Corn anthracnose

​Another fungus that has taken advantage of the minimum tillage practices is Colletrichum graminicola, the cause of anthracnose.  It is most aggressive on weakened plant tissue, causing lesions on seedling leaves during cloudy rainy periods, on senescing leaves and weakened stalks.
 
The fungus remains viable on dead corn leaves and stalks if tissue is exposed on soil surface.  Conidia are produced within a gelatinous material that protects them from dehydration. Spread by splashing water onto seedlings or spread by wind later in the season, these spores germinate when in water on plant material within 12 hrs. Within 24 hours, the hypha form appresoria from which penetration pegs grow into epidermal cells. These infected plant cells respond by producing fungal-inhibiting compounds including hydrogen peroxide. Before the resistance system takes full affect, the fungus keeps the cell alive as it absorbs nutrition from these cells. It then produces hyphal branches expanding into the areas between cells as it switches from existing within living cells (biotrophy) to killing tissue and producing enzymes to digest materials in dead plant tissue (necrotrophy).  This is probably common among corn leaf pathogens that can be called hemibiotrophic pathogens. This mode differs from the rust and smut fungi that are totally biotrophs, dependent solely on living cells
 
After receiving nutrition from the dead tissue, the C. graminicola produces a large number of conidia to spread to other areas.  Most corn hybrids have limited damage from the leaf infection phase from this hybrid.  I am aware of a hybrid in the 70’s that would commonly show many leaf lesions but continued to have good yields and stalk quality.  Others have verified that the leaf disease phase does not lead to the stalk infection phase.
 
Stalk infection by this fungus is confusing.  The fungus causes a black discoloration in the outer rind cells, making it easy to see.  However, inoculation of stalks with the fungus shows that it does not actively kill the stalk pith tissue except only when the tissue is already senescing. A study published in 1980 (Phytopathology 70:534) showed that reducing photosynthesis by removing leaves increased stalk rot from the Anthracnose fungus, just as it did from others such as Gibberella and Diplodia.  It appears that this fungus is basically held off by vigorous, living corn pith tissue but can destroy senescing tissue.  This accounts also for its appearance along with early death of the flag leaf.  The flow of carbohydrates to the kernels depletes sugars from pith tissue first from the upper and lower stalk.  The senescence in the pith in the upper internode allows Colletotrichum graminicola to gain momentum, resulting in black streaks in the rind beginning at the node of that internode.  As a result of the infection and the depletion of sugars the upper flag leaf dies.  Usually this occurs before death of the lower stalk but can signal a potential for eventual stalk rot in the plant if it is not near finishing normal kernel fill.
 
There are single genes available that can inhibit the anthracnose fungus from colonizing the stalk tissue but these do not affect any of the other fungi from inhabiting the stressed corn plant. The gene does not cause any significant reduction in occurrence of stalk rot but only less of it associated with anthracnose. 

​ An interesting discussion of corn and this pathogen can be found at Plant Physiol. 2012 Mar; 158(3): 1342–1358