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Copyright 2005, Board of Trustees, University
NFREC, Quincy Research Report NF-87-2
To Soybean Stem Canker?
by F.M. Shokes,
and R.K. Sprenkel
Florida Agricultural Experiment Station
Institute of Food and Agricultural Sciences
University of Florida, Gainesville
NFREC, Quincy Research Report NF-87-2
WHATEVER HAPPENED TO SOYBEAN STEM CANKER?
by: F.M. Shokes, R.C. Ploetz, and R.K. Sprenkel
In 1983 a major disease epidemic hit soybeans in the western portion of
the Florida panhandle. This disease, known as 'stem canker', devastated some
fields killing grown plants from midseason to maturity and depressed yields
20-50% in fields planted to susceptible varieties. Whatever happened or is
happening to this 'killer' soybean disease? Is there potential for a recur-
rence of the epidemic of 1983? To answer these questions, first let us ex-
plore the nature of the disease and its causal organism.
Stem canker is caused by a fungus that has been known by researchers as
Diaporthe phaseolorum var. caulivora. Since the fungus that we have in the
southeast is slightly different from the one that has been present in the
midwest for a number of years, we call it southern Diaporthe phaseolorum.
This fungus produces two different kinds of spores, both of which can infect
soybeans. In the spring and early summer, when moist conditions prevail,
spores are produced which are capable of infecting soybeans of all ages. The
disease typically develops many days after seedlings are infected, usually
about the time of pod fill. Frequently this disease is not noticed in the
field unless significant symptom development occurs. Conspicuous symptoms
develop only with severe disease. Leaves flag (hang down) and turn brown
between the veins. The leaf stems petioless) die and large brown areas
(cankers) may be seen on the stems. More often than not, these cankers may be
found spreading in both directions from the base of a leaf petiole on the main
stem (see picture on front cover). Green tissue will generally be found above
and below the canker. Plants with cankers may wilt and die. When a plant
dies from stem canker the leaves often remain on the dead plant. In its
early stages, this disease may be confused with anthracnose, but anthracnose
lesions tend to be superficial (they may be scraped off with a fingernail)
whereas stem canker lesions penetrate much deeper into the tissue.
The fungal spores that cause this disease most often infect the plant
where the petiole is attached to the main stem (the crotch) but they may
infect leaves or other plant parts as well. Plants that die from stem canker
in the field are usually of varieties that are moderately to highly suscep-
tible. Varieties which are moderately resistant may be infected but never
develop major symptoms. Resistant varieties such as Braxton or Tracy-M, may
also be infected but usually do not develop cankers in the field.
In 1983 when stem canker first became a problem in Florida, a disease
survey was conducted from September 13-23 (Table 1). A total of 483 fields
were checked, representing 10,789 acres. At that time we were aware only of
the major symptoms associated with the disease. Therefore we were also not
certain about the spread of disease from field to field. We did not want to
enter a field without stem canker after walking through one in which the
disease was present. Fields were scanned with binoculars and only those with
foliar symptoms (leaves flagging and dying) were entered. Plants showing
foliar symptoms were checked for stem cankers.
The incidence (how many plants in a field that are affected) and severity
(how badly plants are affected by disease) of stem canker were high in 1983.
The percentage of fields with symptoms ranged from zero in some counties to
81% of those checked in Escambia county (Table 1). Five counties in the
western and central panhandle had a high occurence of stem canker in 1983.
They were Escambia, Walton, Holmes, Washington and Jackson counties. Santa
Rosa county, immediately adjacent to Escambia county, had very little evidence
of stem canker that year.
In 1984, 567 fields representing approximately 12,404 acres were checked
for stem canker. Foliar symptoms were not as obvious and every fourth or
fifth field was entered and stems were closely checked for symptoms of the
disease, regardless of the occurence of foliar sypmtoms. In 1985 a similar
situation existed as 478 fields, representing approximately 13,170 acres, were
surveyed. The occurence of stem canker was low during 1984 and 1985. Whether
infected plants develop no symptoms, small lesions (cankers) or the plant dies
will depend on known and unknown factors. Our question was, which factors had
changed in these two years versus 1983 that might explain differences noted in
the occurence of stem canker?
One obvious factor to investigate was the weather. Many plant diseases
are dependent on an environment favorable for disease. Two other requirements
for disease to occur are the presence of the pathogen (in this case, the
fungus), and the presence of a susceptible host. We are not yet certain of
the exact weather conditions necessary for major symptom development but we do
know what is necessary for infection. Spores are produced when warm moist
conditions prevail (around 750F with rainfall or very high humidities). These
spores may be windblown or rain splashed onto a plant and, with heavy dews or
light rains, infect the plant when temperatures are within 50-95 F and free
moisture is present. However, some other stress factor must occur at just the
right time for major symptom development to occur. For example, in 1983,
there was a mid-season dry period in many areas where the severity was high.
Some water stress probably occurred in fields in which soybeans were infected
at a much earlier date. If that stress or some other stress occurred at the
critical time (around the beginning pod stage) major symptom development could
occur. Observations on greenhouse grown plants at Quincy lead us to believe
that this is what occurred in the field.
