Sorghum downy mildew (SDM), caused by the fungus Peronosclerospora sorghi, appeared in several sorghum fields in Wharton and Jackson counties of Texas during the spring of 2001 and again in 2002. This disease was once thought to be controlled, so its prominent reappearance was surprising and disturbing. Evidence from one field trial in Wharton county in 2002 suggests that the pathogen is resistant to the Apron/Allegiance seed treatment. Fungicide resistance will make control of this disease more difficult in the future.

Seedlings are pale yellow or have light-colored streaking or mottling on the leaves (Fig. 1), often accompanied by a white fuzzy, growth on the underside of leaves (Fig. 2). These symptoms indicate a systemic infection by soilborne spores (oospores) of P. sorghi that infect young seedlings. Germinating sorghum seed is more prone to infection early in the season, when the soil temperatures are cooler. Leaves that emerge later have white parallel stripes of green and white tissue (Fig. 3). (Do not confuse this striping with iron chlorosis, which results in a pale color in-between veins. The white stripes of SDM are not limited to veins and vary in width.) Later in the season, these striped areas die, turn brown, and disintegrate, resulting in a shredded appearance of the leaf (Fig. 4). Oospores of the fungus are produced in this tissue and eventually end up in the soil.

The white, fuzzy growth on systemically-infected plants indicate the production of short-lived spores, known as conidia. Conidia are produced in cool, humid or wet weather. Conidia become airborne and infect leaves of other plants, causing a local lesion phase of SDM. Local lesions are brown and somewhat rectangular (Fig. 5). Local lesion infections can become widespread throughout a field and be dramatically noticeable, but cause no yield loss and are usually short-lived because seasonal increases in temperature prevent their spread to later-emerging leaves. Most importantly, local lesions do not produce oospores. Under cool, wet conditions, however, infection of young seedlings by conidia can result in systemic infections.

There is no grain yield from systemically-infected plants, which act as "weeds" by decreasing available water and nutrients to nearby, healthy plants, particularly when infected plants occur in patches or clumps.

Why the resurgence?

More than 20 years ago, SDM was a very serious disease of sorghum in the Coastal Bend and Upper Coast growing areas of South Texas. Resistant hybrids provided primary control of the disease until new races (pathotypes) occurred. Many hybrids grown in South Texas during the early 1980's were susceptible to pathotype 3 which allowed this pathotype to became a problem across the region but especially along the Upper Coast However, the widespread use of the fungicide Apron® (metalaxyl) as a seed treatment effectively controlled systemic SDM caused by all pathotypes.

Several factors interacting over many years have contributed to the recent outbreak of SDM. These primary factors are believed to be (1) low seed treatment rates of metalaxyl, (2) continued planting of pathotype 3 susceptible sorghum hybrids, (3) increased monoculture of grain sorghum, and (4) seed treatments with Concep III herbicide seed safeners. The most critical factor is the low seed treatment rate of metalaxyl which is ineffective or less effective in controlling SDM. These low rates then allow the other factors to interactively and progressively increase both the yearly incidence of SDM and the soilborne populations of oospores. The low rates of metalaxyl can also have the effect of selecting for resistant populations, while sorghum monoculture allows such resistant populations to build up in soil. The development of resistance to metalaxyl has happened in at least one field in Wharton county and resistance has probably independently developed in other fields as well.

In 2002, we observed several sorghum fields in Wharton county with high incidences of SDM. These fields were planted to pathotype 3-susceptible hybrids and at least some of these fields were treated with the recommended rate of metalaxyl. Some of these fields will likely have yield losses. Repeated monoculture of these fields will result in the continued build up of SDM oospores in soil, with the increased potential for yield loss in the future.

The indications are that the SDM outbreak is caused by P. sorghi that is a typical pathotype 3. While metalaxyl is ineffective for controlling SDM in some Wharton county fields planted to pathotype 3 susceptible hybrids, there are other hybrids which are resistant to this pathotype. However, metalaxyl treatment of resistant hybrids served to prevent the establishment of new pathotypes that overcome the resistance of those hybrids. When metalaxyl is no longer effective, the chances of a new pathotype developing are increased, particularly under sorghum monoculture. Thus, the use of a SDM-resistant hybrid should not be thought of as a replacement for metalaxyl seed treatment. To do so, while continuing with monoculture, increases the risk of also losing hybrid resistance as a disease control method.

Ideally, SDM control should integrate several methods: fungicide seed treatment, resistant hybrids, and crop rotation, which reduces oospore populations over several years. Such an integrated approach will maintain the longevity of all control methods. At this point in time, the problem with metalaxyl resistance is not widespread, even within Wharton county. Thus, metalaxyl can and should still be used as a seed treatment. This even applies to fields where there is a resistance problem, since it may be possible that the fungicide is suppressing the development of new pathotypes that are sensitive to metalaxyl.

However, in fields where there is a metalaxyl resistance problem, the first objective should be to reduce soil populations of the pathogen through crop rotation. Two years out of sorghum would be a good start; three years would be better. Corn is the only other crop susceptible to SDM, however, infection does not lead to production of oospores. (Johnsongrass is also susceptible to SDM, but it is usually controlled within a field and so, is not a major contributor to the disease problem). After a period of rotation, these fields should be planted with a hybrid resistant to pathotype 3.

In fields where there has been no SDM, metalaxyl should be used on a preventative basis for seed treatment as follows:

Varieties susceptible to pathotype 3:

We recommend a metalaxyl rate equivalent to 1 oz. (dry weight) active ingredient/100 lb seed for SDM control with susceptible varieties. For example, the rate for Allegiance FL is 3.0 fl oz/cwt. The corresponding rate for mefenoxam (also known as metalaxyl-m), the active isomer of metalaxyl, is 0.5 oz. (dry weight) active ingredient/100 lb seed. For example, the SDM control rate of Apron XL® LS, a commercial formulation of mefenoxam, is 1.28 fl. oz. formulation/100 lb. seed. We feel this rate is critical for prevention of fungicide resistance.

Varieties resistant to pathotype 3:

Use a rate of metalaxyl labeled for SDM control with resistant varieties, which ranges from 0.25 to 0.5 oz. (dry weight) active ingredient/100 lb. seed. For example, with Allegiance™-FL, the formulation rate of 0.75 fl. oz./100 lb. seed can be used. The SDM control rate of Apron XL® LS is 0.32 to 0.64 fl. oz. formulation/100 lb. seed.

Refer to the fungicide product label for additional information, particularly for allowable rates, as well as precautions.

Fig. 1: Pale yellow leaf symptom of SDM

Fig. 2: Conidia on leaf underside.

Fig. 3: Striping of leaves (systemic infection)

Fig. 4: Shredding of leaves (source of oospores).

Fig. 5: Local lesions on leaves.