Prepared
by Damon L. Smith
A class project for PP728
Sclerotinia minor Jagger.
Introduction and importance
Sclerotinia minor, the fungus
that causes Sclerotinia blight, white mold and watery soft rots of vegetables,
or lettuce drop, can infect host plants from 21 families, 66 genera, and
94 species. The hosts that have been documented are from the branch Angiospermae.
Most hosts of Sclerotinia minor are in the class Dicotyledonae,
but there are two documented occurrences of S. minor on hosts belonging
to the class Monocotyledonae (12). Sclerotinia minor occurs
worldwide but especially in cool, moist regions. Sclerotinia minor
causes watery soft rots, cottony soft rots, drop, and other diseases of
many important flower and vegetable crops (2). Some common plants that
are susceptible to S. minor include chicory, caraway, baby’s breath,
carnation, and other popular ornamentals. Economically important crops
that S. minor is a pathogen of include soybean, sunflower, common
bean, cucumber, lettuce, spinach, cabbage, sweet potato, irish potato,
pepper, tomato, peanut, and many others (12).
There has been a large amount of research completed on the various crop patho-systems that involve S. minor. This is especially true for S. minor occurring on peanut, Arachis hypogea L. Sclerotinia minor was first identified as a disease on peanut in Australia in 1948. By 1960 reports of S. minor causing root and pod rot on peanut were being reported in Argentina. The first reports of S. minor in the United States were made in Virginia 1971 and then in North Carolina in 1972 (17). Since its inception in the United States the fungal disease has become widespread, having moved into Oklahoma and Texas as well as becoming severe in Virginia and North Carolina. Sclerotinia minor is more damaging than many soilborne pathogens because it has the ability to spread rapidly within the peanut canopy, shows great persistence in the soil, as well as a high level of susceptibility in many hosts. This particular pathogen has caused yield losses of near 80 percent in some areas (17).
Kingdom - Fungi
(Mycetae)
Phylum - Ascomycota
Class - Discomycete
Order - Heliotiales
Family - Sclerotiniaceae
Genus - Sclerotinia
Species - Sclerotinia minor
S. minor, the Causal agent of Sclerotinia blight on peanut. Picture courtesy of NCSU Plant Pathology Extension (14).
Causal agent and signs
The mycelium of S. minor
is white and fluffy. The sclerotia (survival structures) have a black
outer rind, are irregularly shaped, and are approximately (0.5-3.0mm) in
size. Apothecia are rarely seen in the natural environment, but may
occur during February and March or mid-fall on the soil surface.
The apothecia are pale orange to white and have concave or flat tops. If
apothecia do form, they may be 6 mm or more in diameter and contain asci
with ascospores (sexual spores) that measure 8-17 x 5-7 um (3). The
main mode of infection of S. minor is through eruptive germination
of the sclerotia, giving rise to mycelium that infects the plant tissue
(17).
Epidemiology on Peanut
Peanuts become infected with S.
minor in most cases by mycelium from germinating sclerotia. Favorable
conditions for germination and infection include temperatures of 17-21
C and relative humidities of greater than 95 percent (3). In addition,
a soil pH of 6.5 is considered desirable for the germination of sclerotia
in the field (17). In addition, presence of volatile materials from
moist undecomposed plant tissue has been shown to initiate sclerotial germination
in closely related fungi such as Sclerotium rolfsii. Substances
include alcohols such as methanol, aldehydes, esters, and halogenated hydrocarbons
(5). Presence of volatiles has also been shown to be related to sclerotial
germination by S. minor (17). Under optimum conditions peanut leaves,
stems, and pegs that are in contact with the ground can be infected by
the growing mycelium of S. minor. Interestingly, unlike other
species of Sclerotinia, S. minor does not need a food base
of dead or senescing tissue to infect. It has the capability to infect
stems and branches in contact with the soil with no food bases (17).
During severe infections of peanut crops, the top 2.54 cm of soil can be
heavily infested with sclerotia. At the end of the growing season,
sclerotial densities of 50 sclerotia per 100 g of soil are possible (17).
Mechanically injured peanut tissue
is very susceptible to colonization by S. minor. Plants injured
by tractor tires during pesticide application showed a greater incidence
of disease caused by S. minor than non-injured plants (3).
In addition, yield losses correlated to plant injury were about twice as
great as those yield losses in non-injured plants (17).
Sclerotia inside peanut stems. Picture
Courtesy of NCSU Plant Pathology Extension (14).
