Effect of pre-emergence herbicides on bermudagrass recovery from SDS

Be careful what you spray: Some pre-emergence herbicides may limit turf recovery and further weaken the turfgrass system.

Read this story in GCM's digital edition

L.L. Beck, Ph.D.; T. Cooper; A.J. Hephner; C.M. Straw; and G.M. Henry, Ph.D.
July 2013 Preemergence herbicides: clubbing

Exposure to dinitroaniline herbicides may cause
abnormal swelling (“clubbing”) of bermudagrass roots.
Photo by Jim Brosnan

Be careful what you spray: Some pre-emergence herbicides may limit turf recovery and further weaken the turfgrass system.

Spring dead spot (SDS) is a soil-borne disease caused by three closely related ectotrophic, rootinfecting pathogens: Ophiosphaerella narmari, O. korrae and O. herpotricha (1). Spring dead spot symptoms may occur on intensely managed home lawns, athletic fields, golf courses and sod farms located in the transition zone where winter temperatures are cold enough to induce bermudagrass dormancy (16,20).

Disease symptoms are most noticeable when bermudagrass breaks winter dormancy in the spring, but injury may persist into late summer  (7). Symptoms appear as well-defined, bleached, circular patches that range in size from a few inches to a yard in diameter (1,7). Turfgrass plants within the disease patches eventually collapse to the ground, leaving behind sunken necrotic areas (21). The germination of weeds in the center of disease patches may cause a decline in turfgrass aesthetic quality and reduce the playability of turf. In severe cases, bermudagrass may not fully recover from spring dead spot symptoms before the onset of winter, leaving the turf susceptible to further damage from freezing temperatures (14).

Pre-emergence herbicides

Pre-emergence herbicides are often applied to turfgrass stands in early spring to control annual grasses and broadleaf weeds (19). However, certain pre-emergence herbicides may have a negative impact on the growth of bermudagrass turf (9). The use of dinitroaniline (DNA) herbicides, such as prodiamine and pendimethalin, may cause abnormal swelling of turfgrass root tips (“clubbed-roots”), stunting of lateral root growth and/or severely pruned roots when healthy tissue comes into contact with the chemical barrier created in the upper soil profile (9,13). Other researchers (10) have observed noticeable reductions in growth and abnormal root development in bermudagrass plants treated with pendimethalin, prodiamine and dithiopyr. The dinitroaniline herbicide family exhibits low water solubility and readily binds to soil particles, so these chemistries tend to remain near the soil surface and do not leach through the soil profile (10). Therefore, the chemical barrier may remain intact for several weeks to months, until soil microorganisms and other environmental factors degrade these herbicides over time (4). As a result, using certain preemergence herbicides may interfere with bermudagrass recovery in the spring and summer from damage caused by winter desiccation, heavy traffic or disease (2).

July 2013 Preemergence herbicides: Hillcrest

Field experiments were conducted at Hillcrest CC in Lubbock, Texas,
on a Tifway fairway with a history of spring dead spot infestation.
Photos by Gerald Henry

In spring, turfgrass managers often change their focus from spring dead spot control to bermudagrass recovery from disease symptoms. Turf in the center of disease patches is necrotic, so recovery requires encroachment of bermudagrass stolons from surrounding, healthy plants (18). The presence of pre-emergence herbicides in the soil profile may inhibit the rooting of bermudagrass stolons, prolonging disease symptoms and recovery. Though research has been conducted to quantify the effect of pre-emergence herbicide applications on bermudagrass recovery from divot injury (5) and wear/traffic (2), no research has been conducted to determine the effect of pre-emergence herbicides on bermudagrass recovery from spring dead spot disease. Therefore, the objective of our research was to determine foliar phytotoxicity of bermudagrass in response to preemergence herbicide applications and evaluate the effect of spring pre-emergence herbicides on the recovery of a bermudagrass fairway from spring dead spot disease symptoms.

