diseased
kernels
Picture of black point:
Scientific name:Alternaria spp. (1), Cochliobolus sativus, Fusarium spp. (1) , Helminthosporium spp., Pyrenophora tritici-repens (tan spot fungus) (4), plus many others can be involved.
Hosts: Wheat, barley, other small grains and grasses.
Symptoms of black point:
- Glumes and other head tissues covered by black sooty-appearing mold (1).
- Diseased kernels are discolored, weathered, and are black at the ends of the seed (black points).
- The embryos are often shrivelled and brown to black in color (2, 3).
Look-alike symptoms:
Favorable conditions:
- Warm, wet weather during maturation of crop, delayed harvest (1).
- When seed moisture levels excced 20%, coupled with relative humidity above 90%, the amount of black point increases dramatically (3).
Pattern in field: Diseased plants are often uniform in the fields or are associated with wetter, more humid areas of fields.
Infestation levels:
- If embryos are invaded, germination levels will be reduced.
- If plants are infected following germination, plants will be weakened resulting in reduced stands or restricted grain fill (3).
- Seed with black point is more likely to have seedling blight and root rot problems (5)
Life cycle:
- More than 100 species of fungi can be isolated from newly-harvested wheat grain.
- In contrast to storage molds, these fungi are most important in humid field conditions and they infect seed more when relative humidity is greater than 90% and moisture levels are >20%.
- Some of these fungi that developed from infected or infested seed are pathogenic (2).
History in MT and US:
Crop losses: Black point can affect grain quality since food products made from it often have displeasing odor and color. Pigments or other compounds of fungal origin also can cause illness if consumed in sufficient quantity (2).
Cultural controls: There is no way to restrict saprophytic fungi from the field. Generally, seed damage occurs before harvest, but damage will increase if grain is stored at 95% relative humidity with greater than 25% moisture (wet weight basis). Also avoid conditions that promote storage mold growth (2).
Resistant varieties: Some wheat varieties have some resistance mechanisms through anatomical (mechanical) and physiological means (2).
Biological controls:
Chemical controls: Chemical seed treatments containing imazilil or carboxin can improve germination and decrease infection of seedlings grown from diseased kernels (5). Use of seed treatments is strongly recommended when seed lots are infected with black point. While some eradicant and protectant fungicides could potentially be applied to maturing heads during favorable weather for disease, they would rarely be economical (2).
References: 1) Lipps, P.E. 1988. Wheat disease control in
Ohio. Dept. of Plant Path. Ohio State Univ. 2) M.V. Wiese. 1977. Compendium
of Wheat Diseases. APS Press, St. Paul, MN, p.12-13. 3) Riesselman,
J. Black point of cereals. Montana Crop Health Report, September, 22, 1989,
No. 12. 4) Francl, L.J. and Jordahl, J.G. 1992. Spike inoculation of durum
wheat with Pyrenophora tritici-repens and seed symptomology.
Proceedings of the Second International Tan Spot Workshop, Fargo, ND. 5)
Riesselman,m J. Black point and seed quality. Montana Crop Health Report,
April 25, 1988.
Scientific name: Alternaria spp. (2), Cladosporium spp., Sporobolomyces and others.
Hosts: Small grains and grasses
Symptoms: Green to black fungi develop on wheat heads. Sometimes the fungi development progresses to the seeds and black point or kernel smudge develops. In humid climates such as Great Britain, the molds also can develop on leaves (1).
Look-alike symptoms: Black point or kernel smudge refers to the presence of saprophytic or weakly parasitic fungi on the kernels. With sooty molds, the fungi are present more on the heads and glumes.
Favorable conditions: Wet weather during heading through maturation of grain and delayed harvest once grain is mature favor the disease. Heads that are shaded, weakened, undersized, prematurely mature, deficient in nutrients, lodged, or damaged by other diseases also are prone to sooty molds. In some cases, plants weakened by other diseases such as take-all or Cephalosporium stripe are more prone to sooty mold development (1).
Pattern in field:
Infestation levels:
Life cycle:
History in MT and US:
- Problems with sooty molds are rare in Montana, but they can develop any time there are wet, humid conditions while small grains are maturing.
