several feet in diameter can be observed throughout a bermudagrass stand.  The patches remain void of healthy bermudagrass through early summer until lateral growth of adjacent bermudagrass fills in the dead spots.  These dead spots recur on an annual basis, typically becoming larger in diameter each successive year.  The stolons, crowns, and roots of infected bermudagrass plants appear black and rotted.

 It was observed during early descriptions of SDS that the disease was more severe in bermudagrass that experienced a period of dormancy (13,14).  Several research projects conducted under controlled environmental conditions resulted in similar conclusions on the influence of soil temperature on the bermudagrass-O. korrae interaction and the severity of SDS symptoms.  Endo, et al. (4) initiated Koch’s postulates by inoculating ‘Tifgreen’ bermudagrass with isolates of O. namari (15) and incubating the grasses at 55 or 75^oF.  Disease severity was greatest among Tifgreen plants exposed to 55^oF, indicating a cold temperature effect in the disease cycle.  Similarly, Crahay et al. (2) demonstrated when ‘Tufcote’ bermudagrass was infected by O. korrae, symptom expression was more severe at 59^oF compared to 77 or 86^oF.  McCarty et al. (8) concluded from their research of SDS-infected bermudagrass exposed to low temperatures that cold temperatures (23 to 27^oF) induced a higher degree of SDS symptom expression and reduced shoot development.  Nus and Shashikumar (9) reported that bermudagrass plants infected by O. herpotricha or O. korrae are more susceptible to cold damage.

Spring dead spot of bermudagrass has been associated primarily with hybrid bermudagrasses that are intensively managed.  Several management practices, or lack thereof, are considered to be contributing factors for predisposing bermudagrass to SDS.  Early control programs consisted of managing nitrogen levels for healthy turf, reducing the thatch layer, preventing compaction, managing water inputs, and applying fungicides in a preventive manner (1,6).  This disease management strategy remains in extensive use today.  Disturbance of the root zone through cultural practices has been shown to reduce disease severity (11).  Adjusting soil pH (promoting acidic conditions with compounds such as sulfur and manganese) also reduces SDS severity of bermudagrass (3).  To date, fungicides with efficacy for controlling SDS have not been an exclusively reliable tool in the SDS disease management program (6,7).

 Future research should focus on the response of bermudagrass to infection by O. korrae under natural growing conditions in the field, and determination of how this interaction can be manipulated to reduce severity of SDS in bermudagrass.

 Bibliography