Evaluating bermudagrass recovery

Field experiments were conducted during spring and summer 2011 and 2012 at Hillcrest Country Club in Lubbock, Texas, on an Arch fine sandy loam (fine-loamy, carbonatic, thermic Aridic Calciustepts) soil with a pH of 8.2 and organic matter content of 1.5%. Research was located on a Tifway 419 bermudagrass [C. dactylon × C. transvaalensis (L.) Pers.] fairway with a history of spring dead spot infestation. Ophiosphaerella narmari, O. korrae and O. herpotricha were identified from soil samples collected from this location, and no fungicides were applied to the research area the previous spring in order to encourage spring dead spot disease infestation. Plots measured 5 feet × 5 feet (1.5 meters × 1.5 meters) and were arranged in a randomized complete block design with four replications. All experimental areas were mowed 24 hours before herbicide application and twice weekly thereafter at a cutting height of 0.25 inch (0.6 centimeter).

July 2013 Preemergence herbicides: application

Author Leslie Beck applies pre-emergence herbicide to a bermudagrass fairway infested with spring dead spot disease.

Herbicide treatments

Pre-emergence herbicide treatments included Barricade (prodiamine, Syngenta) at 0.651 pound/acre (0.73 kilogram/hectare); Pendulum (pendimethalin, BASF) at 2.23 pounds/acre (2.5 kilograms/hectare), Surflan (oryzalin, United Phosphorus) at 1.49 pounds/acre (1.68 kilograms/ hectare), Dimension (dithiopyr, Dow AgroSciences) at 0.499 pound/acre (0.56 kilogram/hectare), Ronstar (oxadiazon, Bayer Environmental Science) at 3.03 pounds/acre (3.4 kilograms/ hectare), Specticle (indaziflam, Bayer Environmental Science) at 0.031 pound/acre (0.035 kilogram/ hectare), and Tower (dimethenamid, BASF Corp.) at 1.49 pounds/acre (1.68 kilograms/ hectare). Pre-emergence herbicide treatment rates were chosen based on label recommendations for each herbicide.

Herbicide treatments were applied with a CO2-powered backpack sprayer equipped with XR8003VS nozzle tips (TeeJet) calibrated to deliver 32.6 gallons/acre (305 liters/hectare) at 40 psi (276 kPa). Herbicide applications were made on March 15, 2011, and March 23, 2012. A nontreated check was included for comparison. Irrigation at 0.236 inch (0.6 centimeter) was applied immediately following all pre-emergence herbicide treatments to increase infiltration into the soil profile and activate the chemistries.

Data collection

Data collected included percent bermudagrass phytotoxicity (foliar symptoms in response to herbicide application) based on visual assessments and recovery based on digital image analysis. Percent bermudagrass phytotoxicity was visually assessed one and two weeks following preemergence herbicide application on a percent scale relative to the non-treated check, where 0 equaled no bermudagrass injury and 100 equaled complete bermudagrass death. These ratings were conducted to ensure bermudagrass recovery from spring dead spot was not confounded by foliar phytotoxicity symptoms.

July 2013 Preemergence herbicides: table

Digital photographs were taken every two weeks following initial occurrence of spring dead spot symptoms in April until mid-June (14 weeks after treatment). Each trial was located in minimally trafficked landing zones near the beginning of the fairway, so no attempts were made to remove mechanical damage (for example, divots, scalping).

Digital images were analyzed using software to quantify percent spring dead spot cover. Percent spring dead spot cover was converted to percent bermudagrass recovery (over the entire season) by comparing back to initial spring dead spot cover photographs taken in April. Initial spring dead spot cover was approximately 46% ± 5%.

Bermudagrass recovery in response to pre-emergence herbicides

Data for each year are presented separately (Table 1). No bermudagrass phytotoxicity was observed in response to pre-emergence herbicide applications throughout the length of either trial (data not shown).