- Sooty mold was common throughout Montana in the extremely wet summer of 1993 (0).
Crop losses:
Cultural controls:
Resistant varieties: No resistant varieties are known but differences in tolerance are recognized (1). No information for Montana varieties.
Biological controls:
Chemical controls: Several fungicides control sooty molds but use of these is rarely economical (1).
References: 1) M.V. Wiese. 1977. Compendium of Wheat Diseases.
APS Press, St. Paul, MN, p.13-14.
Pictures of common bunt:
symptomatic
and infected kernels
combining
bunt in the 1950s (clouds of spores)
Scientific name: Tilletia tritici or Tilletia laevis (Tilletia caries and Tilletia foetida)
Hosts: Wheat, rye, grasses including Aegilops, Lolium, Agropyron, and Hordeum species (3).
Symptoms of common bunt: Symptoms usually aren't noticed until the plants head out, even though the plants may be moderately stunted (2). Smutted wheat heads are thin and stay green longer than non-infected heads. Infected heads have all or part of the kernels replaced by light-brown smut balls which are filled with dark-brown spore masses. Often some or all of the spikelets are spread apart because the kernels have been replaced with smut balls. The fungus smells like rotting fish when seeds are crushed; infected heads are not shorter as with dwarf bunt (2). Bunt spores released during threshing are combustible and minor explosions have resulted from their ignition by sparks from stationary threshers (3).
Look-alike symptoms:
Favorable conditions: Most infection results from spores carred into the field as contamination on seeds. However, in areas where spores oversummer in the soil, infection of winter wheat can also result from soilborne spores. The spores germinate best when soil of seedbed temperatures are in the range of 40 - 60 F (4). Soil-borne spores of common bunt remain infective in areas where the soil remains dry from the time of harvest until after seeding (5).
Pattern in field:
Infestation levels:
Life cycle: Disease starts at the time of seed germination or seedling emergence. The common bunt fungi infect the shoots of wheat seedlings before the plants emerge from the soil. Most infection results from spores carred into the field as contamination on seeds, but in areas where spores oversummer in the soil, infection of winter wheat can also result from soilborne spores. The spores germinate best when soil of seedbed temperatures are in the range of 40 - 60 F. The fungus then grows within the growing cycle by taking over the ovaries and forming smut balls in place of kernels (4). The fungus is carried on the seed or in the soil (2). Only very young seedlings can be infected. Infection occurs either from smut spores on the seed or spores in the soil close to the seed. Soilborne spores do not survive through the winter (2).
History in MT and US: Common bunt occurs worldwide (4). The species Tilletia caries is widespread in Nebraska and the central Great Plains states. Tilletia foetida is limited to parts of North America and Europe (5).
Crop losses: Common bunt reduces wheat yields and grain quality. It is more frequent and often more damaging on winter wheat than spring wheat (5). The disease not only limits yield directly, by preventing the formation of kernels, but also causes the harvested wheat to be graded as "smutty" and discounted at the market (4). Yield losses of 20 - 30% are not uncommon in favorable areas of the U.S. The maximum yield loss recorded is 88%. However, the widespread use of effective seed treatments can reduce losses to near 0 (5). See Chemical controls below.
Controls: Resistant varieties and chemical seed treatments provide the best control of common bunt. See Resistant varieties and Chemical controls below.
Cultural controls:
1) Wheat seeded early in the fall may escape infection if it can develop through susceptible seedling stages more rapidly than wheat sown late (3).
2) Consider reseeding if therere is decreased stand potential.
3) Crop rotations will not affect diseaes organisms that survive on the seed, such as with the cereal smuts (6).
Resistant varieties: All important commercial varieties of winter wheat are resistant to most races of common bunt. However, some varieties that were formerly resistant to some races are not resistant to new races that come into the area (3). See Chemical controls.
Biological controls:
Chemical controls: All important commercial varieties of winter wheat are resistant to most races of common bunt. However, to prevent the development of new races of common bunt, all seed wheat should be cleaned and chemically-treated.
