Progression and Impact of Laurel Wilt Disease within
Redbay and Sassafras Populations in Southeast Georgia
R. Scott Cameron, James Hanula, Stephen Fraedrich, and Chip Bates
Southeastern Naturalist, Volume 14, Issue 4 (2015): 650–674
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2015 SOUTHEASTERN NATURALIST 14(4):650–674
Progression and Impact of Laurel Wilt Disease within
Redbay and Sassafras Populations in Southeast Georgia
R. Scott Cameron1, James Hanula2,*, Stephen Fraedrich2, and Chip Bates1
Abstract - Laurel wilt disease (LWD), caused by the fungus Raffaelea lauricola and transmitted
by Xyleborus glabratus (Redbay Ambrosia Beetle [RAB]), has killed millions of
Persea borbonia (Redbay) trees throughout the southeastern Coastal Plain. Laurel wilt also
has been detected in Sassafras albidum (Sassafras) in widely dispersed locations across the
southeastern US. We established long-term laurel wilt disease-progression plots in Redbay
and Sassafras stands in southeastern Georgia and monitored them through 4 years to
document mortality rates and investigate long-term effects of LWD on Redbay and Sassafras
survival and regeneration. Laurel wilt disease killed 87.3% of Redbay and 79.5% of Sassafras
trees in the plots. The time from initial LWD detection to inactivity (no new mortality)
in Redbay stands ranged from 1.1 to 3.6 years, with rate of disease progression positively
related to host-tree size and abundance. Larger trees died at a higher rate in both Redbay
and Sassafras stands, and mortality curves were similar for both species. All diseased Redbay
trees died to the ground level, but the majority produced persistent below-ground basal
sprouts, rapidly providing potential replacement stems. Few below-ground basal sprouts
were observed on Sassafras trees killed by LWD, but over a quarter had epicormic shoots that
survived up to several years after infection, and small trees remained alive on most sites, suggesting
some level of tolerance to LWD. Substantial numbers of RAB were only captured in
baited traps located adjacent to plots in an advanced-active stage of disease progression with
abundant infested trees, both in Redbay and Sassafras stands. However, lingering presence
of small numbers of RAB in post-epidemic areas and scattered LWD mortality in small-sized
Redbay regeneration sprouts and seedlings suggest that secondary disease cycles may occur
as Redbay trees there reach greater numbers and size in the future. Documentation of RAB
and LWD spreading in Sassafras in the absence of Redbay supports concern that LWD will
continue to spread into areas with abundant, large Sassafras trees, which would increase the
probability that RAB and LWD will expand into extensive populations of other laurel species
present in the western US and Central and South America.
Introduction
Laurel wilt disease (LWD) is caused by the fungus Raffaelea lauricola T.C. Harrington,
Fraedrich, & Aghayeva and vectored by Xyleborus glabratus Eichhoff (Coleoptera:
Curculionidae: Scolytinae; Redbay Ambrosia Beetle [RAB]), Both were
apparently introduced from Asia through the Port of Savannah, GA, sometime prior
to 2002 when the first RAB was captured in a monitoring trap in Port Wentworth,
GA (Fraedrich et al. 2008). Since that time, the disease has spread rapidly throughout
the coastal plain forests in Georgia, South Carolina, and Florida, killing nearly
all the large, and previously abundant, Persea borbonia (L.) Sprengel (Redbay) and
1Georgia Forestry Commission, Statesboro, GA, 30641. 2USDA Forest Service, Southern
Research Station, Athens, GA 30602. *Corresponding author - jim.hanula@gmail.com.
Manuscript Editor: John Riggins
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P. palustris (Rafinesque) Sargent (Swampbay) trees (while some taxonomists distinguish
P. borbonia and P. palustris as separate species, herein we consider these
taxa as one species that we refer to as Redbay). More recently, LWD has spread into
Redbay stands on the coastal plain of North Carolina and also has been documented
in isolated locations in Alabama, Mississippi, and Texas (Bates et al. 2015). Laurel
wilt was first observed in Sassafras albidum (Nuttall) Nees (Sassafras) in coastal
Georgia (Fraedrich et al. 2008) and subsequently at numerous inland locations
in Georgia (Cameron et al. 2008, 2014), Florida and South Carolina (Smith et al.
2009), Mississippi (Riggins et al. 2011), Alabama (Bates et al. 2013), and Louisiana
(W. Johnson, USDA Forest Service, Pineville, LA, pers. comm.).
The spread of LWD through the southeastern United States has been mapped by
state forestry organizations on a county-wide basis since 2005 (Bates et al. 2015).
More-detailed systematic surveys conducted 2006–2010 documented the local
spread of LWD in Georgia (Cameron et al. 2008, 2010) and illustrated how the
disease advanced in surges and disconnected jumps followed by a more pervasive
infection of most Redbay trees behind the advancing disease front. Koch and Smith
(2008) developed a model predicting the temporal spread of X. glabratus based
on climate, host density, and historical county spread, which provided some early
guidance on how the disease could affect Redbay, but their model underestimated
the importance of long-distance spread assisted by humans (Cameron et al. 2010,
Riggins et al. 2011) and assumed that RAB would not spread in Sassafras in the
absence of Redbay.
The short-term impacts of laurel wilt disease on Redbay and forest communities
have been documented in 2 island maritime forests in northern Florida (Goldberg
and Heine 2009) and southeast Georgia (Evans et al. 2014), and several coastal
plain sites in Georgia (Spiegel and Leege 2013, Maner et al. 2014) and Florida
(Fraedrich et al. 2008, Shields et al. 2011). Redbay trees over ~10 cm diameter at
breast height (1.4 m above the ground; DBH) have been quickly eliminated, leaving
only small-diameter trees and regeneration (Fraedrich et al. 2008, Shields et al.
2011). Evans et al. (2014), reported heavy mortality of Redbay basal sprouts and a
lack of regeneration in an isolated maritime forest, and suggested that Redbay may
become ecologically extinct from coastal forest ecosystems in the southeastern US.
However, these studies have focused on impacts in forests with Redbay at one,
often unspecified, stage of disease progression, and/or in unique areas that may not
be representative of the broader distribution of Redbay.
The complete temporal stand-level spread and long-term effects of LWD on
residual Redbay trees and Redbay regeneration over a broad geographical range
have not been thoroughly investigated. Furthermore, relationships between RAB
populations and stages of disease development, including post-epidemic sites, need
further examination. Descriptions of symptoms, mortality rates, and spread of LWD
in Sassafras stands are lacking, and little is known about disease and RAB spread in
Sassafras communities in the absence of Redbay. Likewise, the long-term effects of
this disease on residual Redbay and Sassafras trees and regeneration after the initial
disease epidemic passes through an area are unknown.
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We established a series of semi-permanent sample plots in southeast Georgia in
front of, at, and behind the advancing laurel wilt disease front and revisited them
semi-annually for at least 4 years to: (1) characterize the progression of mortality
caused by LWD in Redbay and Sassafras, and document regeneration through time
across a variety of geographical, site, and stand conditions; and (2) monitor RAB
abundance associated with defined stages of LWD progression and quantity of infested
host. Results from this investigation will provide a better understanding of
LWD behavior in Redbay and Sassafras, the possibilities for Redbay recovery and
LWD resurgence, as well as insight into the probability of continued spread of RAB
and LWD into the extensive range of Sassafras in the eastern half of the US.