Ronstar. Bermudagrass recovery from spring dead spot was unaffected by applications of Ronstar at 3.03 pounds/acre (3.4 kilograms/hectare). Bermudagrass recovery from spring dead spot in non-treated check plots measured 46% in 2011 and 59% in 2012, which was similar to results for Ronstar treatments (~56%) at 14 weeks after treatment (Table 1). Ronstar is absorbed primarily by shoots of susceptible weeds as they germinate and emerge through the herbicide-treated zone of the soil profile (22). Recovery from spring dead spot requires the encroachment of bermudagrass stolons from surrounding, healthy plants. Bermudagrass stolons that come into contact with Ronstar- treated soil only absorb minimal amounts of the herbicide; therefore, turfgrass rooting is not adversely affected (22). Other researchers have observed similar results in bermudagrass treated with Ronstar (10).

DNA and other herbicide families. Dinitroaniline, pyridine and chloroacetamide herbicides are absorbed by roots and shoots of susceptible weeds as they germinate and emerge through the herbicide- treated zone of the soil profile (15). Stolons that come into contact with these herbicides in the soil may have difficulty rooting because of abnormal swelling of turfgrass root tips and formation of “clubbed roots” (9,13), which potentially reduce bermudagrass recovery from spring dead spot. % bermudagrass recovery from spring dead spot disease.

In our research, Pendulum at 2.23 pounds/ acre (2.5 kilograms/hectare) resulted in only 33% to 38% bermudagrass recovery from spring dead spot at 14 weeks after treatment, regardless of year. Surflan, Barricade, Dimension and Tower applications resulted in 21% to 25% bermudagrass recovery from spring dead spot by 14 weeks after treatment in 2011. In 2012, bermudagrass exhibited similar recovery in response to Barricade (24%) and Surflan (26%), and 33% recovery measured in response to Dimension and 34% in response to Tower at 14 weeks after treatment. These findings support those of other researchers (8,10).

July 2013 Preemergence herbicides: plot

Bermudagrass exhibited the least amount of recovery from spring dead spot at 14 weeks after treatment in response to Specticle applied at 0.031 pound/acre.

However, our results differ from those of other researchers (2) who did not observe differences in the recovery of trafficked Tifway bermudagrass in response to pre-emergence herbicide applications. They found that bermudagrass recovery was similar in response to Ronstar or Pendulum applied at 3.03 pounds/acre (3.4 kilograms/hectare), Barricade at 0.499 pound/acre (0.56 kilogram/hectare), Echelon (prodiamine + sulfentrazone, FMC Corp.) (0.713 + 0.356 pound/acre [0.8 + 0.4 kilogram/ hectare]), and Dimension (0.356 pound/ acre) at one to seven weeks after traffic simulations ceased. The researchers surmised this was due predominantly to bermudagrass growth from underground rhizomes, whereas recovery in our research relied on bermudagrass stolon encroachment. In other research that, like ours, measured bermudagrass recovery from surrounding stolon encroachment of healthy tissue (5), poor regrowth of Tifway bermudagrass was observed in response to applications of Surflan (1.49 pounds/acre [1.68 kilograms/hectare]) (0% regrowth) and Barricade (0.936 pound/acre [1.05 kilograms/hectare]) (3% regrowth) compared to a non-treated check (18%) at six weeks after initial treatment.

Specticle. Bermudagrass exhibited the least amount of recovery (13% to 14%) from spring dead spot at 14 weeks after treatment in response to Specticle at 0.031 pound/acre (0.035 kilogram/ hectare). Specticle is an alkylazine herbicide that controls susceptible grass and broadleaf weeds through the inhibition of cellulose biosynthesis (3). Although Specticle offers turfgrass managers an alternative mode of action for the control of key turfgrass weeds (3,11), long soil residual activity (>150 days) may limit bermudagrass recovery from stress.

