• One or more spikelets or the whole head has a bleached appearance due to premature death of tissues.
• Base of the infected spikelets and portions of the rachis (main stem) sometimes develop a dark brown colour.
• Under favorable climatic conditions the fungus produces small pinkish orange-coloured mycelium and clusters of spores near the base of the kernel. At the end of the season black reproductive structures called perithecia (the fungal sexual stage) may be found on the surface of the glumes.
• Infected kernels are often wrinkled, shrunken and light in weight. The diseased kernels appear white, chalky and sometimes may have a light brown or pink discoloration.
• Up to 15 scabby grains can be contaminated by mycotoxins. G. zeae contaminates grain with deoxynivalenol (DON) (known as vomitoxin) which belongs to the family of trichothecene toxins, and the oestrogenic mycotoxin zearalenone that are harmful to human and animals if consumed.

Confirmation:

• Often, the pathogen only attacks part of the head giving the infected part a white and uninfected part a green appearance.
• Infected spikelets may contain partially-filled seeds.
• Shrivelled grains may appear tan to white, with traces of pink on the seeds.
• Microscopic observations of conidia appear straight or sickle shaped containing 3-7 septa, measuring 25-65 x 2.5-5.0 μm. The exact identification of the Fusarium species based on morphological character is not easy and requires a lot of attention.

Why and where it occurs:

• FHB occurs worldwide wherever wheat is grown and if humid weather is coinciding with flowering. Outbreaks have been reported in Asia, Canada, Europe and South America.
• Ideal conditions for FHB development are; relative humidity above 95% for 40-60 hrs combined with temperatures of 25-30°C.
• Within 7 to 10 days after infection a pinkish mass of conidia form at the base of the diseased spikelets.
• The ascospores germinate in surface moisture on the spikelet and invade the flower. Infections are most serious when the anthers are exposed during flowering.
• New secondary infections of wheat heads are produced mainly by wind dispersed conidia between plants in the same field. This cyclic infection process continues under humid weather conditions on susceptible spikelets.
• The new cycle of ascospores are usually produced too late in the season to cause secondary infection. Ascospores survive in crop residues and contaminated seed.

Causal agent or factors:

• The fungus initially has a short biotrophic phase within the host plant before rapid colonization followed by a necrotrophic phase.
• Factors influencing disease are climate, levels of inoculum wheat growth stage and increased irrigation.
• FHB disease incidence has increased in areas in which wheat is rotated with maize and other cereals, and increases in wheat cropping in humid climatic regions.
• Phylogenetic studies on the FHB fungus have shown that there are different groups species within the Fusarium graminearum species; each of these are limited to different geographical regions.

Host range:

Major hosts include: Triticum aestivum (bread wheat), Triticum turgidum (durum wheat), triticale, Hordeum vulgare (barley), Secale cereale (rye), Oryza sativa (rice), Zea mays (maize), Sorghum bicolor (Sorghum), wild grasses and common weeds.

Life cycle:

Mechanism of damage:

• The FHB ascospores overwinters and survives between harvest and sowing on grass stubble, chaff, cornstalk residue left on the soil surface and infected grain.
• The fungus may live asymptomatic in cornstalks or grass hosts.
• Wind dispersed conidia (asexual spores) or ascospores (sexual spores) infect flower parts, glumes or portions of the spike during damp warm weather.
• The fungus causes physiological changes to the vascular bundle in the rachis, making it partially dysfunctional; this leads to production of small and shriveled kernels or premature death of the spikelets.

When damage is important:

• Percentage yield losses are dependent on: susceptibility of the wheat cultivar, weather, and amount of initial inoculum around the time of flowering and shortly afterwards.
• If the weather is dry during flowering and grain filling then the crop will essentially be scab-free.

Economic importance:
Yield loss is related to the percent of heads and spikelets which are infected and can be as high as 100 percent in some fields.

Management principles:

• In moderate epidemic years, crop rotations that avoid planting of wheat into corn, wheat or barley stubble may reduce disease incidence. Additionally, plowing-in of wheat, barley or corn residue into the soil may also be helpful. However, in severe years, these practices make no difference.
• Avoid planting of very susceptible and susceptible varieties in disease prone areas and near corn fields.
• Rotation with a legume crop between corn and cereal crops enables stubble residues to break down thereby reducing the pathogen inoculum.
• Varieties with moderate to intermediate resistance are available. Resistance to FHB within some varieties is due to: escape of the disease through early or late flowering, restricted development of the disease to one or a few florets per head, or physical barriers to infection of the floret and spikelet.
• To control seed-borne Fusarium, fungicide treatment of wheat seeds is recommended as this controls seedling blight.
• The amount of scabby kernels can be reduced during combine harvesting through the use of fans which blow the light scabby seeds out the back of the combine.

References:

Ban, T., J.M. Lewis and E.E. Phipps (eds.). 2006. The Global Fusarium Initiative for International Collaboration: A Strategic Planning Workshop held at CIMMYT, El Batán, Mexico. March 14 - 17, 2006. Mexico, D.F.: CIMMYT.

Bateman, G.L., R.J. Gutteridge, Y. Gherbawy, M.A. Thomsett and P. Nicholson. 2007. Infection of stem bases and grains of winter wheat by Fusarium culmorum and F. graminearum and effects of tillage method and maize-stalk residues. Plant Pathology 56:604–15.

Dill-Macky, R. and R.K. Jones. 2000. The effect of previous crop residues and tillage on Fusarium head blight of wheat. Plant Disease 84:71-6.

Gilchrist, L. and H.J. Dubin. 2002. Fusarium head blight. In B.C. Curtis, S. Rajaram and H. Gómez Macpherson (eds.), Bread improvement and production. FAO Plant Production and Protection Series. Rome: Food and Agriculture Organisation of the United Nations.

Goswami, R. and C. Kistler. 2004. Pathogen profile: Heading for disaster: Fusarium graminearum on cereal crops. Molecular Plant Pathology 5:515–25.

O Donnell, K., T.J. Ward, D.M. Geiser, H.C. Kistler and T. Aoki. 2004. Genealogical concordance between the mating type locus and seven other nuclear genes supports formal recognition of nine phylogenetically distinct species within the Fusarium graminearum clade. Fungal Genetics and Biology 600-623.

Prescott, J.M., P.A. Burnett, E.E. Saari, J. Ransom, J. Bowman, W. de Milliano, R.P. Singh and G. Bekele. 1986. Wheat diseases and pests. A guide for field identification. Mexico, D.F.: CIMMYT.

Sutton, J.C. 1982. Epidemiology of wheat head blight and maize ear rot caused by Fusarium graminearum. Canadian Journal of Plant Pathology 4:195–209.

Waalwijk, C., R. van der Heide, I. de Vries, T. van der Lee, C. Schoen, G. Costrel-de Corainville, I. Häuser-Hahn, P. Kastelein, J. Köhl, P. Lonnet, T. Demarquet, and G. Kema. 2004. Quantitative detection of Fusarium species in wheat using TaqMan. European Journal of Plant Pathology 110:481–94.

Wiese, M.V. 1987. Scab (Head Blight). In M.V. Wiese (ed.), Compendium of wheat diseases. St. Paul, MN: The American Phytopathological Society (APS Press). Pp. 16-18.

Zillinsky, F. 1983. Common diseases of small grain cereals. Mexico, D.F.: CIMMYT.

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