Canadian Journal of Plant Pathology

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Epidemiology of white mold of white bean in

Ontario

GJ. Boland & R. Hall

To cite this article: GJ. Boland & R. Hall (1987) Epidemiology of white mold of white bean in
Ontario, Canadian Journal of Plant Pathology, 9:3, 218-224, DOI: 10.1080/07060668709501877

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Published online: 29 Dec 2009.

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CANADIAN JOURNAL OF PLANT PATHOLOGY 9: 218-224. 1987

Epidemiology of white mold of white bean in Ontario

G J . Boland and R. Hall

Department of Environmental Biology. University of Guelph,

Guelph, Ontario. NIG2WI
Accepted for publication 1987 06 03

The epidemiology of white mold (Sclerotinia sclerotiorum) of white bean (Phaseolus vulgaris) in Ontario was investigated in
1981 and 1982. Apothecia appeared within the crop in late July and were present for 2 to 4 weeks thereafter. During the 2
weeks preceding the occurrence of apothecia in the field, soil temperatures were in the range 15-30°C and soil matric
potentials were generally > -5 bars. Epidemics started in early August and reached levels > 80% within 2 weeks. Disease first
appeared after closure of the canopy and the appearance of apothecia and petals in the crop, and after rain had initiated plant
surface wetness (PSW) periods of 39-64 h. Subsequent lesions developed after PSW periods as short as 14 h. While disease
progressed, average daily air temperatures were in the range 14-22°C. In controlled environments, disease developed at 15-
25° C, most rapidly at 20° C but not at 30° C, and required PSW periods of at least 54 h. It is concluded that severe epidemics
of white mold can occur in white bean if apothecia, PSW periods > 39 h, air temperatures in the range 15-25° C, and a closed
canopy containing petals occur within the crop at or about the same time.
Boland, G.J., and R. Hall. 1987. Epidemiology of white mold of white bean in Ontario. Can. J. Plant Pathol. 9: 218-224

On a étudié, en 1981 et 1982, l'épidénniologie de la pourriture blanche (Sclerotinia scleroiiorum) du haricot (Phaseolus
vulgaris) sec en Ontario. Les apothécies sont apparues dans la culture à la fin de juillet et furent ensuite présentes durant deux
à quatre semaines. Durant les deux semaines précédent l'apparition des apothécies, la température du sol oscilla entre 15 et
30° C et les potentiels matriciels du sol furent généralement > -5 bars. Les épidémies ont commencé au début d'août et ont
atteint des niveaux > 80% en deux semaines. La maladie s'est d'abord manifestée après la fermeture de la voûte végétale et
l'apparition des apothécies ainsi que des pétales, et après que la pluie eut entraîné des périodes d'humectation de la surface de
la plante (HSP) de 36 à 64 h. Par la suite, des taches se sont développées après des périodes de H PS aussi courtes que 14 h. Au
cours des épidémies, la température moyenne de l'air a varié de 14 à 22°C. En milieu contrôlé, la maladie s'est développée
entre 15 et 25° C, le plus fortement à 20° C mais pas du tout à 30° C, et suite à des périodes de HSP d'au moins 54 h. On conclut
que de graves épidémies de pourriture blanche peuvent survenir dans le haricot si la présence d'apothécies, de périodes de
HSP > 39 h, de température de l'air de 15 à 25°C et d'une voûte végétale contenant des pétales coïncident ou arrivent presque
en même temps.