Methods
Laurel wilt disease impact and progression plots
Field-site description and plant communities. We conducted this field study over
a broad area in southeastern Georgia between latitudes 31–33ºN and longitudes
81–83ºW, encompassing a range of host conditions, stages of disease development,
and ecoregions (Griffith et al. 2001) from the Sea Islands/Coastal Marsh ecoregion,
where the LWD epidemic originated, through the Sea Island Flatwoods and into
the Atlantic Southern Loam Plains to the north and Bacon Terraces to the south
(Fig. 1). We established standardized study plots in Redbay and Sassafras habitats
with specific site selection based primarily on abundance of these species at set
stages of laurel wilt development when the study was initiated. Redbay study sites
roughly fit into 2 plant community types, bay forests and mixed hardwoods, some
of which also included pine, with Redbay generally occupying a mid-story crown
position. Four Sassafras study sites were located in dense open-grown thickets on
deep sandy soils, and 2 others were in mixed hardwood/pine forests together with
Redbay. Geographic location, ecoregion, soil series (USDA, Web Soil Survey),
landscape position, plant community type, plot size, and host species for each of
the study sites, along with common woody plant species associated with bay forests
and mixed hardwood plant communities, are listed in Appendix 1.
Study plot installation and data collection. To document stand-level LWD development,
we established 16 disease-progression plots during late winter through
spring 2009 near the LWD advancing front: 10 with Redbay (R) only, 4 with Sassafras
(S) only, and 2 with both (B) Redbay and Sassafras (Fig. 1). Nine of the
plots—7 Redbay (Ra1–Ra6 and Ba1) and 2 Sassafras (Sa1 and Sa2), each separated
from known diseased trees by 50 m to 15 km—were designated LWD-absent (a)
when the study began. Seven plots—5 Redbay (Rd2–Rd5 and Bd1) and 2 Sassafras
(Sd1 and Sd2)—were designated LWD-active with disease (d) in progress.
We demarcated 4 Redbay post-epidemic plots to document Redbay regeneration,
residual disease, and RAB activity in the aftermath of the initial LWD epidemic.
These plots were located where LWD had passed through ~7 years earlier, and all
susceptible host trees were dead and in an advanced stage of decomposition. We utilized
4 additional Redbay sites (Ra7, Ra8, Ri5, and Ri6) and 2 Sassafras sites (Sa3
and Sd3) for monitoring RAB abundance without installing sample plots (Fig. 1).
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Figure 1. Location, host type, initial disease stage, and laurel wilt (LW)-monitoring plot
numbers superimposed on the southeastern portion of the Ecoregions of Georgia map
(Griffith et al. 2001) Key: RAB = Redbay Ambrosia Beetle, R = Redbay, S = Sassafras, B =
both Redbay and Sassafras, a = LW disease absent at plot initiation, d = disease present,
i = inactive, post-epidemic, * = indicates RAB trapping sites without sample plots. Ecoregions
represented: 75f = Sea Island Flatwoods, 75h = Bacon Terraces, 75j = Sea Islands/
Coastal Marsh, and 65l = Atlantic Southern Loam Plains.
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We laid out study plots using a simplified Carolina Vegetation Survey protocol
(Peet et al. 1998, Wentworth et al. 2008) to facilitate relocation of specific host trees
and document vegetation changes through at least 4 years, 2009–2013 (Fig. 2).
Redbay disease-progression plots (including 2 with mixed Redbay and Sassafras)
and post-epidemic plots consisted of 4 contiguous 10 m x 10 m modules (total =
400 m2) arranged in a square or line to include as many host trees as possible. Five
modules were established on plot Bd1 to incorporate additional Sassafras trees. We
marked the corners of each module with PVC pipe, placed an aluminum tag on a
wire pin at the base of all Redbay and Sassafras trees >2.5 cm DBH in each plot,
and recorded the location of those trees on a map. We documented initial tree diameter,
health (live healthy; live with dieback; LWD wilting = drooping or off-color
leaves; LWD dead = brown leaves or dead from other causes), and number of live
basal sprouts emerging from below ground within 1 m of the base of each tree. We
considered trunks forked below 1.4 m as separate trees. We assumed dead and fallen
Redbay trees in post-epidemic plots were killed by LWD, and estimated their DBH
based on the diameters of the remaining stumps and fallen trunks. We tallied stems
of host regeneration (<2.5 cm DBH, including seedlings and sprouts) in 1 m x 10
m subplots on alternating edges of each module (Fig. 2). We revisited each plot at
~6-month intervals through 4–5 years to record tree condition, number of live basal
sprouts, and presence of epicormic shoots over 1.4 m above ground level for each
tagged host tree, and to count live regeneration stems in subplots.
We used similar procedures for plot installation and subsequent monitoring
of 4 Sassafras plots. Due to the limited distribution or high density of Sassafras
stems, we restricted plots on 2 sites to two 10 m x 10 m modules (total = 200 m2)
and 2 others consisted of one rectangular module, one 90 m2 and the other 50 m2.
We tagged all Sassafras trees >2.5 cm DBH in plots and monitored them every 6
months, except in one plot where Sassafras occurred as a dense thicket, in which
Figure 2. Schematic of LW disease-progression and post-epidemic plot layout and datacollection
methods.
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we therefore tallied trees by 2.5-cm–DBH classes without tagging or following the
trees individually.
Laurel wilt disease diagnosis. Assigning LWD as the cause of mortality in Redbay
and Sassafras was generally based on leaf symptoms (Cameron et al. 2010,
NPDRS 2015). We considered gradual dieback from the apex of crowns and/or
major branches to be not induced by LWD and attributed it to other undetermined
causes, such as suppression, drought, or root disease. Mortality of small branchlets
on Redbay, typical of damage caused by Xylosandrus compactus (Eichhoff) (Coleoptera:
Scolytidae) (Black Twig Borer) also was not attributed to LWD (Dixon
and Woodruff 1982). When the cause of mortality was in doubt, we removed small
patches of bark and outer sapwood to look for the black streaking that is diagnostic
of LWD (Fraedrich et al. 2008). If the cause of mortality was still in doubt, we
collected samples of sapwood and then plated them on a selective agar medium to
confirm presence of R. lauricola (Fraedrich et al. 2008).
Disease-progression and post-epidemic plot data summary
Laurel wilt disease impact in Redbay and Sassafras stands. Variables assessed
on each study plot included: (1) initial and final number and basal area (BA; m2)
per ha of live host trees, (2) number and BA per ha of host trees killed by LWD,
(3) percent of trees and BA killed by LWD, (4) percent of trees that died from other
causes, and (5) initial and final mean DBH (cm) of live Redbay and Sassafras trees.
For 2 plots with both Redbay and Sassafras, we determined host characteristics and
mortality by species and treated them as separate plots. We computed mean mortality
rates among all plots to characterize LWD impact and variation by species
across the broad study area.