Another major difference between 1983 and the 1984 & 1985 seasons was in
the varieties grown throughout the Florida panhandle. A survey was conducted
among seed distributors to identify the varieties and quantities sold during
the three seasons. Soybean seed for planting in 1983 in the severely affected
counties were approximately 59% susceptible and 41% resistant varieties (Table
2). Major changes in varieties purchased for seed were found in following
years. In 1984, only 11% of the soybeans planted in the severely affected
counties were susceptible to stem canker and in 1985, 16% were susceptible.
Similar changes were noted in adjacent counties. However many acres of
susceptible varieties are still grown in other counties of north Florida.
Other work with stem canker has shown that there is considerable variation
within the pathogen population. Using sophisticated techniques for differen-
tiating fungal isolates (fungi from different infected plants), it has been
found that there are at least 29 different groupings. However, there is a
predominance of one type of the pathogenic fungus (Group 1). Implications of
this work are that this particular grouping of the pathogen may have become
established in Florida before isolates of other groups spread into the region.
Although it is impossible to say whether the stem canker fungus came into
Florida on seed, plant debris, or from some other means, we believe that
infested seed played a relatively minor role in the spread of the disease. It
is difficult to find this organism in seed. Where it is found in the seed it
is only present in very low levels, in soybean seed lots throughout the South.
It is very likely that this disease was present in Florida and that the ino-
culum (spore populations) was increasing long before the major epidemic of
1983. Since we know that infection may occur without killing plants or even
causing major symptom development this is very likely. This conclusion is
supported by the fact that resistant and susceptible varieties may be infected
by the fungus and both may develop fruiting structures (which can produce
spores) even if symptoms do not develop. These fruiting structures may
develop in soybean debris and produce spores which can infect soybeans if they
are planted in that field the next season. The fungal population may have
built up in many of our fields in this way, unnoticed until the right
combination of susceptible variety and environment occurred.
Additional research has been conducted at the North Florida Research and
Education Center at Quincy to develop a method of screening breeding lines for
resistance. Field screening is difficult because symptom development is
erratic. Another difficulty is that resistant varieties as well as suscep-
tible varieties may be infected by the fungus. Our research has shown that
the resistance is mainly physiological, expressing itself after infection.
For example, after inoculation of plants in the greenhouse the fungus could be
routinely isolated from tissue not showing symptoms on both resistant and sus-
ceptible varieties and from stem lesions of susceptible varieties. This
agreed with results of isolations of the fungus from field grown plants.
Since the environment is a factor that is difficult to control in the field
and major symptom development is very slow (40-80 days) in the field (even
when it does occur) we sought a quicker way to screen resistant breeding
lines. Working cooperatively with plant pathologists at Dupont De Nemours &
Co. (Wilmington, Delaware), a system was developed whereby plants were inocu-
lated with spores and placed at 22-270 C in a mist chamber for 14 days.
Symptom development occurred by the end of the incubation period. High humi-
dity in these studies placed the plants under a stress and probably provided a
favorable environment for the pathogen to act quickly within the plant. This
system distinguishes varieties of known resistance or susceptibility but
additional work will be needed to validate this technique in the field. This
work is continuing and it is hoped that we will eventually be able to aid
soybean breeders in selecting breeding lines resistant to stem canker.
In conclusion we have documented that there exists a population of a
pathogenic fungus in the Florida panhandle which can cause soybean stem canker
when the right environmental conditions occur and susceptible varieties are
used. Since 1983, we have learned a lot about the fungus itself and how it
infects soybeans. Crop rotation is advisable as well as avo -e of any
Tield where stem canker may have been a problem in recent years. ,, epidemic
of 1983 brought about considerable changes in variety utilization and the best
defense against stem canker is the use of resistant varieties. Some good ones
such as Braxton are available now. Others must be developed by breeders.
Table 3 lists the relative resistance to stem canker of a number of available
soybean varieties. In the Florida panhandle if soybean growers persist in
planting susceptible varieties such as Bragg or Hutton the potential is great
for a recurrence of the epidemic of 1983 whenever the necessary environmental
conditions occur. No one can say for sure when this may happen.
Whatever happened to soybean stem canker? It is still there, waiting, but
we know how to prevent major losses to this disease. Resistant and moderately
resistant varieties are available and should be used. Several of these
varieties have an additional benefit in that they have nematode resistance
that is not present in some of the older susceptible varieties. Growers
should consult their county agent for the latest information on recommended
soybean varieties and follow practices recommended for minimizing this
potentially devastating disease.
The authors would like to thank Dr. C.M. Smith, E.I. DuPont De Nemours &
Company; Dr. C.K. Hiebsch, IFAS-Extension Soybean Specialist; and Dr. T.A.
Kucharek, IFAS-Extension Plant Pathologist, for their help with the stem
Tables 1 & 2 are from a journal publication 'Current Status of Stem Canker
in Florida', published in Plant Disease, Volume 70, July, 1986.