White mold, incited by Sclerotinia sclerotiorum
(Lib.) de Bary, is a common and destructive disease
of bean {Phaseolus vulgaris L.) (Haas & Bolwyn
1972, Purdy 1979, Steadman 1983, Tu &
Beversdorf 1982, Wallen & Sutton 1967) and more
than 360 other species of plants in 65 families
(Purdy 1979). Sclerotiaof the fungus overwinter on
or in the soil and germinate carpogenically to
produce apothecia. Ascospores are the primary
inoculum and require an exogenous source of
energy to infect healthy plant tissues. Senescent
bean blossoms commonly provide this energy.
Thus, epidemics of white mold generally occur
during or after flowering of the crop. Secondary
spread of the pathogen by plant-to-plant mycelial
growth is unimportant (Abawi & Grogan 1979).
Fungicides are used to control the disease but the
efficacy of fungicide treatments is variable,
apparently depending upon numerous factors,
including the timing of the application in relation to
crop phenology, the disease cycle, environmental
conditions affecting infection, coverage of
blossoms and plants, and the required period of
protection from infection (Hunter et al. 1978,
Morton & Hall 1982, Steadman 1979). Elucidation
of the quantitative relationships of pathogen,
weather, and crop factors to disease progress is
needed to develop an accurate system to forecast
the disease and to improve its control by the use of
fungicides. It is likely that details of these
relationships will vary with crop, region, and
cultural practices.
In the only published study on white beans in
Ontario, Haas & Bolwyn (1972, 1973) reported that
disease generally occurred after flowering and was
favoured by soil pH > 7.0, dense canopies, high
individual plant weights, low plant populations,
early seeding, and rows planted at right angles to
the direction of the prevailing winds. They did not
examine the effects of moisture, temperature, or
inoculum. The purpose of the present study was to
observe under field conditions quantitative and
temporal relationships between the occurrence of
white mold in white bean in Ontario and the
presence of apothecia within and outside the field,
closure of the canopy, presence of flowers, periods

218
Published online 29 Dec 2009

of rainfall, matric potential of the soil, duration of
plant surface wetness, and temperature of the air
and soil.
Materials and methods
Field studies. A plot (21 * 21.5 m) of white bean
(cv. Seafarer) was established at the same location
in 1981 and 1982 on sandy loam soil at Arkell,
Ontario. The plot had a history of white mold in
white bean and a severe epidemic had occurred in
1980. The plot was prepared with spring ploughing
and disking in 1981 and spring disking in 1982. The
herbicide Treflan EC (545 g/L trifluralin; Elanco
Prod. Div., Eli Lily and Co. Canada Ltd.,
Scarborough, Ontario) was applied as a preplant-
incorporated treatment at 1.5 L/ ha each year. Spot
applications of Roundup (356 g/L glyphosate;
Monsanto Can. Inc., Mississauga, Ontario) were
applied before planting in 1982 at 2.5 L/ha.
Seeds were chemically treated with B-3 seed
treatment (11.0% diazinon, 16.6% lindane, 33.5%
captan; Chipman Chem. Ltd., Stoney Creek,
Ontario) and sown in 31 rows 72 cm apart at a rate
of 20 seeds per metre of row. The plots were
established on 2 June 1981 and 9 June 1982. In
1982, a 4 m unseeded gap was left in rows 12, 17,
and 23 at the time the main plot was seeded. These
gaps were seeded on 16, 23, and 30 June,
respectively, and, together with the 9 June planting,
were used as observation plots representing four
different planting dates.
Air temperature was recorded with a hygrother-
mograph (model 252; Lambrecht, Goettingen,
Federal Republic of Germany) in a Stevenson
instrument shelter at ground level at the edge of the
plot. Rainfall was measured with a tipping bucket
rain gauge (model P-521; Weather Measure Corp.,
Sacramento, California). In both years, duration of
plant surface wetness (PSW) was monitored with a
DeWit recorder (DeWit, Hengelo, The Nether­
lands) within the crop canopy at 20 cm above
ground level. In addition, in 1982, PSW was
recorded with electrical impedance leaf wetness
sensors (Melching 1974, Hildebrand 1983, Sutton
et al. 1984). Six sensors were wired in parallel and
attached to leaves, petioles, and branches within
the canopy during August. Changes in electrical
resistance were recorded on a Rustrak strip chart
recorder (model 291; Gulton Industries Inc.,
Manchester, New Hampshire). The recording
system was modified to accept alternating current
(Gillespie & Kidd 1978). Soil temperature was
measured with a thermistor placed 2.5 cm below
ground level within the crop and recorded on a
Rustrak strip chart recorder (model 2133; Gulton
Industries Inc., Manchester, New Hampshire). In
BOLAND, HALL: BEAN/WHITE MOLD 219
1982, soil moisture was determined daily by
gravimetric determinations from 15 June to 4
September. Soil samples were taken from the
surface 2-3 cm of soil at three locations within the
field plot. Each sample was weighed before and
after drying at 35° C for 2-3 days. Percent soil
moisture was converted to matric potential from a
soil desorption curve determined using the pressure
plate apparatus (Richard 1965).
Crop stages were determined at weekly intervals
using the soybean growth stage descriptions of
Fehr et al. (1971). Standard descriptions for white
bean were not available. The growth stages
recorded were then divided into vegetative,
flowering, and ripening periods. When all plants
had at least one open flower the field was classified
as being in full bloom. The canopy was defined as
closed when the foliage of adjacent rows touched.
A plant was considered diseased if symptoms of
white mold were detected on any part of the plant,
Disease incidence was expressed as the percentage
of diseased plants in the sample. Disease severity
was calculated as: 2 (severity class * number of
plants in class) * 100/ (total number of plants)
(Grau et al. 1982, Sherwood & Hagedorn 1958).
The severity classes ranged from 0 to 4 where 0 = no
disease, 1 = small lesions less than 5 cm in the
longest dimension, 2 = expanding lesions on
branches or stems, 3 = up to half of branches or
stem colonized, and 4 = more than half of branches
or stem colonized and/or plant dead.
In 1981, the field plot was divided into 310
subplots by establishing 10 subplots 2 m long in
each row. Each subplot extended to 36 cm on either
side of the row. The sample area in each subplot
was located on only one side of the row and was 2 m
long and 36 cm wide. The number of apothecia in
each sample area was counted in all subplots on 22
and 31 July, and in 100 subplots on 13 August. The
mean number of apothecia per sample area was
multiplied by 2 to correct for rating one-half of each
subplot. The presence of apothecia within the field
plot was also determined at frequent intervals.
Disease incidence was determined in 310, 75, 55,
and 33 subplots on 5, 11, 14, and 20 August,
respectively. Environmental variables and crop
development were monitored in the field plot from
2 June to 20 August.
In 1982 the field plot was again marked into 310
subplots. The presence of apothecia in the field was
recorded throughout the season and the number of
apothecia in each subplot was determined on 3 and
11 August. Disease incidence and severity were
rated daily on 100 plants from the field plot after
symptoms were first observed. Detailed observa­
tions on the initiation and expansion of individual
220 CANADIAN JOURNAL OF PLANT PATHOLOGY, VOLUME 9, 1987

