Cephalosporium Stripe of Wheat

Cephalosporium Stripe of Wheat

There is only one true fungal vascular wilt of wheat, Cephalosporium stripe. The disease is also found on most other winter cereals and many wild and cultivated grasses but the greatest economic losses are seen with wheat. Spring cereals and annual grasses are susceptible to take-all but the affects are minimal. The disease was first discovered in Japan in 1930. It has since been found in the United Kingdom and the United States. The first report from the Great Plains came from Kansas in 1972. The first Nebraska field infected with Cephalosporium stripe was found in 1981. The disease can be devastating causes yield losses as high as 50-70%. It can also occur at incidences as high as 100%. The causal organism is Cephalosporium gramineum Nisikado & Nisikado et. al. = Hymenula cerealis Ellis & Everh. The fungus survives between seasons as mycelium and conidia in crop residue on or within 8 cm of the soil surface. Conidia are produced on sporodochia on the residue. Sporodochia are flat and black when dry and raised and yellow-brown when moist. Masses of conidia glisten on the surface when they are being produced. The conidia are soil borne and are transported by water through the soil. They germinate and invade host roots through wounds. Infection occurs in fall, winter or early spring after wounds have been produced by frost injury or mechanical injury from soil heaving. In some cases insect wounds may also serve as an avenue of entry. It has also been reported that wounding may not be necessary in acid soils. The fungus enters the vascular system and is carried upward in xylem vessels. Cephalosporium gramineum sporulates profusely in host tissue forming phialospores and blastospores while mycelial growth is limited. It multiplies at the nodes and produces metabolites which block transport of water and food. Cephalosporium gramineumcan be found in leaf and stem tissue and can survive in crop residue as long as two years. Disease development is favored by prolonged cool wet weather in spring and long growing periods in the fall. Wet soil conditions, fluctuating winter temperatures and acidic soils (pH of 3.9-5.5) also enhance disease development. Cephalosporium stripe is also more severe when wheat is continuously cropped or short rotations are used and when susceptible cultivars are used.

Symptoms

Infection by Cephalosporium gramineum occurs when temperatures are cool but symptoms are most obvious at jointing or heading. Infected plants may be grouped in patches or scattered across a filed. When disease incidence is high the field may have a yellowish cast. The disease gets its name from the stripe symptoms seen on infected leaves. A longitudinal yellow stripe forms on infected leaf blades and extends down the leaf sheath. The vein within the stripe is brown. One or two stripes normally develop on a single leaf and symptoms progress from lower to upper leaves. However, stripes may not develop on all the leaves of an infected plant or on all tillers. The center of the stripe turns reddish brown as the lesion ages. The vascular tissue within nodes is also brown and the discoloration is readily visible when stems are cut longitudinallly. There may also be some discoloration of the tissue immediately below the node. The greatest amount of yield loss is seen when the flag leaf becomes infected. Symptoms are also very evident on heads. Infected plants have smaller heads that are sterile or contain a few shriveled seeds. These plants also tend to head out prematurely with heads that are noticeably shorter than healthy ones. The awns may turn ourtward and whiteheads are produced. Infected tillers are also shorter than normal ones giving the field an overall uneven appearance due to the combination of healthy and affected plants. Lodging occasionally occurs but is not common. When infection occurs on seedlings, their leaves take on a mosaic type of yellowing that is evident in later winter or early spring. Leaves showing this symptoms usually die and are shed before thy form the characteristic stripe symptom.

Plant Health Management

Crop Rotation.

Fields that have shown a high incidence of Cephalosporium stripe should be rotated out of wheat for 3 years. Acceptable crops during that rotation are alfalfa, oats and row crops.

Residue Management.

Destruction of wheat residue subtantially reduces the incidence of the disease. However plowing may not be an option in fields that are part of a conservation tillage program.

Avoid planting too early in the fall.

Plants seeded too early have excessive root growth which provides more points of entry for the pathogen if they become injured.

Resistant Cultivars.

There are cultivars available which show some degree of resistance to Cephalosporium stripe. These cultivars should be used when possible. The cultivars are infected by the pathogen and it is able to reproduce on their crop residue but losses are not as severe as those seen with more susceptible varieties.

References

Shefelbine, P.A., and Bockus, W.W. 1990. Host genotype effects on inoculum production by from infested residue. Plant Dis. 74:238-240.

Watkins, J.E., Doupnik, B. Jr., and Boosalis, M.G. 1985. Cephalosporium stripe of wheat. Cooperative Extension Service, Institute of Agriculture and Natural Resources, University of Nebraska - Lincoln. NebGuide G85-743.

Wiese, M.V. ed., 1987. Compendium of wheat diseases, 2nd ed. APS Press, St. Paul, MN. 112 pp.

Willis, W.G. 1984. Wheat diseases. Cooperative Extension Service, Kansas State University, Manhattan, KS. Publication S-23.

Useful Links

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Caveat

This description is presented for information only and no endorsement is intended for products listed, nor criticism meant for products not mentioned. Always consult the product label before purchasing and using any pesticide.

Material contained on the Links from the page are the responsibility of the linked page's author(s).

This page was researched and drafted by: Jane Christensen, Department of Plant Pathology, University of Nebraska-Lincoln

Disease images were provided by: Dr. David Wysong, Department of Plant Pathology, University of Nebraska-Lincoln

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This page is authored and maintained by:
Dr. J.E. Partridge, Department of Plant Pathology, University of Nebraska-Lincoln

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