Synchronized timelines. We recorded individual host-tree condition, number of
basal sprouts on each host tree, and host regeneration at ~6-month intervals in the
spring (late winter–spring) and fall (late summer–fall) for each plot. Since disease
infection in separate plots and individual trees started at varying calendar dates, we
used synchronized time scales with 6-month intervals to standardize starting points
for summarizing temporal progression variables, including: (1) cumulative mortality
by species and diameter class, (2) number of sprouts per tree before and after
the passage of LWD, and (3) number of host regeneration stems/m 2 (seedlings and
sprouts) through time. We defined the zero point on timelines for disease progression
plots and individual trees within each plot as 6 months (0.5 year) prior to the
observation of the first LWD infected tree or initial symptoms on individual trees
in that plot. For the 5 active plots, which had relatively recent disease episodes in
progress, we estimated the zero point based on the number and condition of infected
and dead trees in the plot at initiation.
In the 7 Redbay disease-progression plots in which LWD was initially absent,
we positioned observations of basal sprouts and regeneration prior to LWD
infection at corresponding negative 6-month intervals up to 1 year before the zero
point on the timeline. We also placed number of sprouts per tree and regeneration
per m2 in post-epidemic plots on synchronized timelines starting at an estimated
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7 years after initial disease infection (based on Redbay disease detection records
[Bates et al. 2015] and decomposition condition of Redbay stumps).
We merged data summaries on synchronized timelines for each plot to calculate
study-wide means for mortality rates by species, basal sprouts, and regeneration.
Since individual plot data were positioned at varying locations on synchronized
timelines, the number of observations for plot averages varied, generally with fewer
replicates at both ends of the time scale for LWD-progression plots. We excluded
from temporal data summaries the plot averages for time intervals with fewer than
4 observations for Redbay and 3 observations for Sassafras.
Cumulative LWD mortality in Redbay and Sassafras. We calculated mean cumulative
percent LWD mortality at 6-month intervals (percent of initial live host trees)
among 12 Redbay plots over a 3.5-year period and 5 Sassafras plots for a 2.5-year
period. Host trees that died from other causes were deducted from the initial numbers
of live trees for this analysis. We charted Redbay and Sassafras cumulative
mortality curves and determined regression trend lines.
Redbay and Sassafras mortality by diameter class. We compared cumulative
percent mortality caused by laurel wilt disease among 3 diameter classes for Redbay
and Sassafras on separate synchronized timelines based on first LWD infection
in each plot, as previously described. We combined individual tree data from the 8
Redbay plots that were observed for 4 years after initial LWD infection, or in which
all Redbay trees were killed by LWD in less than 4 years. Individual tree mortality
data from 4 Sassafras plots observed at least 2.5 years after initial LWD detection
were also merged. We calculated percent mortality at each observation interval
among all trees in three 11.5-cm–DBH classes for Redbay and three 4.6-cm–DBH
classes for Sassafras, and plotted cumulative percent mortality by size class on
separate charts for each species.
Laurel wilt disease progression in Redbay stands. We derived the number of
years that LWD was active in 10 Redbay-only disease-progression plots by subtracting
the date of the first observation of LWD in each plot from the date when
all host trees in the plot were killed by the disease, or when disease progression
ceased (defined as no new LWD infections for at least one year). Since one Redbay
plot (Ra3) remained slightly active at the last field observation, we projected time
to inactivity to 6 months after the final observation, based on the observed mortality
trajectory through 3.5 years. We regressed years that LWD was active in each
plot against initial mean Redbay DBH and total initial Redbay basal area (m2/ha)
to determine if the episode duration was associated to host diameter or basal area.
Too few Sassafras plots were monitored to determine disease progression rate with
respect to DBH and BA for this species.
Basal sprouts, epicormic shoots, and regeneration density in Redbay and Sassafras.
We recorded the numbers of live basal sprouts emerging from below ground
around all tagged Redbay and Sassafras trees throughout the study. We computed
mean basal sprouts per tree within and among plots from synchronized timelines
as described above, excluding from this analysis basal sprouts around host trees
that died from causes other than LWD and sprouts which could not be attributed to
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particular individuals within clumps of trees. In 4 post-epidemic assessment plots,
we synchronized the number of sprouts associated with stumps of Redbay trees
assumed to have died from LWD as above. We determined percentages of Redbay
and Sassafras trees with epicormic shoots >1.4 m above ground level after LWD
infection on all plots. Regeneration density (stems/m2) in 2 size classes (<1.4 m tall
and >1.4 m tall but less than 2.5 cm DBH) was computed for each plot assessment,
arranged on synchronized timelines and summarized as described above.
Redbay Ambrosia Beetle (RAB) population monitoring.
We deployed baited traps immediately outside the perimeter of most LWDmonitoring
plots plus at 6 additional locations (Fig. 1) to track the relative numbers
of RAB in areas at different stages of LWD progression in 2009 and 2010. One
8-funnel Lindgren trap baited with a manuka oil lure (P385-Lure M; Synergy Semiochemicals
Co.) attached to the outside of the upper funnel was suspended on
a rope between two non-host trees ~2 m above ground level and left in the field
throughout August (30 days) each year. We monitored a total of 16 Redbay and 4
Sassafras sites in 2009 and 17 Redbay and 4 Sassafras sites in 2010.
We derived the LWD stage and cumulative DBH of infested host trees at each
trapping site from the late summer/fall assessments for each respective year in
adjacent LWD progression and post-epidemic study plots. Disease progression
stages recognized for RAB trapping sites were: 1) “outside range” of LWD (~5
km to 30 km ahead of the advancing LWD front); 2) “absent-near” where trees
were healthy in plots but LWD was present in trees within ~250 m of the plot;
3) “early-active” where there were recent infections in the plot, but less than 50%
of host trees were wilting or dead from LWD; 4) “advanced-active” where more
than 50% of host trees were wilting or dead; 5) “late-active” where all host trees
were dead or the disease episode was ending, but some dead trees were still standing
with major branches intact; and 6) “post-epidemic” where all host trees were
dead with major limbs broken off and trunks in an advanced stage of decomposition.
We combined data from both trapping years and computed mean numbers of
RAB per day and mean cumulative DBH of infested Redbay trees for each Redbay
disease stage, resulting in a range of 3 to 9 replicates per stage.
Numbers of Sassafras trapping sites were limited to 2 outside range, 2 earlyactive,
1 advanced-active, and 3 late-active. We determined the mean numbers of
RAB per trap per day for Sassafras trapping sites and performed no further analyses
due to limited replication within disease stages.