lesions were made in four observation plots
representing four planting dates. Two groups of 10
consecutive plants in each observation plot
(total = 80 plants) were rated daily for the
appearance of new lesions, lesion size, and
secondary spread of disease. Environmental
variables and crop development were monitored
from 15 June to 20 August.
The presence of airborne inoculum was
monitored throughout the growing season by
placing indicator white bean plants in the field plot
for periods of 4-8 days. Plants were grown until
flowering in a growth room and three pots,
containing two plants each, were placed in the field
plot at approximately 7-day intervals. After
exposure, the pots were placed in a mist chamber
that maintained continuous PSW and were
monitored for symptoms of white mold for up to
7 days.
Growth chamber studies. The duration of PSW
required to produce symptoms of white mold at 15,
20, 25, and 30°C was investigated. Plants were
grown until flowering in a growth room maintained
at 22 ±2° C with a photoperiod of 14 h. Fluorescent
and incandescent lamps provided a quantum flux
(Fig. 1). In 1982, the disease was first observed 3
August and reached 92.0% 16 days later (Fig. 2).
The onset and rapid development of disease was
associated with the appearance of apothecia within
the plot and PSW periods suitable for infection
during (1981) or shortly after (1982) the period of
flowering.
Data on the location of apothecia and the
development of white mold on indicator plants
supported the hypothesis that disease was initiated
by ascospores produced within the field (intrinsic
ascospores). In both years, apothecia were
commonly found outside the field plot along fence
rows and in areas of rough landscaping in
association with weed hosts, the most common
being dandelion (Taraxacum officinale Weber).
These external apothecia were found as early as 20
May 1981 and 31 May 1982, but were rarely found
after the end of June. Conversely, internal
apothecia (those within the field plot) were
abundant immediately before and during disease
development (Figs. 1 & 2)
25,

density at plant height of 150 JUE/ m2/ s. Two plants

in each of 18 pots were inoculated in each rain i
(mm*
experiment, except at 30° C, when only 8 plants
were inoculated. Plants were inoculated at sites 24
1 [
where senescent flower petals had been placed or lemp • • • • # . , . . • m ,.
(C) J • . *. * *
had lodged naturally. These sites were sprayed with #

