Front Cover
 Whatever happened to soybean stem...

Group Title: Research report - North Florida Experiment Station, University of Florida - NF 87-2
Title: Whatever happened to soybean stem canker?
Full Citation
Permanent Link: http://ufdc.ufl.edu/UF00073722/00001
 Material Information
Title: Whatever happened to soybean stem canker?
Series Title: NFREC, Quincy Research report
Physical Description: 12 leaves : ; 28 cm.
Language: English
Creator: Shokes, Frederick M ( Frederick Milton ), 1943-
Ploetz, Randy C
Sprenkel, Richard K
North Florida Research and Education Center (Quincy, Fla.)
Publisher: Florida Agricultural Experiment Station, Institute of Food and Agricultural Sciences, University of Florida
Place of Publication: Gainesville FL
Publication Date: 1987
Subject: Soybean -- Diseases and pests -- Florida   ( lcsh )
Canker (Plant disease) -- Florida   ( lcsh )
Genre: government publication (state, provincial, terriorial, dependent)   ( marcgt )
bibliography   ( marcgt )
non-fiction   ( marcgt )
Bibliography: Includes bibliographical references (leaf 9).
Statement of Responsibility: by F.M. Shokes, R.C. Ploetz and R.K. Sprenkel.
Funding: Research report (North Florida Research and Education Center (Quincy, Fla.)) ;
 Record Information
Bibliographic ID: UF00073722
Volume ID: VID00001
Source Institution: Marston Science Library, George A. Smathers Libraries, University of Florida
Holding Location: Florida Agricultural Experiment Station, Florida Cooperative Extension Service, Florida Department of Agriculture and Consumer Services, and the Engineering and Industrial Experiment Station; Institute for Food and Agricultural Services (IFAS), University of Florida
Rights Management: All rights reserved, Board of Trustees of the University of Florida
Resource Identifier: oclc - 84653765

Table of Contents
    Front Cover
        Front Cover
    Whatever happened to soybean stem cankers?
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        Page 2
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Full Text


The publications in this collection do
not reflect current scientific knowledge
or recommendations. These texts
represent the historic publishing
record of the Institute for Food and
Agricultural Sciences and should be
used only to trace the historic work of
the Institute and its staff. Current IFAS
research may be found on the
Electronic Data Information Source

site maintained by the Florida
Cooperative Extension Service.

Copyright 2005, Board of Trustees, University
of Florida

NFREC, Quincy Research Report NF-87-2

Whatever Happened
To Soybean Stem Canker?

by F.M. Shokes,
R.C. Ploetz,
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


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

canker research.

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
76:(in press).

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
Counties severely
affected during
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

Counties adjacent
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

Counties not
affected by
stem canker in 1983
Gulf nd nd 51 49 33 67
d d
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
susceptible, and
Hiebsch (3).

No data.

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
Jeff 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
Wright MR

a R = resistant, MR
S = susceptible.

= moderately resistant, MS = moderately susceptible,

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