Statistical analyses
We entered the data into Microsoft Excel spread sheets (Microsoft Corp.,
Redmond, WA) and generated sums, cumulative mortality, means, and standard
errors (SE) using basic statistical functions and formulae for the variables to be
assessed. Stand characteristics and impact data were summarized with Microsoft
Excel PivotTable Tools. To determine if there was a size preference among initial
Redbay infections, we used the paired 2-sample t-test in Microsoft Excel Data
Analysis Tools to compare mean diameters (DBH) of the first symptomatic trees in
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7 originally disease-free plots and 1 active plot (with only one initial wilting tree) to
the mean diameters of all Redbay trees. Mean DBH and total BA in10 Redbay-only
plots were normally distributed according to the Kolmogorov-Smirnov test for normality
in the Univariate procedure of SAS (SAS Institute 2000), and we regressed
time to LWD inactivity for each plot against both mean DBH and BA using Excel
Data Analysis Tools. We also regressed mean numbers of RAB per day in 6 LWD
stages against cumulative DBH of infested host in adjacent plots. Graphs were
produced with Microsoft Excel Chart Tools, and we determined best-fit regression
equations to describe the relationships between disease episode duration and mean
DBH, BA, and cumulative percent mortality over time caused by LWD.
Results
Laurel wilt disease impact and progression in Redbay and Sassafras
Impact of laurel wilt disease in Redbay stands. At plot initiation, 4.2 ± 1.83%
(mean ± SE) of Redbay trees were dead from other causes. Laurel wilt disease
killed 87.3% of Redbay trees (93.1% of the basal area) in disease-progression plots,
3.4% died of other causes, and only 9.3% remained alive at the end of the study
(Table 1).
Trees on the 7 Redbay plots initially classified as LWD-absent became infected
with LWD, and disease progression was complete by the end of the study in all
but 1 plot that was projected to be inactive in 1 year. All Redbay trees alive prior
to the arrival of LWD in 6 of the 12 disease-progression plots died within 2 years
after initial disease detection, and only a few small Redbay trees remained alive in
6 other plots. Initial mean DBH of live Redbay trees was 11.6 ± 1.57 cm, and mean
DBH of surviving Redbay trees was 5.2 ± 0.72 cm, the largest of which was 13 cm.
Among 232 Redbay trees that displayed LWD symptoms during the study, all died
to ground level.
Impact of laurel wilt disease in Sassafras stands. At the beginning of the study,
LWD was absent from 3 of the 6 Sassafras disease-progression plots and 11.9 ±
9.21% of Sassafras trees were dead from other causes (primarily due to suppression
beneath a dense hardwoods/pine overstory). Laurel wilt disease was present
Table 1. Initial mean number of live host trees and live basal area (BA), percent of trees and basal
area killed by laurel wilt (LWD), percent mortality by other causes, percent final live trees, and initial
and final mean DBH in Redbay and Sassafras disease-progression plots monitored from 2009–2013
in southeast Georgia.
Initial # % mort. Initial live % BA Initial live Final live
live host % LWD other Final % host BA LWD host DBH host DBH
Host, plot type trees/ha mort. causes live (m2/ha) mort. (cm) (cm)
Redbay, LWD-absent and LWD-active, n = 12
Mean 573.3 87.3 3.4 9.3 6.8 93.1 11.6 5.2
SE 74.38 3.71 1.74 3.24 1.42 2.53 1.57 0.72
Sassafras, LWD-absent and LWD-active, n = 6
Mean 2803.4 80.4 6.0 13.6 7.3 92.7 5.5 3.8
SE 1611.98 6.37 3.23 5.73 3.29 3.23 0.54 0.40
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on all plots by the end of the study, and the disease killed an average of 80.4% of
the Sassafras trees (92.7% of the basal area), while 6.0% died of other causes and
13.6% remained alive at the end of the study (Table 1). In the 2 plots with both
Redbay and Sassafras, LWD killed all Sassafras trees in 1 plot, and only 1 Sassafras
tree remained alive in the other. In 1 Sassafras plot, all initially tagged trees
died, but 2 saplings grew to tree size and were alive at the end of the study. In the
other 3 Sassafras plots, LWD killed 65.0% to 76.2% of host trees and only small
trees remained alive. Mortality due to LWD ceased to expand in one initially active
Sassafras thicket ~1.5 years after plot initiation and did not expand through 2.5
additional years of observation. However, the LWD pathogen remained viable in
stumps in this plot, as confirmed by our ability to readily culture R. lauricola from
wood chip samples taken at the bases of 2 trees that had died 2 years earlier but had
epicormic shoots growing just above the soil level. Disease also lingered in other
Sassafras stands, as indicated by slow continuous mortality at final assessments
and the presence of wilted leaves on epicormic sprouts and black staining in the
sapwood of a few remaining small trees.
Cumulative LWD mortality in Redbay and Sassafras. Cumulative mortality
caused by LWD among initially healthy host trees in 12 Redbay and 5 Sassafras
disease-progression plots followed very similar trajectories (Fig. 3). Host trees died
Figure 3. Mean cumulative percent mortality caused by laurel wilt disease in (A) Redbay
(n = 12, mean DBH = 11.7 cm) and (B) Sassafras (n = 5, mean DBH = 6.0 cm) among trees
alive at plot initiation (excluding mortality from other causes) monitored from 2009–2013
in southeast Georgia. Vertical error bars represent standard error of the mean.
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at a rapid, steady rate up to ~60% mortality through 1.5 years after initial detection
of LWD in plots, and then the rate of increase slowed among the remaining trees.
Disease progression curves were best fit with similar second-order polynomial regression
trend lines for both species.
Redbay and Sassafras mortality rates by host-diameter class. Mean DBH of
the first infected Redbay trees in 8 plots (15.4 cm) did not differ significantly from
the mean diameter of all Redbay trees (12.5 cm) in the plots (t = 1.38, P = 0.210).
Similarly, incidence of LWD among Redbay trees, observed for at least 4 years
and merged from 8 plots, appeared to affect the 3 diameter classes equally at first
detection (0.5 years), with mortality ranging from 18% to 22%, but thereafter mortality
rates increased rapidly for the 2 larger diameter classes (Fig. 4). All Redbay
trees over 25.8 cm DBH were killed by LWD 1.5 years after detection, and all
14.2–25.7-cm-DBH–class trees were dead within 2.5 years. Mortality caused by
LWD progressed more slowly in the smallest DBH-class trees, with 12.3% still
alive after 4 years.
In contrast to Redbay, mortality in Sassafras trees was highest initially in the
largest diameter class where 40% of trees were diseased 0.5 years after initial
detection, while 10% or less where affected in the other diameter classes (Fig. 5).
Sassafras mortality increased greatly in the intermediate and smallest diameter
classes starting 0.5 and 1.5 year, respectively, after initial detection, and incidence
of LWD among all Sassafras diameter classes was 80–100% after 2.5 years.
Laurel wilt disease progression in Redbay stands. The average time from initial
LWD infection to inactivity in 10 Redbay-only disease-progression plots was 2.2
years (range = 1.1–3.7 years). The length of time LWD was active in plots was
inversely related to the initial Redbay mean DBH (P = 0.019) and BA (P = 0.040)
(Fig. 6). Redbay mortality progressed more rapidly and completely in plots with
larger initial mean DBH and BA than in plots with smaller DBH and BA. The 5
plots with the fastest progression were all in “bay forest” plant communities and
Figure 4. Cumulative percent mortality caused by laurel wilt disease in 3 DBH classes
among all individual Redbay trees combined from 8 LWD-progression plots monitored for
4 years in southeast Georgia.
