Northern leaf blight of corn

​Exserohilum turcicum remains alive, but dormant, in diseased, dead leaf tissue on the soil. When temperatures reach 60-80°F, and the leaf is wet for 24-48 hours, this fungus produces hundreds of spores (conidia) on the surface of the old northern leaf blight lesion. Dispersed by wind, these conidia that land on wet corn leaf surfaces will germinate with hyphae, forming appresoria, attach to the leaf surface, send out a penetration peg and enter the leaf epidermal cells within a few hours.  The leaf whorl of a young corn plant is a common site for this infection because of the moisture.
 
The plant tissue near the site of infection reacts to the presence of the intruder by producing anti-fungal products.  These biochemicals not only inhibit growth of this fungus but cause a small chlorotic spot (2-3 mm in diameter) within 48 hours of the infection. This may be sufficient to stop the fungus from progressing in the leaf but with infection by large numbers of spores, a few hyphae can progress on towards the vascular tissue of the leaf.  Once inside the xylem the hyphae essentially fill the tissue with hyphae, causing a mini-wilt in that immediate area. The typical disease symptom of this disease usually starts to be visible about 10 days after infection, as a grey, elongate lesion. These lesions mature about a week later, the fungus eventually stopped from further growth in the corn plant but, with moisture, stimulated to produce more conidia within the lesion anytime during or after the season.  Leaf vascular systems, with multiple branches, are not significantly harmed by a few of these disease lesions but large numbers of lesions will take its toll on movement of sugars in the phloem from the leaves to the roots and developing kernels.
 
Corn varieties vary in the ability to stop Exserohilum turcicum from reaching the vascular tissue of infected leaves. This resistance system, controlled by 3-4 genes, affects the number of lesions that develop.  There are also single, dominant genes that cause specific reactions to the fungus.  These genes are designated as Ht1, Ht2, Ht3 and HtN.  The first three of these interact after the fungus has reached the vascular tissue, causing a chlorotic streak instead of the gray wilted lesion and inhibits most of the fungus’s ability to produce conidia.  The Ht1 gene was effective in the USA for most of the 1970’s, but typical of most single gene resistance systems, the population of the fungus included some individuals with a gene to overcome this resistance.  Eventually it became evident that there were races of the Exserohilum turcicum that could overcome each of the single genes for resistance.  The most stable resistance is the multi-genic one.
 
Dynamics of spore intensity, leaf surface moisture and corn genetic resistance affect whether this disease affects performance of the crop.  Heavy damage usually results in early death of root tissue because of lack of photosynthates reaching the tissues. Early death of root tissue causes general plant wilting, shutting off translocation of sugars to the developing kernels.  Thus, the biggest damage from this leaf disease come in the form of stalk lodging and light grain weight.