Difenoconazole (Dividend, Ciba, 0.25 fl. oz./cwt rate)
Seed treatments include: Captan, Imazalil. (also carboxin, carboxin+captan, carboxin+thiram, maneb+HCB, PCNB+terrazole, TCMTB).
References: (2) Pacific Northwest Plant Disease Control Handbook.
1994. 3) M.V. Wiese. 1977. Compendium of Wheat Diseases. APS Press,
St. Paul, MN, p. 18-20. 4) Cook, R.J. Veseth, R.J. 1991. Wheat Health
Management. APS Press, St. Paul, MN, p. 57. 5) Watkins, J.E. 1978.
"Bunt or stinking smut of wheat", Cooperative Extension Service, U. of
Nebraska, G74-169. 6) Lamey H.A and McMullen, M.P. 1993. "Crop rotations
for managing plant diseases" North Dakota Extension Service. Bulletin PP-705.
.
Pictures of dwarf bunt:
loose
smut, covered smut, and dwarf bunt - slide comparison of three heads
field
shot of stunted plants - dwarf bunt surrounded by healthy plants
Scientific name: Tilletia controversa Kuhn in Rabenh.
Hosts: Winter wheat
Symptoms:
1) Infected plants are very much dwarfed (1/4 to 1/2 normal size) in comparison with healthy plants.
2) Kernels are replaced by smut balls which contain masses of dark smut spores.
3) When smut balls are crushed, a distinctive fishy odor is emitted.
Look-alike symptoms: Dwarf bunt is caused by a newly-described smut fungus species that is closely related to common bunt (Tilletia tritici). Both diseases feature a fishy odor, but dwarf bunt causes much shorter heads. Many common bunt controls are applicable for dwarf bunt. However since Tilletia conroversa infects plants in later growth stages, fungicides needed to control the diseases will differ (see chemical controls) (7).
Favorable conditions:
- Persistant snow cover
- Soil temperatures between 32 and 40 F (9).
- Development of 1 - 3 tillers in the fall (9).
Pattern in field:
Infestation levels:
Life cycle: As with other bunt diseases, infection by the dwarf bunt fungus starts at the time of seed germination or seedling emergence. Teliospores of T. controversa infect the shoots of wheat seedlings before the plants emerge from the soil. Most infection results from spores carried in to the field as contaminants on seed. However, in areas where spores oversummer in the soil, infection of winter wheat also can result from soilborne spores. The dwarf bunt fungus has unique requirements for spore germination and infection. A prolonged period of very low-intensity light accompanied by temperatures between 32 and 40 F is necessary. These conditions generally exist in late fall. Infection can occur at the snow-soil interface when snow falls on unfrozen ground and stays there for several months (7). The spores germinate best when soil or seedbed temperatures are in the range of 40-60 F. Then, the fungus grows witnin the growing point of the infected shoot and completes its life cycle by growing into the ovaries and producing smut balls in place of kernels (7). Unlike those of common bunt, the spores of dwarf bunt may remain alive in the soil for several years (7).
History in MT and US: Dwarf bunt is limited to areas with prolonged snow cover on unfrozen ground. In Montana, dwarf bunt is important only in high-snowfall intermountain valleys in the western part of the state. The disease was first recognized in the United States in Montana in 1935 (9). Elsewhere, the disease occurs in the Pacific Northwest states at relatively high elevations such as in northern and southern Idaho, northern Utah, western Colorado, northeastern Oregon, northeastern Washington, and in parts of the Great Lakes area. The disease also occurs in areas of northeastern states (9). Dwarf bunt does not occur in the Great Plains and the southern states (7).
Crop losses: The disease not only affects yield directly by preventing kernel formation, but it also causes the harvested wheat to be graded as "smutty" and discounted when marketed (7, 9). Quarantines in the Peoples' Republic of China have prevented seed with very low levels of dwarf bunt contamination from being exported to that country (9).
Integrated controls: Integrated control methods that include use of resistant varieties, late seeding, and difenoconazole seed treatments in areas with a history of dwarf bunt will provide the most throrough control (9).
Cultural controls:
- See "Integrated controls" section above for control methods involved cultural controls.