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averaged 1.4 ± 0.12 years to inactivity, 15.7 ± 2.06 cm mean DBH, and 10.8 ± 2.23
m2/ha BA, in contrast to the 5 plots with the slowest progression (4 in mixed hardwood
forests and 1 in a pine plantation) that averaged 2.9 ± 0.30 years to inactivity,
6.8 ± 0.87 cm mean DBH, and 3.7 ± 1.17 m2/ha BA. Also, all Redbay trees in the 5
plots in bay forests died from LWD, while a few Redbay trees remained alive (20.3
± 3.98%) in the 5 plots in mixed hardwood/pine plantation stand s.
Regeneration after laurel wilt disease in Redbay and Sassafras
Basal sprouts around Redbay and Sassafras trees killed by LWD. Prior to LWD
infection, we observed basal sprouts originating from below ground on only a few
Redbay trees, primarily on smaller trees with crown dieback. However, basal sprouts
around Redbay began increasing within 6 months of becoming symptomatic and
continued increasing through 1.5 years after infection by LWD (Fig. 7). Among all
individual Redbay trees, 67.2% had at least one sprout 1.5 years after initial LWD
symptoms were recorded. Although, many below-ground basal sprouts apparently
died between assessment periods, most either re-sprouted or were replaced by new
sprouts, resulting in an increase in the number of sprouts to 3.7 ± 0.64 per tree after 2
years, and sprout numbers remained constant over the next year. In the post-epidemic
assessment plots, 5.1 ± 0.47 Redbay sprouts were associated with stumps of trees
killed by LWD ~7 years earlier. Numbers of sprouts per stump in post-epidemic plots
remained relatively constant through 4 years of observation.
Sassafras did not respond to LWD by producing numerous below-ground basal
sprouts. Only 10.9% of individual Sassafras stems killed by LWD had 1 or more
below-ground sprouts, with a peak of 0.4 ± 0.19 sprouts per tree 2 years after initial
symptoms were detected (Fig. 7).
Incidence of epicormic shoots in Redbay and Sassafras. Epicormic shoots
emerging on stems above 1.4 m were recorded for 6.6% (range = 0–23.3%) of
Figure 5. Cumulative percent mortality caused by laurel wilt disease in 3 DBH classes
among all individual Sassafras trees combined from 4 LWD-progression plots monitored
2.5 years in southeast Georgia.
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Redbay trees and 28.3% (range = 7.7–41.2%) of Sassafras trees killed by LWD in
disease-progression plots. Epicormic shoots on Redbay trees infected with LWD
died quickly as the disease spread rapidly through the crowns and trunks of trees
during the year following the appearance of symptoms. In contrast, some Sassafras
trees that appeared to have died from LWD continued to produce new shoots on
trunks and portions of the crown several years after initial LWD detection in the
tree. Cutting into the stems of these trees revealed black staining typical of LWD,
often beneath 1 or 2 years of apparently healthy radial growth. However, many of
these trees eventually succumbed to the disease and died.
Regeneration density in Redbay and Sassafras disease-progressions plots.
The number of small Redbay (both seedlings and basal sprouts less than 1.4 m tall) was
0.3 stems/m2 in plots at the time of the first LWD infections, but density of stems
increased rapidly to 1.3 stems/m2 from 0.5 to 2 years after LWD detection and remained
relatively constant during the next 2 years (Fig. 8). Very few Redbay stems
Figure 6. Relationship between years that laurel wilt disease was actively killing trees in
plots (episode duration) and (A) initial Redbay mean diameter (P = 0.019, n = 10) and
(B) initial Redbay basal area per hectare (P = 0.040) in southeast Georgia, 2009–2013. Letters
and numbers adjacent to each data point refer to plot identifications for which codes,
locations, site characteristics, and plant community types are listed in Appendix 1.
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less than 2.5 cm DBH but >1.4 m tall were present in the Redbay disease-progression plots
(less than 0.1 stem/m2) through 4.5 years after initial LWD infection.
Numbers of Sassafras regeneration stems less than 1.4 m tall revealed no clear association
with the progression of LWD. Three plots consistently had high numbers of
Sassafras regeneration stems, root sprouts, and seedlings (3.8 ± 0.27 stems/m2),
while 3 other plots consistently had low numbers (0.2 ± 0.03 stems/m2) throughout
the monitoring period. Plots with high numbers of regeneration stems had open
overstory canopies, while plots with little regeneration were covered by dense overstory
canopies. As with Redbay, few regeneration stems less than 2.5 cm DBH and >1.4 m
tall were present in Sassafras plots throughout the observation period.
Redbay response to LWD in post-epidemic plots. All original Redbay trees >2.5
cm DBH were dead to ground level (presumably killed by LWD) when we installed
4 post-epidemic assessment plots in 2009, but numerous basal sprouts and seedlings
were present. In the 4 post-epidemic plots, density of Redbay less than 1.4 m tall at
the first observation was 0.7 stems/m2 and remained nearly constant throughout the
4-year monitoring period. Numbers of Redbay regeneration stems >1.4 m tall consistently
averaged ~0.3/m2 throughout the monitoring period (Fig. 8). Combining
the numbers of regeneration stems in both size classes in post-epidemic plots brings
averages to ~1 stem/m2, which is comparable to the number in disease-progression
plots 4 years after disease initiation.
At plot initiation, only 2 Redbay stems (both 3 cm DBH) had grown to tree size
(>2.5 cm DBH) by ~7 years after the epidemic passed through the area, 1 in each
of 2 separate plots. During the 4-year study, an additional 41 Redbay stems grew to
tree size (39 in plot Ri2 and 2 in Ri1), the largest of which was 3.6 cm DBH after 4
years. Among 43 small Redbay trees in these 2 post-epidemic plots, 4 (9.3%) died
from LWD.
RAB by stage of laurel wilt disease progression.
Redbay Ambrosia Beetles were not captured in areas outside the known distribution
of LWD, and only 6 beetles were caught in areas adjacent to absent-near
Figure 7. Mean numbers of below-ground basal sprouts around individual Redbay and Sassafras
trees before and after infection in LWD-progression plots (Redbay: n = 4–11,
Sassafras: n = 3–5); Redbay data for years 7–11 are from post-epidemic plots (n = 4).
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plots where RAB and LWD were within ~250 m. Relatively few RAB were caught
at early-active and late-active sites (0.38 and 0.54 beetles per day, respectively).
The largest numbers of RAB were trapped in areas where Redbay trees were in the
advanced-active stage of LWD development (mean = 5.7/day; Table 2). A total of 8
RAB were trapped among 4 of 5 post-epidemic sites where the disease had passed
through an estimated 5–10 years earlier.
Figure 8. Mean numbers of Redbay regeneration stems (seedlings and sprouts less than 2.5 cm
DBH) per m2, separated by size class and charted on a synchronized time scale (zero point
on the x-axis is 6 months prior to first detection of laurel wilt in disease progression plots
(n = 4–12). Data for years 7–10.5 years are from post-epidemic plots (n = 4)).