a hand atomizer until runoff with a suspension of 14 J «-! ! ^ L

3500 viable ascospores/mL. Ascospores were gs i vegetative ,i flowering n ûaaning 1
obtained from apothecia collected from the field C B

plot and stored on Millipore filters (Steadman &

Cook 1974) at 3-4°C in a desiccator (Hunter et al. 90-1 r
1982).
Inoculated plants were placed in a mist chamber disease /
(%) | /
that maintained PSW at the treatment tempera­
tures. At regular intervals two pots of plants were 0J -==!_ 1
removed and placed in a nonmisted growth 30i r

chamber at the same treatment temperature. Plants

incubated at 30° C were left in the mist chamber for
108 h. At other temperatures, the periods of 15 J • *-* 1
misting ranged over 60-108 h (15°C), 48-102 h 5i r

(20° C), and 36-90 h (25°C). Plants were usually dry
15-20 minutes after transfer between cabinets.
Observations on the number of lesions per pot were
made 2-3 days after plants were removed from the
mist chamber. The experiment was performed
twice.
Results and discussion
Disease developed rapidly in the field in both
years. In 1981, white mold was first observed 5
August and incidence rose to 82.8% within 15 days
apo
/2 m l I
J, , , , ,j.r....!,..,...-.L.J
Uuly W 20 30 1 August 10 20
DATE
Figure 1. Incidence of white mold (disease) of white bean in
relation to rainfall (rain), mean daily air temperature (temp),
crop growth stage (gs), plant surface wetness duration (PSW),
mean daily soil temperature (soil temp), and mean number of
apothecia per 2 m of crop row (apo/2 m) in a field plot at Arkell,
Ontario in 1981 (C = canopy closure, B = full bloom where each
plant has at least one open blossom, * = apothecia present within
the field plot but not counted).

BC"
PSW
(h) \Z
15
1
5
1
11 24 16 66 42 14 3
■■
20 i 13l i ■ ■n
13 i
30 1 August
Uuly
Figure 2. Incidence of white mold (disease) of white bean in
relation to rainfall (rain), mean daily air temperature (temp),
crop growth stage (gs), plant surface wetness duration (PSW),
mean daily soil temperature (soil temp), mean number of
apothecia per 2 m of crop row (apo/2 m), and matric potential
(soil moist) in the surface 2-4 cm of soil in a field plot at Arkell,
Ontario in 1982 (C = canopy closure, B = full bloom where each
plant has at least one open blossom, * = apothecia present within
the fiefd plot bul not counted).
Indicator plants exposed in the field plot early in
the growing season of 1982 (7 June to 28 June),
before bloom, became diseased in the mist
chamber. During this period, apothecia were
present outside but not inside the field plot. These
results indicate that airborne ascospores from an
external source were present in the plot in June.
Between 28 June and 26 July, indicator plants did
not become diseased and apothecia were not found
inside or within I km of the plot, indicating that
ascospores were not present in the plot during this
period. Subsequently, apothecia developed in both
areas and symptoms developed on indicator plants
exposed in the period 26 July to 19 August.
However, the populations of apothecia outside the
plot during this period were lower than those
observed in the spring and considerably lower than
the populations observed inside the crop.
BOLAND, HALL: BEAN/WHITE MOLD 221
Although we conclude that disease in the field
plot developed mostly from internal inoculum, it is
noteworthy that 0-4 lesions developed per pair of
indicator plants (2 plants/pot) in June when
inoculum from external sources only was available.
It is apparent that severe epidemics could have
developed from extrinsic inoculum if the crops had
been in a susceptible stage at this time. In other
studies, apothecia were not found within the field
and ascospores from external sources were thought
to be important in the epidemiology of diseases
caused by this pathogen (Abawi & Grogan 1975,
Akai 1981, Morrall & Dueck 1982, Stelfox et al.
1978, Williams & Stelfox 1979, 1980). The present
study refers to a field that contained high numbers
of apothecia. The relative importance of extrinsic
and intrinsic inoculum in white mold of white bean
in Ontario remains to be determined.
Apothecia occurred in the plot after soil matric
potentials were maintained at or above -5 bars for
most of a 16-day period (Fig. 2). Similarly, in
previous laboratory studies, sclerotia required
water potentials at or above -7.5 bars for about 10
days or longer (Grogan & Abawi 1975, Morrall
1977, Teo & Morrall 1985) in order to produce
apothecia. In our field study, drying of the soil
occurred during the 16-day period and apothecia
appeared 2 days after rain had rewetted the soil.
Similarly, Morrall (1983) reported the appearance
of apothecia within 4 days after a period of intense
rainfall. We observed sclerotia with apothecial
initials below the soil surface in 1981 before the
crop canopy became closed. It is possible that
sclerotia can germinate carpogenically when
exposed to a series of short, discontinuous periods
of wetting.
Mean daily soil temperatures were in the range
15-30°C for the two weeks preceding emergence of
apothecia and in the range 15-25° C while apothecia
were present (Figs. 1 & 2). This is consistent with
laboratory observations that apothecia are
produced most abundantly between 11 and 15°C
and not at all at 5 or 30°C (Abawi & Grogan 1975,
Saito 1977).
Twenty groups of apothecia outside the field plot
(each group representing one carpogenically
germinated sclerotium) were marked with
numbered pins and observed daily from 27 May to
3 June 1982. During this period the weather became
dry and by 2 June all marked apothecia were
desiccated and shriveled. However, rain fell on 3
June and the soil and surrounding plants remained
wet throughout the day. Thirty-one of the 52
apothecia that were marked on 28 May, and
desiccated on 1 June, reopened on 3 June (59.6%).
Some of these revived apothecia released
222 CANADIAN JOURNAL OF PLANT PATHOLOGY, VOLUME 9, 1987

