Glomerella graminicola

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Glomerella graminicola
Anthracnose Leaf Blight
Scientific classification
Kingdom: Fungi
Phylum: Ascomycota
Subphylum: Pezizomycotina
Class: Sordariomycetes
Order: Glomerellales
Family: Glomerellaceae
Genus: Glomerella
Species: G. graminicola
Binomial name
Glomerella graminicola
D.J. Politis (1975)

Colletotrichopsis graminicola (Ces.) Munt.-Cvetk. (1953)
Colletotrichum graminicola (Ces.) G.W. Wilson (1914)
Dicladium graminicola Ces. [as 'graminicolum'] (1852)
Steirochaete graminicola (Ces.) Sacc. (1923)
Vermicularia melicae Fuckel

Glomerella graminicola ((anamorphic) Colletotrichum graminicola) is a fungus in the teleomorphic phase whose anamorphic phase, Colletotrichum graminicola, causes anthracnose in many cereal species including maize and wheat. Corn is affected in large numbers in the United States by this fungus, especially certain varieties that have been genetically engineered.[1] These engineered varieties are more susceptible to the teleomorph phase of the fungus. It is not until the fungus moves to the teleomorph phase of the lifecycle and begins to produce fruiting bodies that host plants will begin to exhibit symptoms, often on plants depleted in energy after the stress of pollination.[2] Once the pathogen is in a field, producers can suffer huge economic losses. The disease, corn anthracnose leaf blight, is the most common stalk disease in maize and occurs most frequently in reduced-till or no-till fields. As these practices are widespread, as can be the pathogen.[3]

Anthracnose stalk rot

Host and Symptoms[edit]

C. graminicola is a fungal pathogen that colonizes and infects many turfgrass e.g., Bluegrass, Ryegrass, fescue. In addition to the grasses, C. graminicola also infects many grain crops such as barley, wheat, sorghum and corn.[4] The fungus can infect many different parts of the corn plant, typically the kernels, tassels, roots, leaves, stalk and husks. The most common area of infection is the stalk. C. graminicola produces three major symptom types: leaf blight, stalk rot and top die-back. The leaf blight is characterized by round yellowing water soaked lesions on the leaves. These lesions usually occur early in the season and are how this pathogen is distinguished from other diseases. Top die-back is the necrosis of the top leaves and stalk of the corn. This occurs around the same time as grain formation. The stalk rot phase becomes prominent during the late reproductive stages of the corn life cycle. It is characterized by blackening of the pith tissue in the stalk and also of the rind, beginning at the nodes closest to the soil.[5] Along with these symptoms, seedling blight and post emergence damping off are also found.[6]



  • 70-300 μm in diameter
  • Bear prominent, dark, septate spines (setae) up to 100 μm long.


  • Developing at the base of the spines
  • Hyaline to pale yellow, unicellular, sickle-shaped, falcate to fusiform, tapered toward both ends
  • 3-5 x 19-29 μm.


  • Unicellular, hylanine and cylindrical,
  • 4-8 x 8-20 μm.

Growth on PDA

  • Gray and feltlike
  • Conidia and appressoria are numerous when culture are well aerated, and sclerotia sometimes occur.
  • Appressoria are diagnostic: they are tawny brown, irregular-shaped in edge, prominent, and terminal on thickened hyphae.

Disease Cycle[edit]

In the spring, fruiting structures (acervuli) form from corn residue and produce spores (conidia) that are dispersed by wind blown raindrops and splashing.[7] Conidial spores infect young plants through the epidermis or stomata.[6] Anthracnose develops rapidly in cloudy, overcast conditions with high temperatures and humidity. In optimal environmental conditions, conidia can germinate in as little as 6–8 hours in 100% humidity.[7] Initial necrotic spots or lesions can be seen within 72 hours after infection by conidia.[8] Lower leaves that develop lesions provide conidial spores and cause secondary infections on the upper leaves and stalk. Vascular infections primarily occur from wounds caused by stalk-boring insects, such as the larvae of the European corn borer, allowing for conidia to infect and colonize the xylem.[9] From this, anthracnose top die back (vascular wilt) or stalk rot can occur. In the fall, C. graminicola survives as a saprophyte on corn leaf residue. The pathogen can also overwinter on corn stalks as conidia in an extracellular secretion. The secretion prevents conidia from desiccating and protects them from unfavorable environmental conditions.[7] Overwintering on corn residue serves as a vital source of primary inoculum for the leaf blight phase in the spring. The cycle will start all over again when susceptible corn seedlings emerge from the ground in the spring.