- Late seeding (or very early seeding) can minimize infection. NOTE: late seeding can increase risk of winterkill, weeds, soil erosion, and reduced yields.
- Planting spring wheat in problem areas is an option.
Resistant varieties: See "Integrated controls" section above
for controls involving resistant varieties.
WINTER WHEAT VARIETIES:
RESISTANT: Blizzard, Manning, Promontory, Weston, Windridge (Windridge has good resistance, but in areas of high fertility, it can become rank and lodge. Cerone can reduce these problems.)
MODERATELY SUSCEPTIBLE: Meridian
SUSCEPTIBLE: AC Readymade, Agassiz, Arapahoe, Centurk, Cree,
Judith, Neely, Norstar, Norwin, Redwin, Rocky, Roughrider, Tiber, Winalta
(3).
SPRING WHEAT VARIETIES: None listed (4).
Biological controls:
Chemical controls: See "Integrated controls" section above for controls involving chemical controls.
Difenoconazole (Dividend 3FS, CIBA Corp., Greensboro, NC) seed treatment can essentially eliminate dwarf bunt of winter wheat. Dividend, a broad spectrum seed treatment with the active ingredient difenoconazole, was registered in August 1994 (5, 6). Prolonged systemic activity may account for the effectiveness of this compound. Current registrations for wheat range from 1/4 to 1.0 fl. oz. per hundredweight. The rate required is dependent upon the disease complex producers are attempting to control. CIBA currently is recommending the 1.0 fl. oz/cwt. for dwarf bunt control in early seeded winter wheat and the 0.5 oz. rate for wheat seeded after September 15th (5). At the 0.5 oz. rate, Dividend also controls common bunt, loose smut, seed-borne Septoria, general seed rots such as caused by Pencillium, and Fusarium seed scab, and partial control of common root rot. At the 1.0 oz. rate, Dividend is labeled for additional control of Fusarium root rot and take-all root rot, plus some early season foliar leaf disease control (6).
TBZ (fungicide seed treatment) has given erratic control which appears dependent on the length of winter infection (2).
References: 1) Don Mathre, conversation. 2) Pacific Northwest
Plant Disease Control Handbook. 1994. 3) Winter wheat varieties. 1994.
MSU Extension Service Bulletin 1098. 4) Spring wheat varieties. 1994. MSU
Extension Service Bulletin 1093. 5) Riesselman, J.R. 1994. "Dividend seed
treatment registration" Montana Crop Health Report. Aug. 19, 1994,
No. 10. 6) McMullen, M. 1994. "New seed treatment labeled for wheat". NDSU
Pest & Crop Report. Sept. 2, 1994, Issue 17. 7) Wiese, M.V. 1977.
"Dwarf bunt" Compendium of Wheat Diseases. APS Press, St. Paul,
MN, pp. 20-21. 8) Cook, R.J. Veseth, R.J. 1991. Wheat Health Management.
APS Press, St. Paul, MN, p. 55. 9) Sitton, J.W., Line, R.F., Waldher, J.T.,
Goates, B.J. 1993. Difenoconazole seed treatment for control of dwarf bunt
of winter wheat. Plant Disease, v. 77 (11), pp. 1148 - 1151.
.
Pictures of ergot:
on
immiture wheat head in field
Scientific name: Claviceps purpurea
Hosts: Rye is the principle economic host (2). Wheat, barley, oats, triticale, and numerous wild grasses also are susceptible (1,2).
Symptoms:
1) After flowering, but before heading, a sticky conidial stage, or "honeydew" can be observed on infected heads.
2) After the honeydew stage, the ovaries swell and become stroma-like. Their surface is convoluted with a superficial layer of conidiophores (spore-bearing structures) (2).
3) The most obvious symptom is hard, pointed, black to deep purple sclerotia that replace one or more kernels within the head. The sclerotia are several times longer than the kernels and can easily be observed on the head or mixed with the grain.