Table 2. Numbers of Xyleborus glabratus (Redbay Ambrosia Beetle) caught in traps baited with manuka
oil located adjacent to Redbay and Sassafras monitoring plots in varying stages of laurel wilt
disease progression, and mean cumulative DBH of infested Redbay trees in adjacent plots during
August 2009 and 2010.
Cum. DBH (cm)
Trapping of infested host
Host species/LW disease stage* periods Number/day (mean ± SE) (mean ± SE)
Redbay
Outside range 8 0.00 ± 0.00 0.0 ± 0.0
Absent-near 6 0.03 ± 0.01 0.0 ± 0.0
Early-active 4 0.38 ± 0.19 47.8 ± 6.6
Advanced-active 3 5.70 ± 3.83 168.7 ± 53.0
Late-active 3 0.54 ± 0.08 27.3 ± 10.0
Post-epidemic 9 0.03 ± 0.01 0.0 ± 0.0
Sassafras
Outside range 2 0.00 ± 0.00 -
Early-active 2 0.05 ± 0.02 -
Advanced-active 1 3.76 -
Late-active 3 0.10 ± 0.07 -
*Disease stage at the time of trap deployment.
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Numbers of beetles captured at individual Redbay trapping sites were strongly
related to the amount of infested host in adjacent plots, expressed as total infested
DBH at the time of trap deployment, excluding plots without infested host (n = 10,
r2 = 0.80, P < 0.0005). Excluding 1 outlier for which 10 times more beetles were
caught than in any other trap, a strong relationship remained between beetles
caught and amount of infested host (n = 9, r2 = 0.50, P = 0.03).
In Sassafras, we caught the largest number of RAB (109 total, 3.76 beetles per
day) adjacent to the only site in an advanced-active stage of LWD development. We
trapped very few RAB at the early-active and late-active stages, and none in traps
deployed outside the range of LWD (Table 2).
Discussion
LWD impact, progression, and regeneration in Redbay
Final Redbay mortality among 12 sites distributed over a broad area and a variety
of coastal plain ecoregions in Georgia was 87% of trees and 93% of the BA,
which is similar to that reported through portions of the disease process and/or at
more restricted sites in Georgia (Maner et al. 2014, Spiegel and Leege 2013) and
Florida (Fraedrich et al. 2008, Shields et al. 2011). However, this is the first report
of LWD through the entire progression in individual stands over a variety of site/
stand conditions. Disease progression and final mortality rate varied considerably
among sites. All Redbay trees were killed by LWD within 2 years in 6 stands, and
disease progression appeared to stop after larger trees were killed in 6 others. The
diameter of the very first symptomatic trees in plots did not differ significantly
from the average diameter of all trees in plots. However, starting 1 year after first
infections, large Redbay trees were killed more rapidly than smaller trees, possibly
because larger stem silhouettes are more attractive to RAB (Mayfield and Brownie
2013). There was no obvious pattern of spread through the stand, or indication
that the disease spread through root connections from one tree to the next. Episode
duration was inversely related to increasing initial mean diameter and basal area
in stands. Stands with the fastest LWD progression and 100% mortality were all
bay forest plant communities that had a greater abundance of large Redbay trees.
Disease mortality curves and knowledge of factors affecting disease progression
are essential for accurately predicting future spread of LWD.
Once Redbay trees became symptomatic with LWD, their entire crowns generally
died within months, and sprouts emerged at the base of the majority of those
trees. Among 236 Redbay trees determined to be infected with LWD in this study,
all stems and above-ground sprouts died within ~1 year, and no evidence of inherent
post-infection resistance was observed in individual Redbay trees. All initially
healthy Redbay trees died from LWD on 6 sites, but a few small trees up to 13 cm
DBH remained alive on 6 other sites with smaller initial host size and density. Although
putative resistance has been reported among surviving Redbay trees from
6 sites with high levels of LWD mortality (Hughes and Smith 2014), continued
research is needed to determine whether Redbay trees surviving the LWD epidemic
have escaped RAB attack or exhibit some form of host resistance.
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Redbay regeneration (seedlings and sprouts) was abundant and reached a plateau
about 2 years after first symptoms were observed in stands heavily impacted
by LWD. Redbay seedlings were sparse in most disease-progression plots, but we
observed abundant seedling regeneration in one Redbay disease-progression plot
and one post-epidemic plot, suggesting it may be a relatively rare event. In contrast,
below-ground basal sprouting, although variable among sites, was prevalent and
persistent after the passage of LWD.
Heavy mortality of Redbay sprouts and seedlings after LWD has been reported
in areas affected by LWD, and Redbay regeneration is predicted to be of little
consequence in the replacement of Redbay stems after the passage of LWD (Evans
et al. 2014, Spiegel and Leege 2013). Ultimately, this would have significant
impacts on plant communities and on animals that utilize Redbay foliage such
as Papilio palamedes (Drury) (Palamedes Swallowtail). Basal sprouts attached
to the trunk of trees rely on these above-ground stem tissues for water and nutrients
and thus generally are short lived as the main stems die to the ground level
(Del Tredici 2001). Therefore, only basal sprouts originating from below-ground
with potential access to live roots were inventoried in this study. Even though
considerable mortality of below-ground sprouts was observed (often the result
of Black Twig Borer attacks), the numbers of live sprouts increased rapidly
and were maintained through 4 years in disease-progression plots and up to 11
years in post-epidemic plots. Differences in definitions of sprouts and inventory
techniques or, in the case of St. Catherine’s Island, a unique ecosystem not representative
of most Redbay habitat (Evans et al. 2014) may have contributed to
apparent contradictory results regarding Redbay regeneration.
Clumps of Redbay sprouts are commonly observed shortly after clear-cut logging
or prescribed burns, and Redbay is common in the understory and mid-story
of many pine plantations in the southeastern coastal plain. Thus, basal-sprouting
appears to be a reliable and rapid means of regeneration and replacement of Redbay
stems following disturbance, including LWD, and some herbivores may thrive on
flushes of Redbay regeneration in the wake of LWD (Chupp and Battaglia 2014).
LWD impact, progression, and regeneration in Sassafras
Laurel wilt disease killed 80.4% of Sassafras trees in disease-progression plots,
and the Sassafras mortality curve was very similar to that of Redbay through 2.5
years. Large Sassafras trees were killed more rapidly than smaller trees starting with
the first infections. Laurel wilt disease sometimes spreads rapidly from one tree to
the next in dense Sassafras thickets, and black staining typical of LWD has been observed
in Sassafras lateral and runner roots (R.S. Cameron, pers. observ.), suggesting
disease transmission through interconnected roots. Additional studies are needed to
characterize the spread of the LWD pathogen in Sassafras root systems.
Laurel wilt disease has spread intermittently among Sassafras stands in Georgia,
affecting some thickets and individual trees, while others nearby remain apparently
healthy. Disease progression in some Sassafras stands is incomplete. Mortality
stopped in one plot after 90% of trees over 5 cm DBH were killed, and many
small trees remained alive around the periphery of this and other diseased thickets.