Disease Cycle
The mycelium of Sclerotinia minor
attacks lower branches and rapidly invades succulent tissues causing cells
to collapse. The mycelium then develops a white, fluffy mass on the
surface of the tissue as it invades more plant tissue. The plant
is eventually killed and sclerotia are produced in abundant numbers on
the dead tissue. Some sclerotia are shed from the plant tissue into
the soil or can be retained on dead plant tissue as overwintering inoculum.
When conditions are right, the sclerotia germinate into either mycelium
or apothecia (sexual stage of the fungus). In the mycelial stage
the fungus infects a new plant and the cycle starts over again. If
the sclerotia give rise to apothecia (which is a very rare occurrence in
S.
minor) then asci are formed with ascospores (the sexual spores).
When the ascospores mature they are discharged and land on a plant, germinate,
and start the disease cycle over again (3).
Mycelium within the peanut canopy.
Photo courtesy of Joyce
Hollowell.
Signs and Symptoms
Sclerotinia minor can cause
the watery soft rot of many fruits and vegetables except onions and potatoes
(2). In a cool (18 degrees C) moist environment (greater than 95
percent humidity) watery soft lesions occur at sites of infection and the
tissues are rapidly covered with white fluffy mycelium. In peanuts,
all tissues including pegs and pods also show watery lesions and can succumb
to white mycelium (3). The mycelium can penetrate into the tissue
intercellularly and gain nutrients in this manner. Eventually, yellowish-brown
bleached lesions appear on stems and pegs. The leaves become chlorotic
and necrotic, and stems become girdled and die. On the dead plant
tissue, as well as within tissue such as stems, sclerotia form and the
plant tissue is eventually shed to the soil where the sclerotia break off
and become dormant in the soil or can remain on or in plant debris.
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| Mycelium and sclerotia on a bleached peanut stem. Photo courtesy of Joyce Hollowell. | Sclerotia on peanut pods. Picture courtesy of Joyce Hollowell. |
Current areas of Research
Some other research that is being
conducted involves the identification of weed species that maybe found
in or near peanut fields. This is becoming a focus of research as
it is believed that the weeds may act as a source of overwintering inoculum
of S. minor as many weeds do for viral pathogens such as Tomato
spotted wilt virus (TSWV) (1). A weed that has been reported as a
host of Sclerotinia minor is Eclipta prostrata. Eclipta
prostrata is a member of the Asteraceae that has been found
in peanut fields of Oklahoma. Eclipta has become an established
weed in peanut fields, infesting as much as 4,000 ha of irrigated peanut
in Oklahoma (11). High populations of this weed in peanut fields
are thought to be due to excessive rain or irrigation and cool temperatures,
which also favor growth of S. minor (11). Sclerotinia minor
infection and the presence of sclerotia are abundant on many plants of
E.
prostrata. In the lab, E. prostrata tissue had about four
to eight viable sclerotia per 50 mm of lesion, 15 days after inoculation
with S. minor. This information and data suggests that Eclipta
is a potential reservoir for S. minor in field soils in the absence
of peanut plants (11). Eclipta has the potential to be a source
of primary inoculum that can infect peanut crops.
Another weed often found in
and around peanut fields is yellow nutsedge (Cyperus esculentus
L.). In September of 2000, the signs and symptoms of S. minor
were observed on yellow nutsedge in Bertie County by Joyce Hollowell (9).
Diseased plants showing signs and symptoms of S. minor were taken
from the Peanut Belt Research Station at Lewiston-Woodville, NC.
The fungus was isolated from the plant and grown on potato dextrose agar
(PDA). After performing Koch’s Postulates on the fungal isolate,
it was determined that it was indeed S. minor (9). This was
the first time that S. minor was reported on yellow nutsedge.
Although more research needs to be conducted on this weed, it is thought
that it could act as a reservoir for S. minor and a source of primary
inoculum that can infect peanut. In addition, other weeds need to
be examined and their susceptibility to S. minor infection and their
ability to harbor the fungus determined. If such weeds act as alternative
hosts for S. minor it will be necessary to control weed populations
around peanut fields to reduce sources of primary and secondary inoculum.
Weed control around peanut fields is already a high priority to control
TSWV. This will likely become an even larger priority as more weeds
are discovered that can harbor pathogens of peanuts such as S. minor.
S. minor on yellow nutsedge (Cyperus
esculentus L.). Photo
Courtesy of Joyce Hollowell.
