Grain Sorghum Diseases, Occurrence and Management
By Brad Lance
By Brad Lance
Grain sorghum can be affected by a wide variety of diseases, which can cause serious losses of production and profitability. Some diseases occur across a wide area, at levels that do not cause extreme concern in any given field, but may add up to a considerable net loss due to their prevalence. Some diseases are readily detected due to easily identifiable symptoms that noticeably reduce yields. It is important for sorghum growers to be able to identify the diseases that frequently occur in their growing environment.
Plant diseases can mutate and new pathotypes or races can arise in a short time period. Due to the changing nature of plant diseases and yearly fluctuations in environmental conditions, monitoring sorghum production for plant disease incidence should be routine. Most sorghum diseases are readily recognizable and several excellent publications exist for sorghum disease diagnosis. The Compendium of Sorghum Diseases, published by The American Phytopathological Society, is an excellent resource.
Several pathogenic organisms cause sorghum diseases including: fungi, bacteria, and viruses. Host plant resistance varies widely among hybrids. Some diseases, for a variety of factors, do not occur in a given area. Hybrid selection should be based on the diseases that occur in the local growing environment. Some diseases may be managed through crop rotation or other cultural practices that do not require highly resistant hybrids.
This section will examine the symptoms of specific diseases, sources of hybrid tolerance to these pathogens and cultural modifications that may be implemented to reduce the economic impact of sorghum diseases. Pioneer rates sorghum hybrids for resistance to important diseases. This information is available in product catalogs, and in the sorghum products section. Pioneer sales providers, account managers, and area agronomists are excellent resources for specific disease management information.
Seedling blights are often referred to as "damping off diseases." Seedling diseases may be caused by soil-borne pathogens, soil and weather climatic factors, seedling vigor, or any combination of these factors. Pioneer has very stringent seed quality requirements. Every seed lot produced is checked for warm and cold germination and for the presence of disease. This ensures producers the highest quality seed available.
Even with high quality seed, soil-borne fungi can attack seeds and seedlings under certain climatic conditions. Cold, wet soils can severely impact sorghum emergence by weakening the seed, thus allowing pathogens to infect seed and seedlings. Pioneer uses fungicidal seed treatments to guard against seedling diseases.
The first symptom of seedling blight is failure of the seed to germinate which results in rotted seed. In other cases, necrotic tissue may be present, seeds may germinate or the young roots or leaves may have a water soaked appearance. In other cases, seedlings may emerge and then begin to die. There are several fungal diseases associated with seedling blights. The primary seedling disease pathogens are: Pythium, Fusarium, Aspergillus, and Rhizoctonia. These pathogens may occur independently or in combinations to cause seedling disease problems. Using high quality seed, planting only when soils are above 65 F, and use of appropriate seed treatments will minimize seedling disease concerns.
Sorghum leaf blight is a foliar disease caused by Exserohilum turcicum. In 1996, the disease was prevalent in parts of western Texas, but occurred sporadically across the sorghum producing areas of the United States and northern Mexico. Today, this disease is present in many humid areas where sorghum is grown and is favored by moderate temperatures (60 to 80 F). Heavy dew promotes the disease. Dry weather inhibits the establishment of this sorghum leaf blight.
If seedlings are infected, small reddish or tan spots develop on the leaves. As the disease progresses, these spots enlarge, the leaves wilt and turn purplish gray, and the seedling ultimately may die. In more mature plants, long elliptical lesions develop on older leaves and may be reddish-purple or yellowish tan. These lesions vary in color and size according to varying levels of resistance. Most of the lesions occur on older leaves, and then progress to younger leaves. Lesions on older plants have yellowish to gray centers and reddish margins. If the disease is established before boot stage, up to 50 percent yield losses are possible. Sorghum leaf blight can be controlled by rotation to non-susceptible crops and foliar applications of labeled fungicides. Planting resistant hybrids is the most effective management strategy for sorghum leaf blight.
Sooty stripe occurs in areas where warm, humid conditions exist. Sooty stripe occurs primarily in the south central states of the United States such as Kansas, Missouri and Oklahoma.
Sooty stripe is caused by the fungal species Ramulispora sorgi and Ramulispora andropogonis. These pathogens live in leaf tissue on or below the soil surface. These pathogens also infect Johnsongrass, which serves as another source of inoculum. The spores of these pathogens are spread by wind and rain. Removal of inoculum by crop rotation or destruction of infected leaf debris is a viable control method. Use of resistant hybrids will also control this disease.