Backman, P.A., D.B. Weaver and G. Morgan-Jones. 1985. Soybean stem canker:
an emerging disease problem. Plant Dis. 69:641-647.
Hiebsch, C. 1984. Soybean Variety Characteristics. Agron. Facts 165, Univ.
of Fla. 4pp.
Hobbs, T.W. and D.V. Phillips. 1985. Identification of Diaporthe and
Phomopsis isolates from soybean. (Abstr.) Phytopathology 75:500.
Phillips, D.V. 1984. A selective medium for Diaporthe phaseolorum var.
caulivora. (Abstr.) Phytopathology 74:815.
Ploetz, R.C. and F.M. Shokes. 1985. Soybean stem canker incited by
ascospores and conidia of the fungus causing the disease in the
southeastern United States. Plant Dis. 69:990-992.
Ploetz, R.C., R.K. Sprenkel and F.M. Shokes. 1986. Current status of soybean
stem canker in the southeastern United States. Plant Dis. 70:600-602.
Ploetz, R.C. and F.M. Shokes. 1986. Evidence for homothallism and vegetable
compatibility in southern Diaporthe phaseolorum. Can. J. Bot.
Ploetz, R.C. and F.M. Shokes. 1986. Infection of different plant parts of
soybean seedlings by southern Diaporthe phaseolorum and its role in the
development of stem canker symptoms. Can. J. Bot. 64:(in press).
Ploetz, R.C. and F.M. Shokes. 1986. Factors influencing the infection of
soybean seedlings by southern Diaporthe phaseolorum. Phytopathology
Table 1. Occurence of soybean stem canker in Florida during the 1983-1985
acres Fields Fields with
surveyed (no.) surveyed (no.) symptoms (%)a
County 1983 1984 1985 1983 1984 1985 1983 1984 1985
Escambia 1043 2691 1794 47 45 49 81 7 0
Santa Rosa 568 2093 835 41 80 53 2 0 2
Okaloosa 964 793 848 38 27 27 8 0 0
Walton 608 630 1317 29 29 52 52 0 0
Holmes 633 561 610 28 35 36 75 0 0
Washington 1013 647 778 49 48 41 65 8 0
Jackson 2417 988 1040 111 57 56 63 0 0
Calhoun 1554 766 1384 53 58 33 2 7 0
Gadsden 652 378 835 29 29 39 7 0 0
Gulf ns 390 932 ns 10 12 ns 0 0
Madison 993 1273 2192 32 51 55 0 0 0
Jefferson 363 210 ns 26 21 ns 0 5 ns
Hamilton ns 321 ns ns 17 ns ns O ns
Suwannee ns 665 665 ns 30 25 ns 0 0
Total 10,803 12,410 13,176 483 567 478 ---
aFields containing plants with foliar symptoms of stem canker.
symptoms were confirmed by examining plants for stem lesions typical of the
County not surveyed during this season.
Table 2. Percentages of susceptible and resistant soybean varieties
grown in Florida during the 1983, 1984 and 1985 seasons
1983 1984 1985
Seed sales Seed sales Seed sales
1983 epidemic S R S R S R
Escambia 54 46 41 59 17 83
Holmes 30 70 0 100 ndC nd
Jackson 41 59 7 93 0.2 99.8
Walton 87 13 0 100 4 96
Washington 90 10 11 89 55 45
to those severely
affected in 1983
Calhoun 50 50 10 90 3 97
Gadsden 59 41 2 98 3 97
Okaloosa 49 51 31 69 nd nd
Santa Rosa 49 51 21 79 6 94
stem canker in 1983
Gulf nd nd 51 49 33 67
Jefferson 100 0 51 49 36 64
Leon 100 0 100 0 nd nd
Suwannee nd nd 58 42 44 56
aSeed sold by distributors in a given county.
percentage of seed of varieties susceptible (S)
soybean stem canker; S=susceptible or moderately
R=resistant or moderately resistant according to
or resistant (R) to
percentages from total of less than 750 bu. of seed.
Table 3. Relative resistance of soybean varieties to stem canker.
Variety Resistancea Variety Resistancea
Maturity Group V Maturity Group VI
A5939 S A6520 MS
Bedford MS Centennial MR
Deltapine 105 MS Coker 156 MR
Essex MS Davis MR
Forrest S Deltapine 506 MS
Maturity Group VII RA 604 S
A7372 S RA 680 MR
Bragg S S69-96 S
Braxton R Sumter S
Coker 237 S Terra-Vig 606 MR
Coker 317 MS Tracy-M R
GaSoy 17 MS
Govan MS Maturity Group VIII
McNair 700 S Cobb MR
McNair 770 S Coker 338 S
RA 702 S Coker 368 MR
RA 801 S Coker 488 MR
Ransom MS Foster MS
Terra-Vig 708 S Hutton S
Wilstar 790 S Kirby MR
a R = resistant, MR
S = susceptible.
= moderately resistant, MS = moderately susceptible,