Poisoning: Ergot sclerotia contain toxins that can be very harmful to humans, cattle, horses, sheep, swine, and fowl. Ergotism produces two general physiological reactions - constriction of blood vessels and muscle contractions. In pregnant animals, continuous doses of ergot (whether large or small) can cause uterine contractions leading to spontaneous abortion. Small doses often cause a reduction in lactation. Gangrene, caused by a reduction of circulation and tissue degradation, can lead to the loss of extremities, especially toes, ears, and hooves.
In humans, ergotism can cause convulsions and hyperexcitability. Historical descriptions of people going "insane" have been blamed on the consumption of bread made from ergot-infested wheat or rye. Even today, in times of severe grain shortages, people in developing coutries have resorted to consuming ergoty grain. This has resulted in convulsion, gangrene, and death (6).
Lab diagnosis: Before feeding ergoty grain or hay, inspect it carefully. To have it analyzed for toxic content, mail a representative sample to:
Chemistry Station
9 McCall Hall
Montana State University
Bozeman, MT 59717
Your county agent can provide procedures for sampling and shipping the samples.
Look-alike symptoms: Rodent droppings, covered smut
Favorable conditions:
- Wet, warm weather that accompanies and prolongs the flowering period (6).
- The above conditions favor honeydew formation which attracts insect vectors of the disease (2).
- Ergot develops only in grasses that reach maturity (produce heads). For this reason, ergot has been more common in Conservation Reserve Program acreage and other areas in which grasses are not cut or grazed. It is important to monitor small grain crops adjacent to such areas carefully (5).
- Barley varieties infected with barley stripe mosaic virus are more susceptible to infection by the ergot fungus (6).
Pattern in field: Since native grasses often provide inoculum, the disease may be more severe near small grain field margins (3).
Infestation levels:
- The most serious problem assocated with ergot is consumption of infected grain by humans or animals.
- Federal grain grading standards classify grain as "ergoty" if it contains more than 0.3% of ergot bodies (sclerotia) by weight.
- Grain yields rarely are reduced by ergot infections (6).
Life cycle:
1) Hard black sclerotia on the soil surface or residue germinate to produce stromata which form ascospores that are transported by wind or insects to the flowering cereal.
2) A conidial stage known as the "honeydew stage" forms on the infected head. This can be transmitted by insects to other uninfected flowers.
3) Sclerotia form on the heads and drop to the ground or are mixed with the seed for the next year. Infections frequently spread from wild grasses into cultivated cereals. Sclerotia remain viable in soil or in storage with grain for approximately one year (2).
History in MT and US:
- Ergot is indigenous to grasses in temperate areas. These native grasses supply most of the inoculum for grain crop infection.
- Outbreaks of ergot in wheat are sporadic in Montana.
- Ergot has been more common in and near Conservation Reserve Program acreage and other areas in which grasses are not cut or grazed. This is because ergot develops only in grasses that reach maturity (produce heads) (5).
Crop losses: When grain containing ergot sclerotia are fed to livestock, severe livestock losses can occur.
Cultural controls:
- Rotate cereals with a nongrass crop to reduce inoculum. Rotation between wheat and rye is not recommended since both crops are susceptible to ergot (also rye/Triticale- and wheat/grass (esp. Agropyron-rotations should be avoided) (4). Rotations to crops such as safflower, sunflower, fababean, sugar beet, or corn are good choices (6).
- In one cropping season, all the sclerotia will die or rot in the soil allowing susceptible grains to be planted the following year (3, 6).
- Do not plant seed that contains sclerotia.
- Mow or burn native grasses before they flower.
- When ergot is prevalent in native grass on the margins of the field, harvest the outside of the field separately.
- Most sclerotia can be removed from harvest grain by cleaning. 6) Destroy screenings by burning.
- Do not feed to livestock!
- Plant seed containing sclerotia at least 2 inches deep.
- Till sclerotia under to a depth of at least 4 cm so stromata won't reach the soil surface to liberate ascospores (1).
Resistant varieties:
- Unfortunately, no extensive studies have been conducted regarding relative susceptibility of Montana wheat and barley varieties to ergot (6). However, selection of varieties with a low degree of sterility and florets that remain open only for short time periods during pollination and flowering are the best bets (2, 6).
