Phialophora gregata
| Phialophora gregata | |
|---|---|
| Scientific classification | |
| Kingdom: | Fungi |
| Phylum: | Deuteromycota |
| Class: | Deuteromycetes |
| Subclass: | Incertae sedis |
| Order: | Incertae sedis |
| Family: | Incertae sedis |
| Genus: | Phialophora |
| Species: | P. gregata |
| Binomial name | |
| Phialophora gregata (Allington & D.W. Chamb.) W. Gams, (1971) | |
| Synonyms | |
|
Cadophora gregata | |
Phialophora gregata is an Deuteromycete[1] fungus that is a plant pathogen which causes the disease commonly known as "brown stem rot of soybean. P. gregata does not produce survival structures, but has the ability to overwinter as mycelium in decaying soybean residue.[2]
Two strains of the fungus exist;[2] genotype A causes both foliar and stem symptoms, while genotype B causes only stem symptoms.[2] Common leaf symptoms are browning, chlorosis, and necrosis[2] Foliar symptoms which are often seen with genotype A are chlorosis, defoliation, and wilting.[2][3]
There are many ways to manage Phialophora gregata. The most effective form of management is disease resistance,[2] but crop rotation, tiliage, SCN management, and changing the pH of the soil can also be effective [2][4]
Symptoms and Signs
Phialophora gregata’s infection of a soybean plant is accompanied by browning of the plant’s vascular and pith tissues.[2] The plant often exhibits chlorosis and necrosis, as well as leaf browning.[2] Wilting and defoliation are also known to occur.[2] Signs of infection often go unnoticed until reproductive stages of a plant’s life cycle. They can be diagnosed earlier on by opening the stem and visualizing the pathogen. One can visualize signs by cutting open the stem in early stages of infection,[2] but symptoms do not become apparent until after the soybean pod formation.[5]
Depending on which strain infects the plant, and what the environmental conditions are,[6] the effect is more or less potent. Genotype A causes browning of stems as well as foliar symptoms such as interveinal chlorosis, defoliation and wilting.[2][3] Symptomatic leaves have a shriveled appearance, but remain attached to the stem.[3] Genotype B causes only browning of stems.[3]
Secondary symptoms of brown stem rot are stunting, premature death, decrease in seed number, reduced pod set, and decrease in seed size.[3]
Disease from P. gregata is easily confused with Fusarium wilt, due to the similar vascular symptoms observed in both.[7] The diseases could be differentiated through growth on isolation media.[7] The two diseases can be further distinguished by splitting the stems. A split stem with Fusarium infection would have tan or light brown discoloration in the cortex and a normal white pith, while a split stem with P. gregata would have a discolored, reddish brown pith.[5] Root rot and blue masses of spores are symptoms only caused by Fusarium.[5]
Environment
As the disease is soilborne, it is not uncommon to find clusters of diseased plants together.[3] The pathogen proliferates in stem tissues when soil has high moisture content and air temperatures from 70-80 degrees Fahrenheit.[3] Rainy seasons promote brown stem rot.[3] When soil is untilled, the disease is more likely to persist in soil.[3] The incidence of brown stem rot is highest at soil pH ~6.3.[8]
Disease Cycle
The Phialophora gregata fungus is a deuteromycete with a monocyclic life cycle. There are two strains of Phialophora gregata, referred to as genotype A and genotype B.[4] Genotype A causes both foliar and stem symptoms, while genotype B causes only stem symptoms.[2]
The Phialophora gregata fungus produces no survival structures, but can overwinter as mycelium [8] in decaying soybean residue. During overwintering, conidia are produced; these conidia are the inoculum for new plants in the spring.[8] The amount of asexual reproduction that occurs during the winter affects the spring inoculum levels.[8] Infection initially occurs in the roots of young soybean plants, and then spreads to the stem (and foliage, depending on the strain).[2] Generally, early and severe foliar symptoms indicate that the yield losses will be heavier.[4]
Economic Significance
Brown Stem Rot of soybeans is a source of major crop loss. It is not uncommon for soybeans grown in management systems prone for brown stem rot to have yield losses between 10%, with a maximum potential loss of 30%.[2][9] It has been listed as the 3rd most important disease to soybeans in Wisconsin.[2][9] A recent study showed that nearly half the counties in Iowa, from 2006 and 2007, had brown stem rot of soybean.[4]
Management
Disease resistance
Brown stem rot has the uncanny ability to produce yield loss even without obvious symptoms.[9] Due to this and its economic significance, management of brown stem rot has focused on the area of prevention. The resistant forms soybean are currently effective against all strains of brown stem rot,[2] and thus this is a very effective method of management. Commercial soy plant resistance varieties of brown stem rot have been successful in the field. Fungicides are not available.[2][9]
Crop rotation
Crop rotation is used to lower the P. gregata inoculum level in the soil; soybean is the only known Wisconsin host of P. gregata,[2] so 2-3 years of a different crop can rid a field of the pathogen.