Leaf rust and gray leaf spot can be economically damaging in sorghum, especially in moist environments. These foliar diseases are often associated with late planting and ratoon sorghum.
Bacterial leaf spot or Bacterial Leaf Stripe can infect sorghum, but usually only results in cosmetic leaf lesions, not economic losses. These illustrate Bacterial Leaf Stripe.
Head smut is caused by the soil borne fungus Sporisorium reilianum. This pathogen can readily mutate and overwhelm plant resistance mechanisms. There are several known races of head smut, including Southern head smut. The fungal spores live in the soil and germinate in the spring. Spores will actively invade the sorghum plant in the nodal region of the shoot apex. The disease will continue to grow in the plant, actively destroying the reproductive tissues. A black mass of spores replaces some or all of the sorghum head. When infected, some hybrids are dwarfed and will tiller profusely (with all tillers producing smutted heads). Spores move with wind and water to the soil and serve as inoculum for the next year. Since each infected plant produces millions of spores, the threat of infection for the next year is increased. Head smut spores can remain viable for years in the soil. Crop rotation and fungicides cannot control this disease. Head smut can only be effectively managed genetically. Pioneer has many hybrids that are resistant to head smut and continues to screen hybrids for new races of head smut through an extensive screening program.
Loose kernel smut and covered kernel smut are controlled with fungicide seed treatments. These diseases should not be an economic factor due to the widespread use of highly efficacious seed treatments used in sorghum.
Sorghum downy mildew is caused by the fungal pathogen Peronosclerospora sorgi. Downy mildew spores germinate and invade the roots of sorghum seedlings. This type of infection is systemic, in that most of the plant will eventually be infected. Infected seedlings may become chlorotic and die.
Usually, the first leaf with symptoms will show yellowing only on the lower part of the leaf. Under cool conditions, a white "downy" substance may develop on the lower side of the leaves. As the disease progresses, the emerging leaves show parallel stripes of green and white tissue. This white tissue will be necrotic, and the leaves will shred. Infected plants are usually sterile. Sorghum downy mildew can also propagate on Johnsongrass.
Sorghum downy mildew can mutate and form other races. Most sorghum hybrids have genetic resistance to pathotype 1 downy mildew, but resistance to pathotype 3 downy mildew is less prevalent in the sorghum industry.
Fusarium stalk, root, head and seedling diseases are caused by the pathogen Fusarium moniliforme. Other Fusarium species may also cause damage to root and stalk tissue. Crop losses from Fusarium diseases usually range from 5 percent to 10 percent, although losses approaching 100 percent have been documented in localized areas. Yield losses generally occur due to poor grain fill, weakened peduncles, or lodged plants.
Figure 1: Fusarium. Note reddish discoloration in the pith of the stalk or root system. Head in the first photo is from infested plant and shows reduced grain test weight and lack of complete grain fill when compared to unaffected plant on the right.
Disease incidence is sporadic from year to year and is governed by factors such as soil type, weather conditions, fertility, drainage, insect damage, cultural practices and host plant genetics. Fusarium can be identified by light red to dark purple spots on roots, seeds, and stalks, which may be elongated or circular. The fungus spreads to other root and stalk tissues as the growing season progresses. Areas where insect damage has occurred show large areas of red pith. In most cases, when the plant is split longitudinally, the lower two to three internodes exhibit this red pith. Premature plant death during grain development is characteristic of this disease. The leaves appear to be sun scorched or freeze damaged, although the exterior stalk tissue remains green. Lodging may occur on peduncles or stalks. Fusarium overwinters in plant debris and can enter plants by natural wounds, insect damage or machinery damage. The disease appears more severe when periods of cool, moist conditions follow hot, dry, or otherwise stressful growing conditions.
Effective management of the sorghum crop will help control the Fusarium disease. In irrigation situations, manage irrigation to provide moisture throughout the growing season and especially at bloom through hard dough. Effective weed control will reduce stress. Eliminate any potentially damaging insect problems. Maintain good fertility levels. High nitrogen levels with low potassium levels promote stalk rots. Avoid high plant populations and plant hybrids with good levels of resistance to Fusarium.