ascospores by puffing. This appears to be the first
report that desiccated apothecia can revive when
conditions become more favourable.
The phenology of the crop, reproduction of the
pathogen, weather factors, and the occurrence of
disease were interrelated. The prolonged condi­
tions of high soil moisture required for carpogenic
germination occurred as the canopy became fully
closed and disease occurred after apothecia and
flowers appeared in the plot and after closure of the
canopy (Figs. 1 & 2). Other studies have shown that
canopies that provide cooler and wetter environ­
mental conditions favouring apothecial develop­
ment (Schwartz & Steadman 1978) or increased
spore survival (Caesar & Pearson 1983) are
associated with increased infection and disease
development (Weiss et al. 1980a, 1980b). Mean
daily temperatures during disease development (14-
22° C) were in the range suitable for white mold
(Table 1, Abawi & Grogan 1979).
The PSW periods required to initiate lesions in
controlled environment were similar to those
associated with the beginning of epidemics in the
field. In controlled environment chambers,
symptoms did not become apparent without at
least 54 h of continuous PSW at 20°C (Table 1).
Longer PSW periods were required at 15°C and
25°C. Abawi & Grogan (1975) also reported that
48-72 h of continuous PSW were required for
symptoms of disease to appear when ascospores
were inoculated onto senescent blossoms lodged on
bean plants in the mist chamber. Similarly, periods
of PSW associated with the first appearance of
symptoms of disease in the field ranged from 39 h
(Fig. 2) to 64 h (Fig. 1). Although only a few lesions
were visible at this time hyphae were often seen
emerging from colonized blossoms.
Once an epidemic had started, new lesions also
usually developed after extended periods of PSW.
New lesions, originating from senescent, colonized
blossoms, were found on 14 of 16 dates that
observations were made (Table 2). Of 67 lesions
observed, 38 appeared within 24 h after the end of
four extended periods of PSW that occurred from
1-4 August (63 h), 7-9 August (39.5 h), 12-14
August (38 h), and 17-19 August (27.8 h). An
additional 17 lesions appeared in a fourth PSW
period from 21-26 August when five interrupted
periods of dew and rain resulted in a total of 82.5 h
of PSW during a 104-h period. This PSW period
was associated with an increase in disease incidence
in the late-planted plots only. Ten lesions appeared
2-4 days after the first two extended PSW periods
and were associated with periods of wetness caused
by dew lasting for 15.25 h. The two remaining
lesions appeared separately in association with
periods of PSW of 14 and 15 h. Abawi & Grogan
(1975) also reported successful infection of 3 of 51
plants inoculated with an ascospore suspension
after 16 h of leaf wetness in field conditions, and
Blad et al. (1978) found that white mold developed
in association with daily PSW periods of 11-12 h in
irrigated fields in Nebraska. The possibilities that
the pathogen can infect following several
consecutive short periods of PSW or that the
inoculum concentration affects the duration of
PSW required for infection should be explored.
Grogan (1979) observed that much of the
information on the epidemiology of white mold in
Phaseolus species was derived from controlled
environment studies and that more field studies
were required. This study contributes to that
objective. The production of apothecia in the field
was associated with soil temperatures in the range