Researchers (11) have reported that perennial ryegrass cover in plots treated with Specticle at 0.047 pound/acre (0.053 kilogram/hectare) and 0.062 pound/acre (0.070 kilogram/hectare) measured 37% to 48% compared to 88% for a non-treated check 257 days after initial treatment. Reduced recovery in response to Specticle may be explained by other research (12), where hybrid bermudagrass injury on sand-based systems was 25% to 47% at six weeks after treatment in response to Specticle at 0.031 pound/ acre (0.035 kilogram/hectare), while reductions in root length density (>58%) were observed on root systems 2 to 6 inches (5 to 15 centimeters) in depth following applications of Specticle at 0.031 to 0.062 pound/acre (12).

Still other researchers (39) investigated Riviera common bermudagrass root strength in response to sequential applications of Specticle (0.031 or 0.046 pound/acre [0.035 or 0.052 kilogram/ hectare)], Specticle followed by Ronstar (1.99 pounds/acre [2.24 kilograms/hectare]) or Barricade (0.749 pound/acre [0.84 kilogram/hectare]), and Barricade (0.749 pound/acre [0.84 kilogram/ hectare]). No differences in loose stolon number and root strength were observed between the nontreated check and Specticle treatments at 16 weeks after initial treatment; however, bermudagrass root strength was significantly lower in response to sequential Barricade treatments at 16 weeks after initial treatment (17). However, this research examined the response of four-year-old rooted bermudagrass to Specticle applications, whereas our research examined the ability of bermudagrass stolons to encroach from surrounding plants and root in Specticle-treated soil.

Differential responses in spring dead spot bermudagrass recovery from year to year may be attributed to the severe drought conditions experienced in Texas during 2011. The Palmer drought severity index (PDSI) was -4.19 for April and -5.08 for May in Texas during 2011, indicating the most severe drought since 1895 (6). Although research plots were irrigated, high temperatures and low humidity during spring and summer may have increased evaporative demand, thus reducing bermudagrass vigor and subsequent recovery from spring dead spot symptoms.

Pre-emergence herbicide selection may be important when the site has a history of spring dead spot disease pressure. Ronstar can be safely used as a pre-emergence option when bermudagrass is recovering from spring dead spot, while the use of Surflan, Barricade, Dimension, Tower, Pendulum and Specticle may limit recovery and further weaken the turfgrass system.

Acknowledgments

The authors wish to extend appreciation to Paul Dominguez, GCSAA Class A superintendent at Hillcrest Country Club and a 20-year member of the association, for the use of his facility. This research was previously published in the online journal Applied Turfgrass Science as “Effect of pre-emergence herbicides on the recovery of bermudagrass from spring dead spot” by L.L. Beck, T. Cooper, A.J. Hephner, C.M. Straw and G.M. Henry. 2013. doi:10.1094/ATS-2013-0328-01-RS.