The fungus Macrophomina phaseolina causes charcoal rot. Not only is charcoal rot a significant sorghum disease, but it also attacks corn, soybeans, sunflowers, cotton and about 400 other plant species. Charcoal rot is a major disease for sorghum grown in the arid regions of the United States. Dryland production of sorghum is most vulnerable to charcoal rot infection. Anytime grain sorghum is stressed after bloom and into the fill period, charcoal rot can be a problem. High plant populations, leaf diseases, hail damage, mechanical damage, excess nitrogen fertilization, and insect feeding may increase post-flowering stress and allow pathogens to enter the roots. This disease is especially damaging when warm, moist growing conditions are followed by hot, dry conditions during grain fill. Infected roots show water soaked lesions, which will turn black. Lodging will occur and entire fields may be affected. If a lodged plant is split open, the pith will be black and resemble charcoal. Control of charcoal rot is similar to controlling Fusarium rot. Eliminating stress following bloom may not always be feasible in dryland situations. However, controlling nitrogen rates, utilizing appropriate plant populations, and minimizing insect feeding, can go a long way in reducing charcoal rot incidence and severity. Hybrid selection is very important in combating this disease. Although there is no known genetic resistance to charcoal rot, many Pioneer hybrids exhibit good tolerance to this disease. Select hybrids with good scores for charcoal rot, standability, and drought tolerance to minimize the effects of charcoal rot.
Anthracnose is caused by the fungal pathogen Colletotrichum graminicola (Ces.) and is divided into three categories based on where the damage occurs in the plant: leaf anthracnose, panicle (grain) anthracnose, and anthracnose stalk rot. Lesions begin on the lower leaves and progress up the plant. The lesions appear as oval to elongate water soaked spots. As the lesions increase in size they become tan with a wide border that can vary from a reddish orange color to a purple or tan color. When the host tissue dies, dark fruiting bodies known as acervuli develop and form conidiospores. The conidiospores have a creamy to pinkish color and serve as the source inoculum for secondary and panicle infections.
Panicle anthracnose occurs as plants start to mature. Infections in the panicle are generally caused when conidiospores formed from the leaf lesions are splashed onto the panicle by either rain or irrigation water. Infected panicles are light in weight, can mature early, and often display varying levels of sterility.
Anthracnose stalk rot occurs in much the same way as panicle anthracnose. While infection can occur anytime throughout the growing season, mature plants are generally the most at risk. The infection occurs when the condiospores are either splashed or blown onto the stalks. Initial symptoms include a water-soaked discolored appearance in the lower portion of the stalk. These lesions will become reddish in color and be mixed in with healthy stalk tissue.
Anthracnose will overwinter on plant debris that remains on the soil surface, and can also survive in the seed. Warm and wet conditions create a favorable environment for the pathogen to readily reproduce and spread. Planting resistant hybrids, use of seed treatments, crop rotation, and tillage are viable options for helping to control anthracnose.
Sorghum ergot is a fungal disease formerly confined to the African and Asian continents. However, over the past few years this aggressive disease has affected sorghum producers in Australia, and the American continents. In 1996, the first reports of sorghum ergot in the Caribbean and Mexico were received. Since that time, ergot has been reported across the sorghum growing areas of North America. This article provides insight on sorghum ergot’s unique pathological characteristics, potential for the extent and range of damage, and control measures.
Any sorghum field has the potential to be affected by this disease, which infects primarily via airborne spores. Pollinating florets are the site of infection. Once pollination has been achieved, the risk of infection is past. The first visual symptom of infection is the production of thick, sugary honeydew from infected florets. This honeydew contains infectious spores and produces a bloom of white, powdery spores on the surface of the honeydew. Other non-pathological fungi can later colonize the sugary honeydew, producing a brown or black spore mass. Any condition that limits pollen production or viability has the potential to increase the severity of infection in commercial production or seed production. Hybrid seed production fields will be at the highest level of risk due to the presence of male-sterile plants that require pollen from other plants to achieve fertilization. Fields that do not “nick” closely will be at very high risk if the disease is present. Some forage hybrids have a higher potential for infection than commercial grain sorghum due to a number of forage/hay hybrids that are male-sterile. These hybrids will be extremely likely to be infected in the presence of sorghum ergot spores.
To control infection levels and reduce the production of disease spores, these hybrids should be cut for hay before heading and intensive grazing on heading plants should be minimized. Commercial grain sorghum production is least likely to be infected, but conditions causing poor pollen production and viability can increase risk of infection. A prominent example of this scenario is a field which is late-planted and pollinates during very cool conditions in early fall or late summer. Cool conditions inhibit sorghum pollen production. Very humid conditions and prevailing winds from the direction of known infectious sites will move this disease cross-country. Areas at moderate to high risk of experiencing sorghum ergot include all of the major sorghum-producing areas of the Plains states. Southeastern states are currently considered to be a low to moderate risk.