Disease Management[edit]

Since C. graminicola is found to survive on corn residue, specifically on the soil surface; one of the most effective methods of control is a one-year minimum of crop rotation to reduce anthracnose leaf blight.[10] A study in 2009 showed more severe symptoms of leaf blight due to C. graminicola when grown on fields previously used for corn in comparison to fields previously used for soybean.[5] Other management methods include the use of hybrid selections and tillage systems. Keeping in mind, hybrid selection may be resistant to leaf blight but they are not necessary resistant to other fungal diseases such as stalk rot. Tillage systems that are able to fully bury corn residue deep underground along with one year crop rotation will reduce the source of inoculum greatly. More work is still needed in order to determine the influence of buried and surface corn residues as a source of inoculum for corn anthracnose.³


Corn anthracnose caused by Colletotrichum graminicola is a disease present worldwide. This disease can affect all parts of the plant and can develop at any time during the growing season. This disease is typically seen in leaf blight or stalk rot form. Before the 1970s, Anthracnose was not an issue in North America. In the early 1970s, north-central and eastern U.S was hit with severe epidemics. Within 2 years of C.graminicola’s appearance in Western-Indiana sweet corn production for canning companies were nearly wiped out and production no longer exists there today.[7]

Anthracnose stalk rot was seen in many U.S corn fields in the 1980s and 1990s. A survey conducted in Illinois in 1982 and 1983 found that 34 to 46% of rotted corn stalks contained C. graminicola.[11] Estimates on yield grain losses from anthracnose leaf blight and stalk rot range from zero to over 40%. This is dependent on hybrid, environment, timing of infection, and other stresses.

The impacts of C. graminicola are predicted to increase as the use of Bt corn becomes more common. Bt engineered corn has been seen to have a greater proportion of stalk rot and be more susceptible to C. graminicola compared to strains without Bt.


Once conidia germinate on corn leaves, a germ tube differentiates and develops into an appresoria and allows C. graminicola to penetrate epidermal cells.[12] Germination and appressorium formation occur best in the temperature range (15-30°C)[7] Interestingly, penetration occurs in a much narrower temperature range (25-30°C). In order to penetrate the cell wall, the fungus first pumps melanin into the walls of the appressorium to create turgor pressure in the appressorium. The melanin allows water into the appressorium cell but nothing out. This builds up an incredible amount of turgor pressure which the fungus then uses to push a hyphae through the corn cell wall. This is called the penetration peg. The penetration peg then grows, extends through the cell extracting nutrients and the host cell wall dies.[6] Hyphae migrate from epidermal cells to mesophyll cells. As a defense response, the cells produce papillae to prevent cell entry but is typically not seen successful. It is believed C. graminicola has a biotrophic phase because the plasma membrane of the epidermal cells is not immediately penetrated after invasion into the epidermal cell wall. Between 48–72 hours after infection, C. graminicola shifted from biotrophic growth to nectrotrophy (lesions appear). This is when secondary hyphae invade cell walls and intercellular spaces.[8]


  1. ^ "information page". Retrieved 2015-11-11. 
  2. ^ "Anthracnose Stalk Rot". Retrieved 2015-11-11. 
  3. ^ "Anthracnose Leaf Blight | Field Crops". Retrieved 2015-11-11. 
  4. ^ Hsiang, T.; Goodwin, P.H. (July 2001). "Ribosomal DNA Sequence Comparisons of Cholletotrichum Graminicola from Turfgrasses and other Hosts". European Journal of Plant Pathology. 107 (6): 593–599. doi:10.1023/A:1017974630963. Retrieved November 11, 2015. 
  5. ^ a b Jirak-Peterson, Jennifer C.; Esker, Paul D. (2011-02-08). "Tillage, Crop Rotation, and Hybrid Effects on Residue and Corn Anthracnose Occurrence in Wisconsin". Plant Disease. 95 (5): 601–610. doi:10.1094/PDIS-11-10-0837. 
  6. ^ a b c "THE VAILLANCOURT LAB". THE VAILLANCOURT LAB. University of Kentucky. 
  7. ^ a b c d e Bergstrom, Gary C.; Nicholson, Ralph L. (1999). "The Biology of Corn Anthracnose: Knowledge to Exploit for Improved Management". Plant Disease. 83 (7): 596–608. doi:10.1094/pdis.1999.83.7.596. 
  8. ^ a b Mims, C. W.; Vaillancourt, L. J. (2002). "Ultrastructural Characterization of Infection and Colonization of Maize Leaves by Colletotrichum graminicola , and by a C. graminicola Pathogenicity Mutant". Phytopathology. 92 (7): 803–812. doi:10.1094/phyto.2002.92.7.803. PMID 18943278. 
  9. ^ Carson, M. L. (1999). White, D. G., ed. Compendium of Corn Diseases: Anthracnose Leaf Blight. St. Paul, MN: American Phytopathological Society. pp. 21–22. 
  10. ^ "Anthracnose Leaf Blight and Stalk Rot of Corn, AC-0022-01". Retrieved 2015-10-20. 
  11. ^ Anderson, B; White, D (1987). "Fungi associated with cornstalks in Illinois in 1982 and 1983". Plant Disease. 71 (2): 135–137. doi:10.1094/pd-71-0135. 
  12. ^ Politis, D.J.; Wheeler, Harry (1973). "Ultrastructural study of penetration of maize leaves by Colletotrichum graminicola". Physiological Plant Pathology. 3 (4): 465–471. doi:10.1016/0048-4059(73)90056-8. 

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