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2015 Vol. 14, No. 4
Sassafras appears to have some degree of tolerance to LWD as many trees continue
to produce new sapwood long after infection. Thus, some trees are not killed completely
to the ground level and produce epicormic sprouts that grow into branches
off the trunk or lower crown for at least several years after infection, despite the
presence of the pathogen in the trees.
Sassafras proliferates rapidly through root suckers and produces seeds at a
relatively young age, which are readily disseminated by wildlife. Sassafras is also
known to produce both basal sprouts from stumps of young trees and abundant root
suckers from long lateral runner roots, which are instrumental in the rapid colonization
of openings in wooded areas and open fields, resulting in dense and relatively
pure stands (Gant and Clebsch 1975, Griggs 1990). Regeneration by seedlings and/
or root sprouts was abundant in half the Sassafras study sites, and numerous smaller
trees on the periphery of most thickets remained apparently healthy many years
after initial infection.
Sassafras is widely distributed throughout the eastern US, and our data suggest
it will likely to be severely impacted by LWD, especially larger trees. However,
through intermittent disease spread, host tolerance, and prolific seedling and rootsprout
regeneration, Sassafras will likely continue to persist, at least as small trees,
in the presence of laurel wilt disease.
RAB populations related to disease progression
Redbay Ambrosia Beetles use olfactory cues in finding hosts and are attracted to
volatiles emitted from cut Redbay (Hanula and Sullivan 2008; Hanula et al. 2008;
Kendra et al. 2011, 2014). Although not definitively confirmed, circumstantial evidence
suggests that at least some of the first trees that RAB attack and infect with
R. lauricola in new areas are already damaged and emitting cues for attraction and
boring. Among 4 sites in our study with no known LWD within at least several km,
the very first tree confirmed with LWD in the area had broken limbs from storm
damage (2 sites), dieback, or damage from human activity.
We captured no RAB in traps placed outside the known range of LWD and only
a few in plots where LWD-infected trees were within ~250 m. Increasing numbers
of RAB were caught during the early-active stage of disease progression. As RAB
brood began emerging from the first infested trees, populations increased rapidly
along with Redbay mortality, which reached 70% within 1.5 years after initial
disease detection. During this rapid disease-progression phase, larger-diameter
Redbay trees died at a higher rate than smaller ones, possibly reflecting RAB preference
for larger silhouettes (Mayfield and Brownie 2013) at a time when the area is
inundated with host volatiles, perhaps making point sources of chemical cues more
difficult to locate. The largest numbers of RAB were captured in monitoring traps
during the advanced-active stage, starting ~1.5 years after the first symptomatic
trees were observed. This stage occurred after 50% of Redbay trees had died and
RAB brood emergence was likely at its peak (Maner et al. 2013). Numbers of RAB
decreased during the late-active disease-progression stage when most host trees had
died and conditions for brood production were deteriorating within trees.
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Low numbers of RAB captured at 4 of 5 post-epidemic trapping sites and observations
of a few small-diameter Redbay trees killed by LWD adjacent to 3 of 4
post-epidemic plots indicate that low-level populations of RAB have survived in
these areas up to 11 years after the passage of the original LWD epidemic. These
findings are similar to those of Maner et al. (2014) confirming that RAB populations
drop to very low levels after suitable hosts are eliminated by LWD, possibly
allowing Persea spp. populations to recover after the epidemic moves through an
area (Hanula et al. 2008). Over the longer term, the continued success of the RAB
in southeastern forests will depend on its ability to find and utilize hosts that are
on average much smaller in diameter and occur at lower densities than occurred
when the beetle first arrived. As Redbay trees reach greater diameters and densities,
however, LWD incidence may increase within localized areas.
Sassafras has been less attractive to RAB than Redbay or Swamp Bay in most
trapping experiments (Hanula et al. 2008, Kendra et al. 2014, Mayfield and Hanula
2012), yet Sassafras has been shown to be a suitable host for RAB (Mayfield et al.
2013). Since RAB were trapped adjacent to an isolated advanced-active Sassafras
stand in this study, and LWD has killed Sassafras trees in widely separated locations
in the southeastern US where no Redbay are nearby (Bates et al. 2015), it is clear
they can reproduce and sustain populations on Sassafras alone.
If RAB and R. lauricola can survive in colder climates to the west and north as
Formby et al. (2013) suggest, the disease has a high potential to continue spreading
and cause significant impacts in areas of abundant, large Sassafras trees. Perhaps
more importantly, Sassafras may provide a reservoir of RAB and R. lauricola over
a large area and long period of time, thus increasing the probability that the disease
will be spread via human movement to other susceptible Lauraceae like Umbellularia
californica (Hook. & Arn.) Nutt. (California Bay Laurel; Mayfield et al. 2013)
and Persea americana Mill. (Avocado) in California.
Disease management
Management of LWD in forested areas may be impractical, except possibly in
high-value, isolated host populations, such as island communities, where prompt
sanitation and removal of infected trees may slow the spread. The relatively slow
initial progression of LWD observed in isolated Redbay stands in this study indicates
there is a narrow window of opportunity to slow LWD through early detection
and complete removal of the first infested trees.
Currently, it appears LWD will continue to spread and impact Redbay populations
across the southeastern and south-central US. Laurel wilt disease was recently
detected in Redbay in isolated counties in east Texas and it is likely to spread to
the far western range of the species in south Texas. In addition, the disease is now
spreading in Sassafras beyond the distribution of Redbay. The rate of spread has
been much more rapid than originally predicted, in large part because of the human
transport of infested host material and the efficiency of RAB as a vector. Thus, the
most crucial management option would involve discovery of pathways of introductions
into new areas and implementing means to prevent these long-distance
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movements into disease-free areas in the southeastern US and other parts of the
New World where there is an abundance of Lauraceae species of both ecological
and economic importance.
Conclusions
Laurel wilt disease progression in Redbay stands starts slowly with a few trees
of varying sizes, but mortality increases rapidly, especially in larger trees, as RAB
populations build to high levels. The rate of spread is greater within Redbay stands
with higher densities of larger diameter trees, best represented in bay forests where
nearly all trees >2.5 cm are killed within 2 years after the first symptomatic trees
are observed. In stands with sparser and smaller-diameter trees, disease progression
may last up to 4 years, sometimes becoming apparently inactive with a few
small Redbay trees remaining alive. Abundant seedling regeneration appears to be
infrequent after Redbay stands are decimated by LWD, but below-ground basal
sprouts proliferate around most stumps within a year after trees are killed. This appears
to be an important regeneration strategy for Redbay after LWD, and may lead
to persistence and slow recovery for Redbay. However, low numbers of RAB and
scattered LWD mortality in small Redbay trees continue on most sites up to 11 years
after the initial epidemic, which suggests that the disease will persist at endemic
levels and will continue to impede Redbay recovery.