Biological controls: Some fungi, like Fusarium roseum, hyperparasitize C. purpurea and offer promise for biological control (2).
Chemical controls:
References: 1) Pacific Northwest Plant Disease Control Handbook.
1994. 2) Wiese, M.V. 1977. "Ergot" Compendium of Wheat Diseases.
APS Press, St. Paul, MN, pp. 14-16. 3) NDSU Pest Report, "Ergot",
July 30, 1993, No. 13. 4) Lamey H.A and McMullen, M.P. 1993. "Crop rotations
for managing plant diseases" North Dakota Extension Service. Bulletin PP-705.
5) Riesselman, J. 1992. Ergot potential in cereals. Montana Crop Health
Report, August 7, 1992, No. 10. 6) Riesselman, J., Baldridge, D. and Rumley,
J. 1983. Ergot and its contol. Monguide. Montana State University Cooperative
Extension Service, MT8318.
.
Pictures of fusarium scab:
comparison
of healthy and scabby kernels
Scientific name: Fusarium spp. (2) Fusarium graminearum (1) and Fusarium roseum
Hosts: Small grain crops (Hard red spring wheat and durum wheat are the most commonly infected. Barley and oats also are susceptible but infections are more rare in these crops. Corn also is a susceptible host (Corn root rot and corn stalk and ear rot)(7).
Symptoms of Fusarium scab:
- Florets in affected heads are killed, bleached white and develop salmon-pink to orange spore masses on the edges of their glumes.
- Kernels in infected florets are shriveled, whitish to pinkish in color and have poor germination (1).
Look-alike symptoms:
Favorable conditions: Rare in Montana, but can occur when rain persists through the flowering period of the crop, or there are 48 hours of continuous moisture at the time of flowering. Wheat-wheat rotation or corn-wheat (or vice versa) rotation since the wheat scab fungus is the same one that causes Gibberella stalk rot of corn (1). The vomitoxins that may be produced by the scab fungus on the head do not form after the grain reaches 22-25% moisture.
Pattern in field:
Infestation levels:
Life cycle: The causal fungi are facultative, nonparasitic organisms that may also infect other plant parts (roots, leaves, seedling blights) (4). Involved Fusarium spp. reside in the soil and on old stubble and straw. The same organisms can also cause disease of the roots, foot, and crown of wheat. The pathogens have simple nutrient requirements and are nearly always present as saprophytes.
History in MT and US: Severe infections in eastern ND, Minnesota, Manitoba, August 1993. Isolated incidents in Montana, 1993. Scab was severe in parts of Washington and Idaho in 1982 and 1984.
Crop losses: Significant yield losses result from flower sterility and poor seed filling (4). In ND, the total yield loss from scab in 1993 is estimated to be about 90 million bushels while estimated yield loss was 36 million bushels in 1994. No data on loss estimates for barley or durum wheat (2). In 1994, estimated average yield losses in HRS wheat from scab were 24% in NE, 12% in EC, 9% in SE. Losses would have been much higher if the average in affected counties had been planted to much more susceptible cultivars (2).
Toxin production:
Fusarium species that cause scab sometimes but not always produce one or more mycotoxins at the time of harvest. These chemicals may be toxic to livestock and man and may remain stable in flour and bread.
Several mycotoxins may be produced by F. graminearum in wheat seeds. One of major concern is deoxynivalenol (DON) which also is known as vomitoxin. DON is produced in wheat seeds while still in the field so it is already present when the grain goes into the bin. The grain must be at about 23% moisture or more before the Fusarium can grow.
Current U.S. guidelines suggest that DON should not exceed 2 ppm in raw wheat and 1 ppm in bread. These regulations are only guidelines in the US. Canadian regulations are more strict (6).
Cultural controls:
Fall tillage: Plowing under infected residue aids in decomposition of the residue and prohibits release of spores in the following year (3).
Rotation: Rotation to non-host plants such as beans or sugar beets can greatly reduce inoculum levels.
A corn-wheat rotation is NOT effective since both crops are scab hosts (3). The most serious scab problem is likely to arise if wheat is planted into corn stubble to cornstalk trash. The scab organism survives in corn residue and is readily available to infect the wheat head if favorable warm and wet conditions occur at the time of pollination.
