Sclerotinia sclerotiorum: Difference between revisions
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| binomial = ''Sclerotinia sclerotiorum'' |
| binomial = ''Sclerotinia sclerotiorum'' |
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| binomial_authority = (Lib.) de Bary, (1884) |
| binomial_authority = (Lib.) de Bary, (1884) |
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| synonyms = |
| synonyms = |
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''Hymenoscyphus sclerotiorum'' |
''Hymenoscyphus sclerotiorum'' |
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<small>(Lib.) W. Phillips, (1887)</small><br> |
<small>(Lib.) W. Phillips, (1887)</small><br> |
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The pathogenic fungus ''Sclerotinia sclerotioum'' proliferates in moist environments. Under moist field conditions, ''S. sclerotiorum'' is capable of completely invading a plant host, colonizing nearly all of the plant’s tissues with [[mycelium]]. Optimal temperatures for growth range from 15 to 21 degrees Celsius. Under wet conditions, ''S. sclerotiorum'' will produce an abundance of mycelium and [[sclerotia]]. The fungus can survive in the soil mainly on the previous year’s plant debris. Like most fungi, ''S. sclerotiorum'' prefers darker, shadier conditions as opposed to direct exposure to sunlight. |
The pathogenic fungus ''Sclerotinia sclerotioum'' proliferates in moist environments. Under moist field conditions, ''S. sclerotiorum'' is capable of completely invading a plant host, colonizing nearly all of the plant’s tissues with [[mycelium]]. Optimal temperatures for growth range from 15 to 21 degrees Celsius. Under wet conditions, ''S. sclerotiorum'' will produce an abundance of mycelium and [[sclerotia]]. The fungus can survive in the soil mainly on the previous year’s plant debris. Like most fungi, ''S. sclerotiorum'' prefers darker, shadier conditions as opposed to direct exposure to sunlight. |
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==Life Cycle== |
==Life Cycle== |
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The lifecycle of ''Sclerotinia sclerotiorum'' can be described as monocyclic, as there are no secondary inoculums produced. During late summer/ early fall the fungus will produce a survival structure called a sclerotium either on or inside the tissues of a host plant. The following spring the dormant sclerotia will germinate to produce fruiting bodies called [[apothecia]], which are small, thin stalks ending with a cup-like structure about 5-15mm in diameter (similar in shape to a small [[mushroom]]). The cup of the apothecium is lined with acsi, in which the [[ascospores]] are contained. When the ascospores are released from the asci, they are carried by the wind until they land on a suitable host. The ascospores will then germinate on the host and begin to invade the host’s tissues via mycelium, causing infection. ''S. sclerotiorum'' is capable of invading nearly all tissue types including stems, [[foliage]], flowers, fruits, and roots. Eventually white, fluffy mycelium will begin to grow on the surface of the infected tissues. At the end of the growing season, ''S. sclerotiorum'' will once again produce sclerotia. The sclerotia will then remain on the surface of the ground or in the soil, on either living or dead plant parts until the next season. The lifecycle will then continue respectively. |
The lifecycle of ''Sclerotinia sclerotiorum'' can be described as monocyclic, as there are no secondary inoculums produced. During late summer/ early fall the fungus will produce a survival structure called a sclerotium either on or inside the tissues of a host plant. The following spring the dormant sclerotia will germinate to produce fruiting bodies called [[apothecia]], which are small, thin stalks ending with a cup-like structure about 5-15mm in diameter (similar in shape to a small [[mushroom]]). The cup of the apothecium is lined with acsi, in which the [[ascospores]] are contained. When the ascospores are released from the asci, they are carried by the wind until they land on a suitable host. The ascospores will then germinate on the host and begin to invade the host’s tissues via mycelium, causing infection. ''S. sclerotiorum'' is capable of invading nearly all tissue types including stems, [[foliage]], flowers, fruits, and roots. Eventually white, fluffy mycelium will begin to grow on the surface of the infected tissues. At the end of the growing season, ''S. sclerotiorum'' will once again produce sclerotia. The sclerotia will then remain on the surface of the ground or in the soil, on either living or dead plant parts until the next season. The lifecycle will then continue respectively. |
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==Control== |
==Control== |
