An Overview of Goss's Bacterial Wilt and Blight

Goss’s bacterial wilt and blight of corn is an economically serious disease of susceptible dent and specialty corn hybrids and varieties. This disease (most commonly called Goss’s wilt) is caused by the bacterium Clavibacter nebraskensis. Grain yield loss from severe Goss’s wilt infections can exceed 50 percent.

Goss’s wilt was first observed in south-central Nebraska in 1969, and was reported in neighboring states soon after that. The disease’s prevalence was low throughout the region from the 1980s through the early 2000s. However, between 2006 and 2017, Goss’s wilt reemerged in these states and was reported in many other U.S. states and two Canadian provinces.

Currently, the known distribution of Goss’s wilt reaches as far east as Indiana, west to Colorado, south to Texas, and as far north as Manitoba and Alberta. To date, the disease has not been confirmed outside the continental United States and Canada.

This publication describes Goss’s bacterial wilt and blight symptoms, describes disorders commonly confused with the disease, and recommends management strategies.

Symptoms

Goss’s wilt can cause leaf blight and systemic wilt symptoms. Leaf blight is the most common symptom and may occur at any growth stage. Leaf symptoms include elongated tan to grayish-brown lesions that have irregular or wavy margins that extend parallel to the veins (Figure 1). Before the tan lesions form, young lesions appear as streaks of light green tissue with water soaking on the leaf (Figure 2). The tan lesions can affect large sections of leaf area — more than 60 percent of the leaf area on infected plants may be killed (Figure 3).

Dark green to black, scattered, water-soaked spots (“freckles”) develop in the lesions (Figure 4). When the lesions are exposed to sunlight, small, glossy droplets of dried bacterial ooze may appear. When dried, this ooze may look similar to dried varnish (Figure 5).

The systemic wilt phase is less common than the leaf blight phase and is often first observed in the early vegetative stages of growth (corn growth stages V2-V6). When the wilt phase develops, the infection may discolor xylem tissues or cause a slimy stalk rot, which is followed by wilting and plant death (Figures 6-8). Systemically infected plants may wilt and appear drought stressed. Corn plants may have weak stalks and an increased susceptibility to lodging.

Disease Cycle

Figure 9 shows the disease cycle for Goss’s wilt. Infested corn residue is the primary source of inoculum for Goss’s wilt. The pathogen overwinters in infested corn residue on or near the soil surface. Infested residue may allow the pathogen to survive on the soil surface for at least 10 to 15 months. Burying infested residue reduces the pathogen’s survival.

The Goss’s wilt pathogen can also survive in other plant species. Confirmed hosts include grain sorghum, annual ryegrass, sudangrass, several foxtail species, johnsongrass, large crabgrass, shattercane, big bluestem, little bluestem, and wooly cupgrass. These and other grasses may also be sources of inoculum to infect corn.

The bacterium is likely splashed from infested residue or grasses onto the surface of corn leaves. The disease typically develops after the bacterium enters wounds in leaves caused by hail, blown soil, or wind. However, wounds may not be required for infection.

The pathogen can spread systemically in plants after leaves are infected. Although infection that leads to significant yield losses typically occurs during the vegetative growth stages, symptoms often become most visible and severe after silking (R1 growth stage). The bacterium can spread short distances within a field by contacting leaves on adjacent plants and between fields across country roads during the growing season.

In addition, wind and equipment can spread infested leaves or other plant material from field to field. Seed can be infected at very low levels but is not known to be an important means of dissemination; however, it may play a role in introducing the disease into new areas or specific sites within fields.

Conditions that Favor Disease

Planting hybrids susceptible to Goss’s wilt, practicing reduced tillage, and planting continuous corn in fields with a history of the disease can favor outbreaks in subsequent growing seasons. Strong storms, wind, sandblasting, and hail that injure corn leaves allow the pathogen to enter and infect the plant.

Disease development is favored by warm (80°F) weather. Very hot (greater than 95°F) or cool (less than 70°F) temperatures may impede disease development. The disease may occur in fields regardless of irrigation practices, although irrigation may enhance disease progression.

Yield Loss and Impact

Many states have documented yield losses in susceptible corn hybrids during the leaf blight phases of the disease. Fields infected during vegetative growth stages can experience yield losses of more than 50 percent. No hybrids are completely resistant (immune) to Goss’s wilt, but yield losses for resistant hybrids are greatly reduced compared to susceptible cultivars (Figure 10).

Diagnosis

Goss’s wilt can be confused with several other diseases. Therefore, we recommend that you have a diagnostic laboratory confirm suspected samples. Diagnosing this disease is based on noting the presence of the characteristic symptoms and signs (as noted above), confirming the presence of the pathogen, and observing bacterial streaming from the lesions (Figure 11).

Diseases and Other Conditions with Similar Symptoms

Disease Management

The best way to manage Goss’s wilt is to plant highly resistant corn hybrids. Additional control can be achieved by rotating crops with nonhosts (such as soybean, dry bean, small grains, or alfalfa) to help reduce the primary inoculum for the subsequent corn crop.

Because the bacterial pathogen survives in infested residue, tillage that buries residue may reduce the disease. It may also be beneficial (where feasible) tocontrol grassy weed hosts and practice tillage that buries infected residue after harvest. Fungicides are ineffective and other chemical sprays have not been consistently effective at reducing symptoms or preserving yield.

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Acknowledgments

Authors

Dean Malvick, University of Minnesota; Tamra Jackson-Ziems, University of Nebraska-Lincoln; and Alison Robertson, Iowa State University.

Reviewers

Tom Allen, Mississippi State University; Gary Bergstrom, Cornell University; Kaitlyn Bissonnette, University of Missouri; Carl Bradley, University of Kentucky; Emmanuel Byamukama, South Dakota State University; Martin Chilvers, Michigan State University; Alyssa Collins, Pennsylvania State University; Travis Faske, University of Arkansas; Andrew Friskop, North Dakota State University; Austin Hagan, Auburn University; Doug Jardine, Kansas State University; Nathan Kleczewski, University of Illinois; Daren Mueller, Iowa State University; Pierce Paul, The Ohio State University; Adam Sisson, Iowa State University; Damon Smith, University of Wisconsin; Albert Tenuta, Ontario Ministry of Agriculture, Food and Rural Affairs; Lindsey Thiessen, North Carolina State University; and Kiersten Wise, University of Kentucky.

Photo Credits

All photos were provided by and are the property of the authors and reviewers except Figure 3 by Kyle Jensen, Corteva Agriscience; Figure 11 by Nolan Anderson, Purdue University; and Figures 13 and 15 by Gary Munkvold, Iowa State University.