Another topic of S. minor that has not been researched extensively is the interaction of plant architecture and S. minor. Little is known about how the fungus infects peanut and what part or parts of the peanut plant are most susceptible to infection of S. minor. In addition, there has been minimal research conducted concerning the interaction between the environment and S. minor infection. Dow, et al(8) found that the optimum temperature of germination, mycelial growth, and infection was 20-25 C. Ninety-five to 100% relative humidities were also favorable (8). Imolehin, et al.(10) studied the effects of temperature and moisture on sclerotial production, germination, and infection by S. minor on lettuce tissue. In the lab, the optimum temperature for sclerotial germination was 18C, while 12C was the optimum temperature for sclerotial formation. Solute potentials of –7 bars was optimal for mycelial growth, while germination of sclerotia was optimal at –1/3 bars (10). Research on soil moisture and temperature and its effects on S. minor germination and growth needs to be conducted in field studies to determine the true environmental influences on the behavior of S. minor. Better understanding of these areas is needed in order to better understand how to control the fungus. If more understanding and better control of the fungus are not obtained this problem may become of epidemic proportions in the near future.
Literature Cited
2. Agrios, George N. Plant Pathology 4th Edition. San Diego: Academic Press, 1997. P 355-358.
3. Backman, P.A., et.al. 1997. The compendium of peanut diseases, second edition. American Phytopath. Soc. Press, St. Paul. 34-35.
4. Bailey, J. 2001. Peanut Disease Management. Pages 85-104 in: 2001 Peanut Information. Jordan D.L., Spears, J.F., York, A.C., Brandenburg, R.L., Brown, A.B., Bailey, J.E., and Roberson, G.T. eds. North Carolina Cooperative Extension Service, Raleigh, North Carolina.
5. Beute, M.K., and R. Rodriguez-Kabana. 1979. Effect of volatile compounds from remoistened plant tissue on growth and germination of sclerotia of Sclerotium rolfsii. Phytopathology 69: 802-805.
6. Bowen, C., Melouk, H.A., Jackson, K.E., and Payton, M.E. 2000. Effect of a select group of seed protectant fungicides on growth of Sclerotinia minor in vitro and its recovery from infested peanut seed. Plant Dis. 84: 1217-1220.
7. Chappell, G.F., Shew, B.B., Ferguson, J.M., and Beute, M.K. 1995. “Mechanisms of Resistance to Sclerotinia minor in Selected Peanut Genotypes.” Crop Science 35:692-696.
8. Dow, R.L., Porter, D.M., and Powell, N.L. 1988. Effect of environmental factors on Sclerotinia minor and Sclerotinia blight of peanut. Phytopathology 78: 672-676.
9. Hollowell, J.E, and Shew, B.B. 2001. Yellow Nutsedge (Cyperus esculentus L.) as a host of Sclerotinia minor. Plant Dis. 85: 562.
10. Imolehin, E.D., Grogan, R.G., and Duniway, J.M. 1980. Effect of temperature and moisture tension on growth, sclerotial production, germination, and infection by Sclerotinia minor. Phytopathology 70: 1153-1157.
11. Melouk, H.A., Damicone, J.P., and Jackson, K.E. 1992. Eclipta prostrata, a new weed host for Sclerotinia minor. Plant Dis. 76: 101.
12. Melzer, M.S., Smith, E.A., and Boland, G.J. 1997. “Index of Plant Hosts of Sclerotinia minor.” Can. J. Plant Pathology 19:272-280.
13. Myco Site: Research http://biologi.uio.no/bot/ascomycetes/fungi.htm. December 3, 2001.
14. North Carolina State University Plant
Pathology Extension Website http://www.ces.ncsu.edu/depts/pp/notes/Peanut/gallery/sminor.htm
October 16, 2001.
15. Oklahoma Cooperative Extension Service: Soilborne Blight Diseases of Peanut. http://www.agweb.okstate.edu/pearl/plantdiseases/f-7186.html. October 16, 2001
16. Prophyta online: Contans®WG the biological plant-protection agent against Sclerotinia disease. http://www.prophyta.com/contans.html. November 28, 2001.
17. Porter, D.M., Smith, D.H., and Rodriguez-Kabana, R. 1982. Peanut Plant Diseases. Pages 326-410 in: Peanut Science and Technology. H.E. Pattee and C.T. Young eds. American Peanut Research and Education Society, Inc., Yoakman, Texas.
18. Sherwood, J. L., Beute, M. K., Dickson, D.W., Elliot, V.J., Nelson, R.S., Opperman, C.H., Shew, B.B. 1995. Biological and Biotechnological Control Advances in Arachis Diseases. Pages 160-206 in Advances in Peanut Science. H.E. Pattee and H.T. Stalker eds. American Peanut Research and Education Society, Inc., Stillwater, Oklahoma.
NC State, A&T State University Cooperative Extension: Peanut Page
Georgia Cooperative Extension Service: Georgia Commodities
University of Illinois Extension: Sclerotinia Disease
University of California: Agriculture and Natural Resources: Sclerotinia Diseases
NC State Peanut Pathology Extension Leader
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