Economic damage can occur in a number of ways. Most prevalent is damage to seed production fields. A prophylactic spray program of an approved fungicide will need to be used in seed production areas, if the possibility of infection is high. Secondly, grain production can be lost in commercial fields, especially in late-flowering fields. Probably the most significant risk to commercial grain production is the poor harvestability of fields with honeydew on leaves and grain heads. Honeydew coated plant parts can coat harvesting equipment with a gluey substance that can adhere to critical combine parts such as grain augers, headers, and sieves.
There are no known sources of resistance to sorghum ergot that can be easily integrated into today’s commercial sorghum hybrids. A long-term solution may be the integration of resistance genes via biotechnology. Pioneer is a leading innovator in the use of biotechnological processes in sorghum. However, very little has been accomplished in the field of grain sorghum biotechnology when compared to other commercial crops such as corn, soybeans, and cotton. Any commercial hybrid resistance is many years away, whether achieved via biotechnology or traditional plant breeding.
Chemical control measures that have been used successfully in sorghum seed production consist of a 5-7 day interval of 3-4 applications of a triazole fungicide such as propiconazole. The economics of applying fungicides to ordinary grain or forage production is not likely to be feasible. The rates and sequential treatments required for good control of ergot will probably be in the $30 to $50 per acre range.
Seed produced in an ergot-infested environment can have some viable spores in a crusty residual coating that often accompanies ergot infection. Seed treatment fungicides can disinfect seeds that have some ergot residue on the seed coat. Conventional topical treatments such as captan and fludioxonil will control the spores present on ergot-encrusted seeds.
Ideal conditions for ergot infection are high humidity and cool temperatures (70 F). Most sorghum (especially in south and central Texas and eastern Kansas) pollinates during periods of high temperatures. This may somewhat blunt the effects of the fungus in these growing areas. Commercial sorghum production in the high plains is at risk for ergot infection due to the cool conditions that can be prevalent during pollination. Very late planted fields will be most at risk due to the extended period of time required for pollination to occur when temperatures fall below 60 F.
Many viruses can infect sorghum plants. The main difference between viruses and other pathogens is that viruses do not actively penetrate plant tissue. Viruses must be transmitted (vectored) to the plant, usually by aphids and leafhoppers.
The two primary viruses infecting sorghum are maize dwarf mosaic virus (MDMV), shown here on maize, and sugarcane mosaic virus. Aphids transmit both of these diseases after feeding on plant reservoirs containing the virus. Maize dwarf mosaic virus is primarily vectored from Johnsongrass and other grass species. SMV Sugarcane mosaic virus can be vectored from the same plant species as MDMV, with the addition of sugarcane. Control of insect vectors and alternate hosts of the diseases will provide some suppression. Genetic resistance offers the best control of these diseases.
(This section was written by John Jaster SRA in Taft)
There are many different diseases and types of diseases that can affect a sorghum crop in a given year. The easiest way to differentiate between any disease races is to compare the disease reaction of known tolerant and known susceptible hybrids. This can be done in the field where side by sides are planted or sent to special greenhouses and grown on virulent sets of known inbreds to determine the race. Again this is a relative test. Some diseases like anthracnose can overwhelm genetic resistance if greenhouse conditions are just right. Plant pathologists are not able to differentiate races by looking at the pathogen under a microscope. Some molecular markers in the future might be able to do this. Do not send plant samples to a lab expecting race identification unless a battery of greenhouse tests on living differentials are performed. The smart thing (easiest and cheapest) to do is plant the known resistant and susceptible hybrids in a sick field and do side by side evaluation in the field at the time of disease expression. Consulting with the local extension plant pathologist in your area can help to determine what if any testing needs to be done, as well as details on how to collect and prepare samples for testing.
Brad Lance holds a Bachelor of Science degree in entomology from Texas Tech University. He currently serves as the Business Director for the Heartland Business Unit and previously served as a Technical Information Manager for the Western sales region. He spent a number of years as quality control manager at the Pioneer sorghum seed production location in Plainview, Texas and has worked as a Field Sales Agronomist since joining Pioneer Hi-Bred International in 1982.