Septoria glume blotch (extended information)

Disease Name:
Septoria glume blotch, Stagonospora nodorum blotch or glume blotch

Phaeosphaeria nodorum (E. Müller) Hedjaroude
Anamorph Stagonospora nodorum (Berk.) Castellani and E.G. Germano


  • Phaeosphaeria nodorum infects leaf, stem and causes discoloration of the spike in the symptom known as glume blotch.
  • P. nodorum lesions are initially red-brown surrounded by a yellow halo. Flecks are lens-shaped lesions 3-6mm by 6-19 mm.
  • Early leaf symptoms include yellowing at the site of infection and tip burn of the leaf.
  • The chlorotic front expands to form oval-shaped lesions on the leaf, with the majority of hyphae running parallel to the vasculature of the leaf.
  • Within the chlorotic areas, small regions of necrosis are often evident. With age they may develop gray-brown centers.
  • Pycnidia (spore-producing structures) can form throughout the lesion.
  • Pycnidia of S. nodorum are light to dark brown and circlular and three times bigger than pycnidia of M. graminicola.


  • P. nodorum lesions with pycnidia are difficult to see by eye as they are light color and buried in the leaf tissue.
  • After a week or so under conditions of controlled humidity, pycnidia will begin to form in the lesion. The release of pycnidiospores (conidia), usually oozing in a mass of pink-pigmented cirrus, is preceded by the swelling of a single point on the pycnidial surface forming a protuberance which ruptures the cuticle.

Why and where it occurs:

  • Septoria glume blotch can be found in all wheat growing areas of the world.
  • Infections of P. nodorum occur over a wide temperature range ideally between 20 to 27°C with wet and windy weather conditions.
  • The fungus is able to infect all above-ground plant parts and overwinters in the field on infected stubble where the sexual stage occurs.
  • Successive rounds of asexual reproduction and dispersal can distribute P. nodorum throughout the plant canopy.
  • Up to 16 hrs of wetness is required for infections to occur and within 10-20 days secondary spores are produced in lesions.
  • Infection is highly dependent on the plant’s stage of development and happens before spike emergence; it becomes more severe later in the season.
  • Further spread can lead to glume blotch as a result of direct attack of glumes by the fungus.
  • The disease is also seed transmitted.
  • The presence of wheat stubble, volunteer wheat, susceptible grasses and diseased seeds sustains survival of the disease from year to year. These become sources of the fungi (inoculum) for infection of the new wheat crop.

Causal agent or factors:

  • Windborne ascospores or seedborne pycnidiospores are the main source of primary inoculum
  • Following primary infection, asexually produced, rain-splashed pycnidiospores contribute to epidemic development during the remainder of the growing season, in particular under wet and warm weather conditions.
  • The wide dispersal of ascospores via wind would suggest that sexual crossing would be ecologically compulsory in natural populations of the fungus. This would predict a more or less equal preponderance of the two mating type idiomorphs MAT-1 and MAT-2.
  • M. graminicola and P. nodorum may occur individually either early or later in the season respectively, but frequently occur together in the same field and on the same plants. However, within a geographical region, the relative prevalence of both pathogens may vary depending on temperature patterns and varieties.

Host range:

Although most closely associated with wheat, P. nodorum is also pathogenic on barley (Hordeum vulgare).There are reports on wild grasses which the pathogen may use as alternate host.

Life cycle:

Mechanism of damage:

  • The pycnidiospores or ascospores germinate on the wet leaf surface and enter the leaf tissue through natural openings (stomata) or directly through the epidermal tissue.
  • Moisture is required for all stages of infection: germination, penetration, mycelial development and formation of pycnidia.
  • The fungus produces a toxin which kill plant cells around the infection points.
  • The host-specific toxin ToxA produced by the wheat pathogens P. tritici-repentis and P. nodorum interacts with the product of the dominant plant gene Tsn1 to induce necrosis. The ToxA gene is thought to have been acquired by P. tritici-repentis from P. nodorum through a recent horizontal gene transfer event.

When damage is important:

  • Percentage yield losses are dependent on susceptibility of the wheat cultivar, weather conditions (wet and windy with moderate temperatures), and availability of inoculum on diseased stubble, volunteer wheat or use of diseased seeds.

Economic importance:

Stagonospora nodorum blotch may cause up to 30% loss of yield in wheat.

Management principles:

  • Practices such as crop rotation can reduce incidence.
  • Initially, carboxin was used to treat wheat seeds against infection, but it has been replaced in the last 10–15 years by systemic triazole ergosterol biosynthesis inhibitors.
  • Application of fungicide at a suitable time such as difenoconazole and triadimenol will effectively control most outbreaks.
  • It is important to plant varieties with the highest available level of resistance. The degree of resistance varies in different cultivars ranging from highly susceptible to moderate resistance.
  • Wide crosses involving Aegilops tauschii have found that resistance is controlled by single genes, but it is not yet clear whether these genes can usefully be introgressed in bread wheat.
  • No complete resistance has been found in the existing wheat gene pool.


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Contributors: H. K. Buhariwalla, E. Duveiller, and P. Kosina