Laurel wilt disease has spread out of the Redbay range and into Sassafras in parts
of Georgia. The disease mortality curve and preference for larger trees are similar
to that in Redbay. Progression in thickets can be rapid, apparently moving through
clonal root systems, but the disease process slows or stops in some Sassafras stands
for unknown reasons. Epicormic shoots and lingering decline in individual trees
may be evidence of host resistance in Sassafras. Further investigation of the spread
of LWD in Sassafras root systems and within stands in a wider variety of habitats
and geographical locations is needed to evaluate the potential for spread over its
extensive range.
Documentation of LWD progression in Redbay and Sassafras provides a better
understanding of disease epidemiology and baseline data for modeling the spread of
LWD. Observations of successful RAB development, disease behavior, and broadening
distribution of LWD in Sassafras in the absence of Redbay, indicate a potential
for disease spread through Sassafras populations in North America, increasing the
likelihood it will eventually expand its range to the western US and Central and South
America where members of the Lauraceae are more diverse and abundant.
Acknowledgments
Funding for this Evaluation Monitoring (EM) Project was provided by the USDA Forest
Service, Forest Health Protection, Southern Region and the Georgia Forestry Commission.
We thank Dr. Joel Gramling (The Citadel) for help with plot design and sampling protocol,
and Susan Best and Mike Cody for assistance in the laboratory.
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2015 Vol. 14, No. 4
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Appendix 1. Characterization of laurel wilt disease progression monitoring plots and Xyleborus glabratus (Redbay Ambrosia Beetle) trapping
sites, with initial disease status, county location, ecoregion, soil series, landscape position, plant community type, plot size, and host
species (R = Redbay, S = Sassafras, and B = both) present in southeastern Georgia.
Plot ID/ Plot
disease size
statusA County Ecoregions of GeorgiaC Soil series Landscape positon Plant community typeD (m2) Host
Ra1 Emanuel Atlantic Southern Loam Plains Kinston- Upper stream terrace Bay forest 400 R
Bibb
Ra2 Jenkins Atlantic Southern Loam Plains Rains Intermit. stream head Mixed hardwood forest 400 R
Ra3 Bacon Bacon Terraces Surrency Intermit.stream head Mixed hardwoods, pond pine 400 R
Ra4 Emanuel Atlantic Southern Loam Plains Pickney Upper stream terrace Bay forest 400 R
Ra5 Ware Bacon Terraces Surrency Bayhead Bay forest, pond pine 400 R
Ra6 Pierce Bacon Terraces Chipley Upper stream terrace Bay forest, pond pine 400 R
Ba1 Jenkins Atlantic Southern Loam Plains Kershaw Upland side slope Mixed hardwoods, pine 400 B
Bd1 Screven Atlantic Southern Loam Plains Surrency Bayhead Mixed hardwoods, pine 500 B
Rd2 Bulloch Atlantic Southern Loam Plains Rutledge Upper stream terrace Bay forest 400 R
Rd3 Tattnall Atlantic Southern Loam Plains Osier Upper stream terrace Mixed hardwood, pine 400 R
Rd4 Appling Bacon Terraces Surrency Bayhead Mixed hardwood, pine 400 R
Rd5 Brantley Okefenokee Plains Mascotte Upland flatwoods Pine plantation, saw palmetto 400 R
Ri1 Bryan Sea Islands, Coastal Marsh Leon Coastal flatwoods Mixed hardwood, pond pine 400 R
Ri2 Chatham Sea Islands, Coastal Marsh Ellabelle Coastal flatwoods Mixed hardwoods 400 R
Ri3 McIntosh Sea Islands, Coastal Marsh Rutledge Bayhead Bay forest, oaks 400 R
Ri4 Bulloch Sea Island Flatwoods Rutledge Stream head Mature mixed hardwoods, pine 400 R
Sa1 Jenkins Atlantic Southern Loam Plains Troup Sand ridge Pine plantation, mixed hardwoods 200 S
Sa2 Jenkins Atlantic Southern Loam Plains Troup Sand ridge Pine plantation, agric. field edge 50 S
Sd1 Bulloch Atlantic Southern Loam Plains Cowarts Upland side slope Roadside, adjacent pine plantation 200 S
Sd2 Screven Atlantic Southern Loam Plains Fuquay Sand ridge Fence row between agricultural fields 90 S
Ra7B Emanuel Atlantic Southern Loam Plains Kinston- Stream head Mixed hardwoods NA R
Bibb
Ra8B Wheeler Atlantic Southern Loam Plains Osier-Bibb Stream terrace Mixed hardwood forest NA R
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Plot ID/ Plot
disease size
statusA County Ecoregions of GeorgiaC Soil series Landscape positon Plant community typeD (m2) Host
Ri5B Wayne Sea Island Flatwoods Kinston- Bayhead Mixed hardwoods, pine 400 R
Lynchburg
Ri6B Evans Atlantic Southern Loam Plains Rutledge Bay swamp Bay forest NA R
Sa3B Jenkins Atlantic Southern Loam Plains Fuquay Sand ridge Roadside, adjacent pine plantation 140 S
Sd3B Bulloch Atlantic Southern Loam Plains Fuquay Sand ridge Fence row between agricultural fields NA S
APlot ID and initial disease status key: R = Redbay, S = Sassafras, B = both Redbay and Sassafras, a = LWD absent at initiation, d = LW
disease active at initiation, i = inactive, post-LW disease epidemic, NA = not applicable.
BRAB trapping sites only.
CGriffith et al. (2001) Ecoregions of Geor gia.
DRedbay sites in this study generally fit into 2 plant community types, bay forests or mixed hardwoods, some of which also included Pinus
spp. (pine). In addition to Redbay, the most common woody plant species on the bay forest sites were: Gordonia lasianthus (L.) Ellis
(Loblolly Bay), Magnolia virginiana L. (Sweet Bay), Cyrilla racemiflora L.(Titi), Ilex glabra (L.) Gray (Gallberry), and Lyonia lucida
(Lamarck) K. Koch (Fetterbush). Woody species present on the mixed hardwood/pine sites included Acer rubrum L. (Red Maple), Liquidambar
styraciflua L. (Sweetgum), Liriodendron tulipifera L. (Yellow-poplar), Sweet Bay, Nyssa sylvatica Marshall (Blackgum), Redbay,
Quercus nigra L. (Water Oak), other Quercus spp. (oaks), Gallberry, Fetterbush, Myrica cerifera L. (Wax Myrtle), and Titi. Smilax sp.
(greenbrier vines) were present on both bay and mixed-hardwood forest sites, but were especially prolific on bay forest sites. Pinus serotina
Michaux (Pond Pine) was an important component on 3 bay forest and 3 mixed hardwood/pine sites. Pinus elliottii Engelmann (Slash
Pine) or P. taeda L. (Loblolly Pine), was present in several other mixed-hardwood/pine sites. Two plots were established in managed pine
plantations, one Slash Pine and the other Loblolly, with Redbay in the mid-story. The Loblolly Pine plantation was an upland flatwoods site
with Serenoa repens (Bartram) Small (Saw Palmetto) as a major understory component. Sassafras disease-progression plots were generally
located on disturbed sites, adjacent to open fields, with thickets of nearly pure Sassafras. However, 2 plots with both Redbay and Sassafras
present were classified as mixed-hardwood/pine plant communities .