Irigated wheat planted after corn is a high risk rotation practice, because the continuous wet conditions are very favorable for scab infection (7).
Fertility: At the Langdon Experiment Station in ND, low fertility (50 lb N) resulted in higher disease than high fertility (80 lb N) (3).
Irrigation: Avoid sprinker irrigation during flowering (1).
Swathing: The vomitoxins that may be produced by the scab fungus on the head do not form after the grain reaches 22-25% moisture. If swathing could get the moisture level down faster than straight cutting, then it may be beneficial, AS LONG AS THE SWATHED GRAIN DOESN'T GET RAINED ON AND MOLD. So the weather forecast is important in this decision (5).
Resistant varieties: In ND, 2375, and Butte 86 are considered more tolerant of scab infection. Grandin is moderate in response (2). Evaluations of HRS and durum variety response to scab are being conducted in ND (fall 1994). Scab severity and vomitoxin production are being compared in the varieties (3).
Biological controls:
Chemical controls:
Seed treatments:
In areas of severe scab occurance, there can be seed quality concerns. If seed germinations are below 90%, use seed treatments (3). Seed treatments containing TCMTB or thiram will reduce Fusarium contamination on seed used to plant a subsequent crop, but will have no effect on head blight.
Foliar fungicides:
No effective fungicides currently are available. In 1994, trials were established in MN and ND to evalulate whether flowering to early post-flowering applications of benomyl and/or mancozeb may significantly reduce scab infection and spread. Initial indications, based on scab severity ratings, indicate some positive results. However, yield differences have not yet been determined (3).
References: 1) Lipps, P.E. 1988. Wheat disease control in
Ohio. Dept. of Plant Path. Ohio State Univ. 2). McMullen. 1994. "Estimates
of Scab losses in HRS wheat. NDSU Crop and Pest Report, Sept. 2,
1994, Issue 17. 3) McMullen. Scab losses in HRS wheat".Sept. 2 1994. "Scab
management for 1995". NDSU Crop and Pest Report, Sept. 2, 1994,
Issue 17. 4) Wiese, M.V. 1977. "Head blight or scab" Compendium of Wheat
Diseases. APS Press, St. Paul, MN, pp. 16-17. 5) NDSU Pest Report,
"To swath or not to swath", August 13, 1993. 6) Cook, R.J. Veseth, R.J.
1991. Wheat Health Management. APS Press, St. Paul, MN, p. 58. 7)
Lamey H.A and McMullen, M.P. 1993. "Crop rotations for managing plant diseases"
North Dakota Extension Service. Bulletin PP-705.
Picture of loose smut:
loose
smut, covered smut, and dwarf bunt - slide comparison of three heads
Scientific names: Ustilago tritici
Hosts: Wheat, barley, (infrequent on rye) (2).
Symptoms:
symptoms
on heads - progressively more severe
Symptoms become apparent between heading and maturity. Diseased heads emerge before healthy ones. Diseased heads are blackened and very distinctive from green, healthy heads. A thin membrane encloses a dry olive-black spore mass. Spores disperse by wind and after only a few days, only the rachis remains (2).
Look-alike symptoms: Loose smut produces rather distinct symptoms on heads.
Favorable conditions: Infections occur only during flowering and are favored by wet weather and cool to moderate temperatures (16-22 C)(2).
Pattern in field:
Infestion levels:
Life cycle: The loose smut fungus is strictly seedborne (3,8). The loose smut fungus comes into the field within the embryoes of seed. Once the infected seeds germinate, the fungus again becomes active. It grows upward in the plant within the growing points to where the heads are forming. Where the kernels should be, the fungus forms a loose mass of spores. The formation of these spores is timed so that they can be blown to the open flowers of neighboring plants, where they invade the ovaries to repeat the cycle (8).
History in MT and US: Occurs worldwide.
