SOYBEAN SUDDEN DEATH SYNDROME IN KENTUCKY
Donald E. Hershman
Soybean sudden death syndrome (SDS)
was first discovered in Arkansas in 1971, but was not recognized as a serious
soybean disease until 1984. Since that time, the disease has been confirmed
in 9 states including Alabama, Arkansas, Illinois, Indiana, Kentucky, Louisiana,
Missouri, Mississippi and Tennessee. While SDS is not a serious problem
every year, severe infections can reduce yields by as much as 80%. These
losses result from premature defoliation, flower and pod abortion, pod
drop and reduced seed size. Indirect yield losses and seed quality problems
may also be a factor due to higher levels of pod- and stem-infecting fungi
where plants die prematurely as a result of SDS.
SDS has appeared in 20 west Kentucky
counties since 1984. The most severe episodes of the disease have occurred
in highly productive river bottom fields, especially those with a history
of soybean cyst nematode (SCN) infestation. Early-planted full season soybeans
are more often and more severely affected than are double crop soybeans
or late planted full season soybeans.
Initially, the cause of SDS was elusive,
with mechanical, cultural, environmental and biological factors all considered
as possible causes. Early studies involving soil fumigation indicated that
the origin was biological. Subsequent work in Arkansas and Mississippi
proved that SDS is caused by a strain of the common soil fungus Fusarium
solani (FS-A). This result has been confirmed by work in Indiana and
Missouri and is now generally accepted.
Although FS-A is the primary organism
associated with SDS, other pathogens may also be involved in disease development.
The most studied of these is the soybean cyst nematode. Mississippi researchers
found that while SCN is not required for severe SDS to occur, SCN at sufficient
levels exacerbates foliar symptoms, leading to early and severe SDS. This
finding is important, since the disease's timing and severity, relative
to soybean development, determines how much yields are reduced.
In addition to SCN, other soybean pathogens
(foliar and root/stem infecting) are being studied for their potential
role in SDS development. Preliminary data suggest that any stress factor
(biological, mechanical or environmental) may magnify SDS symptom expression
and cause SDS-affected plants to deteriorate earlier and more severely
(i.e. to die prematurely).
Symptoms first appear as random, irregularly-shaped
yellow blotches of various sizes. Blotches occur between the veins of leaflets
and can start at any level in the canopy of plants. As the disease progresses,
blotches run together and begin to turn brown. At first this effect is
most pronounced in the tops of plants. At this stage the disease becomes
recognizable from the road.
With time, you see large dead areas
between the veins with the veins remaining green. Affected leaflets eventually
die and either stay on the plant or fall to the ground. In the latter case,
the petioles remain attached and the plants look as though they have been
fed on by grasshoppers.
Severe defoliation in the early to
mid-reproductive stages may be accompanied by flower and pod abortion and
drop of developing pods. Fully expanded pods, although they may ripen prematurely,
rarely drop off the plants. Premature ripening, however, may lead to higher
levels of pod- and stem-infecting fungi which could indirectly lower yields
or seed quality.
Root and Stem Symptoms
In addition to foliar symptoms, roots
and stems of plants with SDS also show characteristic symptoms. Root symptoms
precede foliar symptoms and appear as a general deterioration of taproots
and lateral roots. Nitrogen-fixing nodules also deteriorate and are non-functional.
The internal portion of affected taproots turns a milky gray-brown. This
general discoloration extends up the stem for several nodes, but the stem's
core remains healthy (i.e. white).
SDS symptoms are the result of root
infections by FS-A. The fungus cannot be isolated from tissue above the
soil line. Recent research has indicated that foliar symptoms are the result
of a fungus-produced plant toxin. The fact that plants occasionally recover
after showing earlier foliar symptoms further suggests toxin activity.
Symptoms of SDS can begin in plants
at almost any stage of development; however, in Kentucky symptoms rarely
develop before the mid pod fill stages. While the name "sudden death syndrome"
suggests the plants' rapid and complete demise, death, if it occurs, can
come very slowly or affected plants may recover. Hot and dry weather during
pod development is most often associated with the remission of SDS symptoms.
SDS is most prevalent and severe during
wet, cool growing seasons. Crops planted early when soil moisture and temperatures
are higher and lower, respectively, also seem to be at greatest risk. However,
severe SDS has been noted in late-planted soybeans.
The link between soil moisture and
SDS, while suspected by many, was confirmed through work in Mississippi.
Workers there found that root infection by FS-A was highest and SDS more
severe under conditions of continuous, high soil moisture during the early
vegetative stages of crop development. It is common to be able to isolate
FS-A from soybean roots as little as 2 weeks after planting. Thus, under
field conditions, a long period exists between root infection by FS-A and
the development of foliar symptoms.
SDS typically begins in fields as spots
('hot spots') or streaks. This may be followed by symptom development throughout
the field. Although the reason behind the development of hot spots is not
clear, researchers speculate that these areas in fields are most favorable
to root infection by FS-A and/or the development of symptoms. Conditions
which favor these processes are still being worked out, but probably include
higher soil moisture, higher SCN populations, and slowed or enhanced root
development, among other factors.
Research in Kentucky and field observations
throughout the mid south indicate that cropping sequence has little effect
on SDS development. This is probably due to the widespread distribution
of FS-A and its ability to survive for long periods in the roots of many
crop and weed plants, in plant residues and in the soil. However, a questions
remains as to rotation's effect on other diseases which may indirectly
affect SDS. It seems logical that moderating any stress factor by crop
rotation would lessen the potential for severe SDS to occur. This, however,
has yet to be proved.
Cultivars differ in their response
to SDS; however, researchers have had a hard time pinning down a consistently
favorable response from many cultivar. This situation is not likely to
change until we better understand the factors favoring and determining
SDS severity. The development and use of environmentally-controlled tests
for the rapid screening of soybeans against FS-A, should help identify
cultivars with the highest and most consistent level of resistance. The
long-term goal is to identify resistance genes and begin an SDS breeding
program using either conventional breeding techniques or biotechnology.
While control measures for SDS are
still under development, using the following practices, in an integrated
approach, should help reduce the disease's overall impact.
•Plant cultivars which have performed
well in the presence of SDS. To determine which cultivars to plant, use
test results from as many locations and years as possible. Give preference
to cultivars with resistance to other important diseases in your area.
•Plant more than one cultivar, preferably
from different maturity groups.
•For full season soybeans, delay planting
for as long as possible. Early May plantings are at generally higher risk
than are late May/early June plantings.
•Plant parts of fields or different
cultivars at different times.
•Use any cultural practices which reduce
plant stress (good fertility and weed control) and control other diseases
which might augment the effects of SDS (e.g. SCN).
•Improve drainage in field.
•Harvest affected fields in a timely