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Control of white mold on crops can depend greatly on specific cultural practices and the application of chemical sprays. Crops that are highly susceptible to white mold should be planted in well drained soils. Also, properly spaced plants or maintaining growth in the fields will help to maintain good air circulation and create microclimates that are less favorable for disease development (Pohronezny 25). Fields with heavy disease pressure may also be flooded for a period of four to five weeks so as the sclerotia may lose their viability(Pohronezny 25). This may not be a practical measure and may be why chemical sprays are used. Fumigating the soils with broad spectrum fungicides can be effective in controlling sclerotia (Pernezyny, Momol and lopes 23). During the growing season, however, applying contact and systemic fungicides during times of the plants greatest susceptibility (flowering and senescence) will give the greatest amount of protection against disease. Crop rotation with cereals in fields with high levels of disease incidence can help in reduction of inoculums. Rotation should last for at least three years since sclerotia can be viable for at least this long. |
Control of white mold on crops can depend greatly on specific cultural practices and the application of chemical sprays. Crops that are highly susceptible to white mold should be planted in well drained soils. Also, properly spaced plants or maintaining growth in the fields will help to maintain good air circulation and create microclimates that are less favorable for disease development (Pohronezny 25). Fields with heavy disease pressure may also be flooded for a period of four to five weeks so as the sclerotia may lose their viability(Pohronezny 25). This may not be a practical measure and may be why chemical sprays are used. Fumigating the soils with broad spectrum fungicides can be effective in controlling sclerotia (Pernezyny, Momol and lopes 23). During the growing season, however, applying contact and systemic fungicides during times of the plants greatest susceptibility (flowering and senescence) will give the greatest amount of protection against disease. Crop rotation with cereals in fields with high levels of disease incidence can help in reduction of inoculums. Rotation should last for at least three years since sclerotia can be viable for at least this long. |
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* [http://www.extento.hawaii.edu/kbase/crop/type/s_scler.htm Crop Knowledge Master] |
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* http://www.ag.ndsu.edu/pubs/plantsci/hortcrop/pp899w.htm] |
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*http://www. |
* [http://www.ars.usda.gov/Research/docs.htm?docid=20320] |
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*[http://www.ars.usda.gov/Research/docs.htm?docid=20320] |
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==References== |
==References== |
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{{reflist}} |
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<references /> |
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1. Agrios, George N. Plant Pathology. 5th ed.. Burlington, MA: Elsevier Academic Press, 2005. 546-550. Print. |
1. Agrios, George N. Plant Pathology. 5th ed.. Burlington, MA: Elsevier Academic Press, 2005. 546-550. Print. |
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4. [http://www.ars.usda.gov/Research/docs.htm?docid=20320] |
4. [http://www.ars.usda.gov/Research/docs.htm?docid=20320] |
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[[File:Sclerotinia sclerotiorum at Phaseolus vulgaris, sclerotiënrot stamsperzieboon.jpg|260px|thumb|left|Sclerotinia sclerotiorum on bushbean]] |
[[File:Sclerotinia sclerotiorum at Phaseolus vulgaris, sclerotiënrot stamsperzieboon.jpg|260px|thumb|left|Sclerotinia sclerotiorum on bushbean]] |
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[[Category:Plant pathogens and diseases]] |
[[Category:Plant pathogens and diseases]] |
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[[Category:Sclerotiniaceae]] |
[[Category:Sclerotiniaceae]] |
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{{Leotiomycetes-stub}} |
{{Leotiomycetes-stub}} |
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{{plant-disease-stub}} |
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[[ca:Sclerotinia sclerotiorum]] |
[[ca:Sclerotinia sclerotiorum]] |
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Revision as of 16:21, 4 February 2013
| Sclerotinia sclerotiorum | |
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| Sclerotinia sclerotiorum on Phaseolus | |
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| Species: | S. sclerotiorum
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| Binomial name | |
| Sclerotinia sclerotiorum (Lib.) de Bary, (1884)
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| Synonyms | |
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Hymenoscyphus sclerotiorum (Lib.) W. Phillips, (1887) Peziza sclerotiorum Lib., (1837) | |
Sclerotinia sclerotiorum is a plant pathogenic fungus and can cause a disease called white mold if conditions are correct. S. sclerotiorum can also be known as cottony rot, watery soft rot, stem rot, drop, crown rot and blossom blight (Agrios 546). A key characteristic of this pathogen is its ability to produce black resting structures known as sclerotia and white fuzzy growths of mycelium on the plant it infects. These sclerotia give rise to a fruiting body in the spring that produces spores in a sac which is why fungi in this class are called sac fungi (Ascomycetes). This pathogen can occur on many continents and has a wide host range of plants. When S. sclerotiorum is onset in the field by favorable environmental conditions, losses can be great and control measures should be considered.