Crop losses: Quantity and not quality is affected by loose smut as opposed to seedborne bunts and covered smut. Yield loss is directly proportional to number of heads infected. Usually losses are less than 1%, but losses up to 27% have been reported (2). In barley, higher levels are common: Horsford barley injury levels can equal 25%. Losses are directly proportional to infection levels (3).
Cultural controls: Plant certified seed (3). Crop rotation does not reduce diseases caused by organisms that survive on or in the seed, as with cereal smut fungi (9).
Resistant varieties:
Biological controls:
Chemical controls: Seed treatment with systemic fungicides. Captan, Imazalil. (also carboxin, carboxin+captan, carboxin+thiram, (1))
References: 1) Lipps, P.E. 1988. Wheat disease control in
Ohio. Dept. of Plant Path. Ohio State Univ. 2) Wiese, M.V. 1977. "Loose
smut" Compendium of Wheat Diseases. APS Press, St. Paul, MN, pp.
21-22. 3) Pacific Northwest Plant Disease Control Handbook, 1994.
7) Cook, R.J. Veseth, R.J. 1991. Wheat Health Management. APS Press,
St. Paul, MN, p. 55. 8) Cook, R.J. Veseth, R.J. 1991. Wheat Health Management.
APS Press, St. Paul, MN, p. 57. 9) Lamey H.A and McMullen, M.P. 1993. "Crop
rotations for managing plant diseases" North Dakota Extension Service.
Bulletin PP-705.
Scientific names: Aspergillis
spp. and Penicillium spp. (1)
Hosts: Small grains (other crops)
Symptoms: Where infections are well established, embryoes are killed and darkened beneath the bran coat. Infected seed often has a musty odor. Excessive fungal growth can induce heating, "caking", and seed decay. Sometimes grain is darkened or even charred (bin burned) by prolonged exposure to heat generated in storage. Storage molds on the surface of wheat seed are not detrimental. Internal infections, however, decrease germination. The fungi primarily invade embryoes so that many kernels that appear healthy are damaged (1).
Look-alike symptoms:
Favorable conditions: Warm temperatures, seed injury, contaminant debris, and moisture promote storage molds. Most of the fungi grow optimally between 30 and 33 C, and can grow between 5 and 40 C. Seasonal or daily temperature fluctuations in storage bins can cause moisture migration and condensation that may permit fungal growth on grain that is otherwise suitably dry (1).
Pattern in field:
Infestation levels:
Life cycle: The fungi responsible for storage molds are species of Penicillium and Aspergillis. They grow best at about 75 F, but they can still grow at temperatures down to 40 F. These fungi have the unique ability to grow at relative humidities down to a lower limit of about 70%. Below this minimum relative humidity of the air or the equivalent moisture status of the grain, the fungi cannot obtain enough water to maintain the turgor pressure necessary for their growth.
Wheat equilibrated with 70% relative humidity has a moisture content of about 13%. This is wet enough for the growth of the most extreme types of these water-stress-tolerant fungi. At progressively higher temperatures and relative humidities, more and more species of Aspergillis and Penicillium can grow.
Grain at 18% moisture is ideal for the maximum growth of some Aspergillis species. Grain stored at 20% moisture with equivalent relative humidity at 90% can support the growth of many different fungi.
History in MT and US:
Crop losses: Both Aspergillis and Penicillium contain members that produce mycotoxins that are toxic to man and animals and reduce palatibility of the grain. The large numbers of air-borne spores produced can cause respiratory diseases in man and animals (1).
Cultural controls: The best prevention of storage mold growth is to maintain grain moisture content below 12 - 12.5% (3). Usually, grain with less than 12 - 12.5% moisture (wet weight basis) stored below 20 C and 70% RH will not be damaged (1,3). Periodic grain sampling and testing for heating, moisture content, germinability, and fungi are recommended. Avoid injuring seed during harvest (1).
Resistant varieties:
Biological controls:
Chemical controls: Available only for grain to be used as seed (1).
References: 1) Wiese, M.V. 1977. "Storage molds" Compendium of Wheat Diseases. APS Press, St. Paul, MN, p. 11. 2) Cook, R.J. Veseth, R.J. 1991. Wheat Health Management. APS Press, St. Paul, MN, pp. 57-58.
