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.
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L.L. Beck, Ph.D.; T. Cooper; A.J. Hephner; C.M. Straw; and G.M. Henry, Ph.D.
Exposure to dinitroaniline herbicides may cause
abnormal swelling (“clubbing”) of bermudagrass roots.
Photo by Jim Brosnan
careful what you spray: Some pre-emergence herbicides may limit turf recovery
and further weaken the turfgrass system.
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).
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 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).
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).
Author Leslie Beck applies pre-emergence herbicide to a bermudagrass fairway infested with
spring dead spot disease.
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 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.
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).
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).
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.
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).
Bermudagrass exhibited the
least amount of recovery from
spring dead spot at 14 weeks
after treatment in response
to Specticle applied at 0.031
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.
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.
(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).
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
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
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.
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.
- 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.
- 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.
- 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.
- 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.
- 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.
(verified June 10, 2013).
- Dawson, B. 2011. A drought for the
centuries: It hasn’t been this dry in Texas since 1789. Texas Climate News, Dec. 19, 2011.
- 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.
- 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.
- 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.
- Fishel, F.M., and G.E. Coats. 1994.
Bermudagrass (Cynodon dactylon) sod rooting as influenced by preemergence herbicides. Weed Technology 8:46-49.
- Henry, G.M., J.T. Brosnan, G.K. Breeden et
al. 2012. Indaziflam programs for weed control in overseeded bermudagrass turf.
- 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.
- 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.
- Nus, J.L., and K.Shashikumar. 1993. Fungi
associated with spring dead spot reduce freezing resistance in bermudagrass. HortScience 28:306-307.
- Parka, S.J., and O.F. Soper. 1967. The
physiology and mode of action of the dinitroaniline herbicides. Weed Science 25:79-87.
- 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.
- 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).
- 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.
- Turgeon, A.J. 2011. Turfgrass Management.
9th ed. Prentice Hall, Upper Saddle River, N.J.
- Wadsworth, D.F., and H.C. Young. 1960.
Spring dead spot of bermudagrass. Plant Disease 44:516-518.
- 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.
- 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 (email@example.com) is an associate professor in the
department of crop and soil sciences, University of Georgia, Athens, Ga.