Hosts and Symptoms
Common hosts of white mold are herbaceous, succulent plants, particularly flowers and vegetables. It can also affect woody ornamentals occasionally, usually on juvenile tissue. White mold can affect their hosts at any stage of growth, including seedlings, mature plants, and harvested products. It can usually be found on tissues with high water content and in close proximity to the soil. One of the first symptoms noticed is an obvious area of white, fluffy mycelial growth. Usually this is preceded by pale to dark brown legions on the stem at the soil line. The mycelium then cover this necrotic area. Once the xylem is affected, other symptoms occur higher up in the plant. These can include chlorosis, wilting, leaf drop, and death quickly follows. On fruits, the initial dark lesions occur on the tissue that comes in contact with the soil. Next, white fungal mycelium covers the fruit and it decays. This can occur when the fruit is in the field or when in storage.[1]
Importance
White mold affects a wide range of hosts. It is known to infect 408 plant species. Its diverse host range and ability to infect plants at any stage of growth makes white mold a very serious disease. The fungus can survive on infected tissues, in the soil, and on living plants. It affects young seedlings, mature plants, and fruit in the field or in storage. White mold can spread quickly in the field from plant to plant. It can also spread in a storage facility throughout the harvested crop. Some crops it affects commonly are soybeans, green beans, sunflowers, canola, and peanuts.[2]
Environment
The pathogenic fungus Sclerotinia sclerotioum proliferates in moist environments. Under moist field conditions, S. sclerotiorum is capable of completely invading a plant host, colonizing nearly all of the plant’s tissues with mycelium. Optimal temperatures for growth range from 15 to 21 degrees Celsius. Under wet conditions, S. sclerotiorum will produce an abundance of mycelium and sclerotia. The fungus can survive in the soil mainly on the previous year’s plant debris. Like most fungi, S. sclerotiorum prefers darker, shadier conditions as opposed to direct exposure to sunlight.
Life Cycle
The lifecycle of Sclerotinia sclerotiorum can be described as monocyclic, as there are no secondary inoculums produced. During late summer/ early fall the fungus will produce a survival structure called a sclerotium either on or inside the tissues of a host plant. The following spring the dormant sclerotia will germinate to produce fruiting bodies called apothecia, which are small, thin stalks ending with a cup-like structure about 5-15mm in diameter (similar in shape to a small mushroom). The cup of the apothecium is lined with acsi, in which the ascospores are contained. When the ascospores are released from the asci, they are carried by the wind until they land on a suitable host. The ascospores will then germinate on the host and begin to invade the host’s tissues via mycelium, causing infection. S. sclerotiorum is capable of invading nearly all tissue types including stems, foliage, flowers, fruits, and roots. Eventually white, fluffy mycelium will begin to grow on the surface of the infected tissues. At the end of the growing season, S. sclerotiorum will once again produce sclerotia. The sclerotia will then remain on the surface of the ground or in the soil, on either living or dead plant parts until the next season. The lifecycle will then continue respectively.
Control
Control of white mold on crops can depend greatly on specific cultural practices and the application of chemical sprays. Crops that are highly susceptible to white mold should be planted in well drained soils. Also, properly spaced plants or maintaining growth in the fields will help to maintain good air circulation and create microclimates that are less favorable for disease development (Pohronezny 25). Fields with heavy disease pressure may also be flooded for a period of four to five weeks so as the sclerotia may lose their viability(Pohronezny 25). This may not be a practical measure and may be why chemical sprays are used. Fumigating the soils with broad spectrum fungicides can be effective in controlling sclerotia (Pernezyny, Momol and lopes 23). During the growing season, however, applying contact and systemic fungicides during times of the plants greatest susceptibility (flowering and senescence) will give the greatest amount of protection against disease. Crop rotation with cereals in fields with high levels of disease incidence can help in reduction of inoculums. Rotation should last for at least three years since sclerotia can be viable for at least this long.
External links
- Index Fungorum
- USDA ARS Fungal Database
- Crop Knowledge Master
- http://www.ag.ndsu.edu/pubs/plantsci/hortcrop/pp899w.htm]
- [1]
References
1. Agrios, George N. Plant Pathology. 5th ed.. Burlington, MA: Elsevier Academic Press, 2005. 546-550. Print.
2. Pohronezny, K. L. "White Mold." Compendium of Tomato Diseases. 1st ed. St. Paul, MN: The American Phytopathological Society, 1991. Print.
3. Pernezny, K, M. T Momol, and C. A Lopes. "White Mold." Compendium of Pepper Diseases. 1st ed. St. Paul, MN: The American Phytopathological Society, 2003. Print
4. [2]