Table 1. Effects of temperature and duration of plant surface wetness on incidence of lesions produced on bean
plants inoculated with ascospores of 5. sclerotiorum

Number of lesions per number of inoculation sites after the following periods of
Temperature continuous plant surface wetness (h)a
(°C) 36 42 48 54 60 66 72 78 84 90 96 102 1(
30
exp. 1 0/36
exp. 2 0/44
25
exp. 1 0/18 0/24 0/14 0/16 0/12 4/11 12/21 4/8 18/23
exp. 2 0/13 0/15 0/19 0/12 0/12 0/13 4/16 4/8 6/12
20
exp 1 0/8 l/ll 1/11 3/11 2/11 10/13 10/13 10/15
exp. 2 0/24 1/28 2 / 3 3 3/18 12/24 6/22 7/26 9/18 11/28
15
exp. 1 0/27 0/23 0/23 0/23 0/24 1/22 4/19 5/29 13/33
exp. 1 0/26 0/23 0/26 4/24 8/24 8/24 10/24 11/20 16/21
^Plants were removed at 6-hour intervals and placed in growth chambers maintained at the same treatment
temperatures without plant surface wetness. Plants were rated for lesions 2-3 days after removal from mist
chambers.
 BOLAND, HALL: BEAN/WHITE MOLD 223

Table 2. Time and duration of plant surface wetness (PSW) in a field plot of white
bean during August 1982 in relation to the appearance of lesions of white mold and
increases in disease severity.

Time of Time of
Date initial initial PSW No. of new Disease
in wetness dryness duration lesions/80 severity
August (h) (h) (h)' plants2 index3
1-4 1830 1330 63.00 5 34
4-5 2030 1145 15.25 0 108
5-6 2030 1145 15.25 9 88
6-7 2100 1215 15.25
7-9 1930 1100 39.50 17(3)* 140
9-10 2015 1030 14.25 7 183
10-11 1930 1015 14.75 0(2) 198
11-12 2000 1115 15.25 1 174
12-14 1900 0900 38.00 3(3) 230
14-15 1915 0900 13.75
15-16 1845 0945 15.00 1 285
16-17 1830 0830 14.00 1 239
17-18 1900 0930 11.75
18-19 1845 0745 13.00
19 1015 1315 3.00 4 280
19-20 2145 0930 11.75 2 276
20-21 1830 1045 16.25
21-23 2030 1030 38.00 1 313
23 1300 1445 1.75 1
23-24 1830 0830 14.00
24-25 1500 0915 18.25 8 322
25-26 2015 0645 10.50 7(1)
'Plant surface wetness from 1-4 August was measured with a De Wit recorder. All
other measurements were made with electrical impedance leaf wetness sensors.
2
Number of new lesions observed in 20 plants at each of four planting dates (80 plants
total).
^Disease severity index =
2 (Severity Class * number of plants in class) ir.n.

Total number of plants

classes are 0 = no disease; 1 = small lesion(s) less than 5 cm; 2 = expanding lesion on
branch or stem; 3 = up to half of branches or stem colonized; and 4 = more than half of
branches or stem colonized and/or plant death,
♦Numbers within parentheses represent lesions initiated by secondary spread of
disease (mycelial spread from diseased to nondiseased tissues).

14-30°C and soil matric potentials generally > -5
bars. The disease developed after canopy closure,
the onset of bloom, the appearance of apothecia in
the field and the persistence of moisture on plant
surfaces for periods of 39 h or more. We have
identified the quantitative and temporal relations
of these factors to disease occurrence, but their
relation to disease severity and their application to
disease prediction remain to be determined.
The financial support of the Natural Sciences and Engineering
Research Council of Canada and the Ontario Ministry of
Agriculture and Food is gratefully acknowledged.
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