Fusarium Head Blight (FHB)

FHB infection causes important economic losses wherever cereal crops are grown. The FAO put yield losses worldwide as high as 50%.  Yield losses in wheat can range from 5 – 75% depending on severity and time of infection.  

The last time we saw a high incidence of FHB in wheat crops in the UK was 2007 when 80% of crops showed visible symptoms. In that year HGCA winter wheat trials nationally showed an 8% drop in yield on the previous 5 year average. However, this year has been wetter and cooler indicating that the yield losses will be higher. Yield loss occurs as a result of poor grain fill as well as poor grain set.

Pathogens responsible

All the fungi responsible for FHB are present in the soil. There are two groups of fungus involved; Fusarium and Microdochium. Fusarium species include F. culmorum, F. graminearum, F. avenaceum, F. poae and the recently discovered F. langsethiae. The Microdochium species include M. nivale and M. majus.  F. culmorum, F. graminearum are the main culprits in the development of mycotoxins including the highly toxic trichothecene mycotoxins, such as deoxynivalenol (DON) and zearalenone (ZON).

DON contamination of grain is most severe in wheat crops following grain maize. DON is considered the most important mycotoxin produced by F. graminearum and has been shown to cause vomiting in both animals and humans, often resulting in feed refusal in livestock. DON can also reduce starch and protein concentration in grain. ZON is a strong estrogenic compound which causes reproductive problems in animals, such as cattle, swine and poultry.

There are legal limits for fusarium mycotoxins deoxynivalenol (DON) and zearalenone (ZON) in wheat intended for human consumption and guidance limits for grain for feed.

Source of infection.

Crop residues from previous cereal crops are main source of infection. The spores are splashed up through the crop on to the ears. However, it is highly likely that conidia are transported by rain up through the canopy from leaf layer to leaf layer in a series of steps before finally being splashed on to the ear. Fusarium graminearum can also release spores in to the air in the spring especially if warm and humid and these airbourne spores can travel for miles.

Infection is classified into 5 types. Type 1 infection refers to the initial infection of a spikelet, Type 2 is when this initial infection spreads through the wheat ear to other spikelets.  Types 3 – 5 refer to effect on grain size, grain retention, yield tolerance and breakdown of mycotoxins.

Infection takes place as the mycelia grow along the surface of the spikelets and any anthers that are protruding from the floret. Once inside the floret the mycelium colonise the developing grain. During colonization of wheat heads, marked alterations in the host tissues occur, including degeneration of cytoplasm and cell organelles, and disintegration of host cells. This degradation suggests that FHB pathogens may secrete corresponding cell wall–degrading enzymes. Most infections occurred on the inner surfaces of lemma, glume, palea, and rachis, and not necessarily through anthers.

Breeding Resistance

Conventional plant breeding.

FHB resistance can be divided into five components. Of these, resistance to initial infection (type I) and resistance to spread within infected tissue (type II) are the two key mechanisms contributing to the so-called ‘field resistance’. Resistance to Type (III) grain size and number retention, (IV) yield tolerance, and (V) decomposition or non-accumulation of mycotoxins are less common.

The cultivar Sumai 3, a Chinese variety, and its derived lines are the most commonly used sources of Type II resistance in breeding programmes. It also has a much lower level of DON accumulation in the harvested grain. Type V resistance, which refers to a low DON concentration in the grains from infected spikes, is also a priority for wheat breeding programs.

Genetic engineering.

Still in its infancy - the use of particle acceleration to introduce antifungal protein (AFPs) genes to produce transgenic wheat at the University of Minnesota resulted in germplasm that reduces severity of FEB by 20-30%. In China researchers using an antibody derived from chicken and an antifungal peptide from Aspergillus giganteus resulted in enhanced Type 1 resistance.

Factors influencing the development of FEB.

Severe epidemics of FEB occur when there is a large amount of inoculum, suitable weather for infection and host plants at a susceptible growth stage, i.e. at flowering. Regions with intense wheat and, or maize cultivation are likely to have greater concentrations of airborne inoculum.  The disease occurs wherever cereals are grown and is a major problem in the US, Australia, China and Europe.

The predominant FHB pathogen worldwide is  Fusarium graminearum. In cooler maritime areas of northwestern Europe, commonly occurring FHB species are F. culmorum, F. avenaceum, and Microdochium species. In field sampling across Europe, including the UK, it was not uncommon to have all six species (F. graminearum, F. culmorum, F. poae, F. avenaceum, and two Microdochium species) present at one site.

Cultivations: minimal cultivations increase the risk of infection as these leave crop residues on the surface as a source of inoculum.

Plant height: The Rht2 dwarfing gene has been used extensively in modern wheat breeding programmes to reduce the height of wheat. Work carried out at CSIRO in Australia compared isolines of wheat with and without the dwarfing gene.  Tall isolines all gave better type I resistance than their respective dwarf counterparts. One theory is that shorter plants tend to be more susceptible to FHB because the ears are closer to the soil surface, leading to more ready dispersal of spores from infected debris on the soil surface near the spikes. The researchers found that when they raised the dwarf isolines so that the ears were at the same height as the tall isolines the difference in type 1 resistance disappeared.

Weather:  
UK 2012. March was the third warmest March on record. It was also the fifth driest and third sunniest March. This followed an unusually dry mild winter all perfect conditions for fusarium development in early spring.  Wet weather ever since and particularly in June when wheat crops were flowering gave near perfect infection conditions. The wet July has only helped in the development of the disease.

Mathematical models for predicting Fusarium outbreaks have used the following criteria.
 (1) ascospore spread: in the growth stages 39/41-61, at least one rain (≥4 mm), then one or more warm days (average temperature ≥16°C); (2) infection of the heads by ascospores: immediately after the spread of the ascospores in the growth stages 55-69, at least two days with rain ≥2 mm and temperature ≥17°C. (3) production of macroconidia on the upper leaves and infection of the heads: immediately after the spread of ascospores a moist (and cool) weather period; infection of the heads by high numbers of macroconidia even at low temperatures.

Fungicide control

Results from controlled experiments in the US, which were designed to mimic high disease pressure, show that Prosaro (prothioconazole + tebuconazole) was better than tebuconazole alone. However, in these experiments no product gave better than about 65% control of Fusarium head blight. European work has shown very variable fungicide results which were explained mainly by high differences in the disease and crop development under changeable weather conditions. Relatively low temperatures and rainy weather during application at the prolonged flowering stage was considered the probable cause of poor control in 2008.

Microdochium species are resistant to Strobilurins.

Biological control.

Research using competitive fungi or the bacteria Pseudomonas has shown good control of Fusarium species and in reducing DON levels in grain.

Could the disease have been controlled?

The primary time for control is still considered to be when 50% of the ears in a crop of wheat are at the start of flowering. However, not only is this a difficult growth stage to predict with accuracy but this year it also coincided with wet and windy conditions. Getting the timing right over large acreages of wheat this year was a challenge for even the most geared up farmers.

The most effective T3 fungicide for FEB control is a mixture of prothioconazole + tebuconazole but when the disease pressure is high like this year 60% control still leaves an awful lot of spikelets infected.
CropMonitor results show that this year the main fungus present on blighted ears is Microdochium nivale. This year also saw obvious symptoms of this fungus on leaves within the canopy.

The cool wet April through to July favoured this pathogen and the intense rainfalls would have helped it move up through the canopy. The miserable weather also resulted in long delays between the T1 and T2 fungicides allowing the fungus to establish on leaf layers. Therefore, the epidemic was poised to happen. An application of prothioconazole between T1 and T2 may have helped but the chances of this being achieved were slim at best.