Literature cited

  1. Baird, J.H., D.L. Martin, C.M. Taliaferro et al. 1998. Bermudagrass resistance to spring dead spot caused by Ophiosphaerella herpotricha. Plant Disease 82:771-774.
  2. Brosnan, J.T., G.K. Breeden, A.W. Thoms and J.C. Sorochan 2011. Preemergence herbicide efficacy under athletic field traffic. Online. Applied Turfgrass Science doi:10.1094/ATS- 2011-1128-01-BR.
  3. Brosnan, J.T., G.K. Breeden, P.E. McCullough and G.M. Henry. 2012. PRE and POST control of annual bluegrass (Poa annua) with indaziflam. Weed Technology 26:48-53.
  4. Capo-chichi, L.J.A., J.M. Goatley Jr., W. Philley et al. 2005. Dinitroaniline-induced genetic changes in bermudagrass. Crop Science 45:1504-1510.
  5. Cooper, T., and G.M. Henry.2010. Bermudagrass divot recovery in response to dinitroaniline preemergence herbicides. Proceedings Southern Weed Science Society 63:57. (Abstract) Online. www.swss.ws/NewWebDesign/Proceedings/Archives/ 2010%20Proceedings-SWSS.pdf (verified June 10, 2013).
  6. Dawson, B. 2011. A drought for the centuries: It hasn’t been this dry in Texas since 1789. Texas Climate News, Dec. 19, 2011.
  7. Dernoeden, P.H., J.N. Crahay and D.B. Davis. 1991. Spring dead spot and bermudagrass quality as influenced by nitrogen source and potassium. Crop Science 31:1674-1680.
  8. Fagerness, M.J., F.H. Yelverton and R.J. Cooper. 2002. Bermudagrass [Cynodon dactylon (L.) Pers.] and zoysiagrass (Zoysia japonica) establishment after preemergence herbicide applications. Weed Technology 16:597-602.
  9. Fishel, F.M., and G.E. Coats. 1993. Effect of commonly used turfgrass herbicides on bermudagrass (Cynodon dactylon) root growth. Weed Science 41:641-647.
  10. Fishel, F.M., and G.E. Coats. 1994. Bermudagrass (Cynodon dactylon) sod rooting as influenced by preemergence herbicides. Weed Technology 8:46-49.
  11. Henry, G.M., J.T. Brosnan, G.K. Breeden et al. 2012. Indaziflam programs for weed control in overseeded bermudagrass turf. HortTechnology 22:774-777.
  12. Jones, P.A., J.T. Brosnan, D.A. Kopsell and G.K. Breeden. 2012. Soil type and rooting depth affect hybrid bermudagrass injury with preemergence herbicides. Crop Science 53:660-665.
  13. Mitra, S., and P.C. Bhowmik. 2005. Root pruning preemergence herbicides affect root development of Kentucky bluegrass (Poa pratensis L.). International Turfgrass Society Research Journal 10:1227-1232.
  14. Nus, J.L., and K.Shashikumar. 1993. Fungi associated with spring dead spot reduce freezing resistance in bermudagrass. HortScience 28:306-307.
  15. Parka, S.J., and O.F. Soper. 1967. The physiology and mode of action of the dinitroaniline herbicides. Weed Science 25:79-87.
  16. Perry, D.H., M. Tomaso-Peterson and R. Baird. 2010. Seasonal variation in frequency of isolation of Ophiosphaerella korrae from bermudagrass roots in Mississippi and pathogenicity and optimal growth of selected isolates. Mycopathologia 169:395-402.
  17. Post, A.R., and S.D. Askew. 2011. Effects of indaziflam on bermudagrass [Cynodon dactylon (L.) Pers.] quality and root strength. Proceedings Southern Weed Science Society 64:97 (Abstract). Online. www.swss.ws/NewWebDesign/Proceedings/Archives/2011%20Proceedings-SWSS.pdf (verified June 10, 2013).
  18. Tredway, L.P., M. Tomaso-Peterson, H. Perry and N.R. Walker. 2008. Spring dead spot of bermudagrass: A challenge for researchers and turfgrass managers. Online. APSnet Features. doi:10.1094/APSnetFeature-2008-0108.
  19. Turgeon, A.J. 2011. Turfgrass Management. 9th ed. Prentice Hall, Upper Saddle River, N.J.
  20. Wadsworth, D.F., and H.C. Young. 1960. Spring dead spot of bermudagrass. Plant Disease 44:516-518.
  21. Walker, N.R. 2009. Influence of fungicide application timings on the management of bermudagrass spring dead spot caused by Ophiosphaerella herpotricha. Plant Disease 93:1341-1345.
  22. Yelverton, F. 1995. Strategies for turfgrass weed control with preemergence herbicides. North Carolina State University, Raleigh, N.C. Online. www.turffiles.ncsu.edu/articles/tf0071.aspx (verified June 10, 2013).

L.L. Beck is an instructor in the department of plant and soil science, Texas Tech University, Lubbock, Texas; T. Cooper is a sales representative for Dow AgroSciences, Houston; A.J. Hephner is a turf and ornamental market specialist for FMC, Knightdale, N.C.; C.M. Straw is a graduate research assistant and G.M. Henry (gmhenry@uga.edu) is an associate professor in the department of crop and soil sciences, University of Georgia, Athens, Ga.