Issue No. 19, Article 3/July 30, 2004
Northern Corn Leaf Blight: Why Are We Seeing This Disease?
Many of you have noted that northern corn leaf blight (NCLB) has been pretty easy to find this season on hybrid corn varieties. In evidence were the very large diagnostic lesions that indicate a susceptible reaction. Why would you be seeing susceptible lesions with qualitative and quantitative resistance to NCLB in hybrids when at most what we should be seeing is a resistant flecking-type symptom?
Susceptible lesions of NCLB. (Photo by Matt Montgomery.)
Here's a little review for a disease that has been exhibiting a slow and steady resurgence for the past several years. NCLB is caused by the fungus Setosphaeria turcica; the conidial state that causes our troubles is Exserohi-lum turcicum (syn. Helminthosporium turcicum). Symptoms of NCLB are long, elliptical, grayish or tan lesions. Infection is initiated when free water is present on the leaf surface for 6 to 18 hours and the temperature is between 65°F and 80°F. The lesions show up on the bottom leaves first. Heavy dews, frequent light showers, high humidity, and moderate temperatures (64°F to 84°F) favor NCLB. The fungus overwinters in corn debris, or the spores can be windblown over long distances. Generally, water splashing on infested debris causes the initial lower-leaf infections.
Genes for resistance to races of the fungus have long been used for effective management in our hybrid field corn. The major genes are Ht1 and Ht2, which confer resistance to races 1 and 2, respectively. There are also some additional quantitative genes and some additional genes for resistance to race 2. For a long time, we have held that in our area race 1 is usually not a problem, since most commercial hybrids have the Ht1 gene for resistance. Race 2 is in some areas and can infect hybrids that have only the Ht1 gene for resistance, so the other genes for resistance to race 2 have been incorporated into many commercial hybrids.
How can the increase in NCLB be explained? First, consider that the field environment has been excellent for infection by this disease: high moisture, long dews, and cooler temperatures. That is interesting, but if our hybrids have qualitative or quantitative resistance, then we shouldn't be seeing susceptible lesions from infection.
Well, is it possible that there is a new race creating the problem? University of Illinois corn pathologist Professor Don White indicates that race 1 is still the most frequently isolated race in Illinois. So, while a new race is possible and always worth consideration, it probably doesn't totally explain the situation we have been seeing. The next thing to find out is whether the hybrids you are growing or recommending actually have resistance to the disease bred into them. They may not have any at all.
Studies in more tropical climates (with long dew periods) have shown that the fungus can overcome genetic resistance in "nonadapted" hybrids. Well, we are not growing nonadapted hybrids, so that doesn't help explain things. The extended dew periods may have some merit, but it hasn't been tested for this situation.
At this juncture, the most reasonable explanation is that hybrids without resistance are being selected. Check it out. If susceptible lesions are present despite appropriate resistance selection, then a new race is the next best explanation. A last-resort explanation, if neither of those explanations can be documented, is that perhaps we are beginning to see fungal adaptation to longer periods of dew. This is not very likely, by the way, and certainly not worth considering as any kind of explanation at all if the resistance background of the hybrid is unknown.