Tillage
More decomposition of soybean residue results in less pathogen, as the fungus can only survive on soybean residue. Therefore, tillage can be effective. Once the soybean residue has decomposed, the survival of P. gregata is drastically decreased. It is common for farmers to practice both crop rotations and tillage in a cyclic fashion.[10] This is done by conducting little to no tillage when a soybean crop is planted after corn, followed by intensive tillage when a corn crop is planted after soybean.[10]
Management of Soybean Cyst Nematode (Heterodera glycines)
P. gregata is often found to be more severe in the presence of SCN;[2] soybean plants showing resistance to SCN have been found to produce greater yields.[2] Soybean plants with resistance to both SCN and genotype A of P. gregata can grow normally, even when both pathogens are present.[4]
Monitoring soil pH
Soil pH has been shown to have an effect on brown stem rot. Maintaining a soil pH of 7.0 reduces the risk of disease the greatest.[2]
External links
References
- ↑ Weidong, Chen, Lynn E. Gray, James Kurle, and Craig Grau. "Specific Detection of Phialophora Gregata and Plectosporium Tabacinum in Infected Soybean Plants Using Polymerase Chain Reaction." Molecular Ecology 8.5 (1999): 871-77. Web.
- 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 Grau, C. "Brown Stemrot of Soybeans." <http://fyi.uwex.edu/fieldcroppathology/files/2010/11/bsr_063.pdf>
- 1 2 3 4 5 6 7 8 9 Robertson, A. & Tabor, G. “Soybean Brown Stem Rot.” Iowa State University. <http://www.extension.iastate.edu/Publications/PMR1004.pdf.>2012.
- 1 2 3 4 5 Robertson, A.E. and Nutter, F.W. Iowa Soybean Disease Survey. www.soybeandiseasesurvey.info
- 1 2 3 Monsanto. "Brown Stem Rot and Sudden Death Syndrome in Soybean." Lewis Hybrids. Lewis Hybrids, 2010. Web. <http://www.lewishybrids.com/files/File/Agronomic%20Spotlight%20-%20Brown_Stem_Rot_Sudden_Death_Soy.pdf?PHPSESSID=0c6bc72c5c097a7e80e53605fd2effce>
- ↑ Westphal, Andreas, Scott Abney, and Gregory Shaner. "Diseases of Soybean: Brown Stem Rot." Purdue University Department of Botany and Plant Pathology and USDA-ARS, May 2006. Web.
- 1 2 Smith, S. N. "Association of Phialophora Gregata with Fusarium Solani F. Sp. Pisi in Garbanzo Beans in California." APS Net 83.9 (1999): 876.1. Web.
- 1 2 3 4 Pedersen, Palle. “Brown Stem Rot.” <http://extension.agron.iastate.edu/soybean/diseases_bsr.html> 2006.
- 1 2 3 4 Grau, Craig, and Nancy C. Kurtzweil. "Brown Stem Rot: Management and Variety Options." The Yields II Project: Research-Based Management Information. Soybean Research and Development Counci, Oct. 2003. Web.
- 1 2 Dorrance, Anne E., and Dennis R. Mills. "Brown Stem Rot of Soybean." Ohio State University, 2008. Web. <http://ohioline.osu.edu/ac-fact/pdf/0035.pdf>.