The culprit primarily responsible for Fusarium head blight is the fungus Fusarium graminearum and its spore form Gibberella zeae. Although several other species of Fusarium may be involved, F. graminearum appears to be the most important in North America. This fungus can also cause a seedling blight, root rot of small grains, and stalk rot of corn. It is widely distributed and present wherever barley, corn, and wheat are grown.

The Infection Cycle
Fusarium species exist as saprophytes on crops (organisms that feed on dead or decaying matter). The sexual state (perithecia) of the fungus develops on these residues in the spring (see figure). Resultant spores are airborne and capable of traveling long distances. They may be wind-blown or rain-splashed from the crop residues onto the developing heads of wheat or barley plants.

It is generally believed (though this theory is currently being reexamined) that Fusarium first becomes established on the extruded anthers (pollen bearers) of a plant and then grows into the developing kernel. Thus grain crops (particularly wheat, where the head is not protected by the flag leaf during pollination) are most susceptible during flowering and for a period of time thereafter. Infection is most common during moist, warm weather. These initial infections can lead to additional spore production (asexually) and secondary infections that may occur on other kernels within a single head, kernels in adjacent plants, or even plants in neighboring fields.

Spread and Control in the Field
Crop residues, including straw, chaff, and small infected kernels, that are left in the field serve as a good growth medium for Fusarium, and thus may perpetuate the disease cycle into subsequent crop years. There is little question that the minimum tillage practices commonly used in the western half of the United States for soil conservation have directly led to today's Fusarium problems.

Control of the fungus is problematic. All barley cultivars, old and new, are very susceptible to FHB; attempts are being made to breed in a resistance to the disease. Fungicides are largely ineffective and costly, and thus are not generally applied in North America. Growers groups have requested a crisis exemption from the EPA that would permit the use of two triazole-based fungicides in attempting to control FHB on barley and wheat. These fungicides can reduce FHB severity by 40-50% by controlling the spread of the fungus, but are ineffective under high disease pressure. New fungicides are continually being evaluated. Careful and diligent crop rotation and moldboard plowing are of some help, but airborne spores can always drift in from neighboring farms.

Toxins Produced by the Fusarium Fungus
A wide array of fungi produce mycotoxins in small grains, but not all toxins are produced under all conditions (8). Aspergillus sp. fungi produce aflatoxins, which are primarily of concern to producers and consumers of corn, peanuts, and cottonseed. Small grains are not at high risk for these toxins in the United States. Similarly, a range of mycotoxins common to agricultural crops -- including fumonisins (produced by another species of Fusarium called Fusarium moniliforme), ochratoxin (produced by Aspergillus ochraceous and also by several species of Penicillium fungi), and citrinin (produced by Penicillium fungi) -- are a legitimate public health concern but are not typically encountered in malting barley.

Barley kernels after three days of germination. The kernel on the left had not germinated and shows extensive fungal growth. Pinkish and/or black discoloration are characteristic of heavily infected kernels. By contrast, the kernel on the right shows limited signs of infection and displays normal rootlet growth.

The FHB fungus produces a number of toxins specific to the Fusarium genus. Zearalenone (F-2 toxin) is primarily responsible for causing hyperestrogenism (feminization) in livestock at concentrations of about 1 ppm. Higher concentrations can interfere with conception, ovulation, implantation, fetal development, and viability of newborns (9). The FHB fungus also produces a number of trichothecene toxins, namely T-2, nivalenol, diacetoxyscirpenol, and deoxynivalenol (DON), also known as vomitoxin. DON is the most common mycotoxin associated with small-grain production in North America (5) and the most common toxin occurring on barley in the upper midwestern United States (6).

Deoxynivalenol (DON) and toxicity: With an LD50 (lethal dose in mice in 50% of treatments, in mg of toxin per kg of mouse body weight) of 70, DON is one of the least toxic trichothecenes (the lethal dose for nivalenol and T-2, for example, is 4). The effects of DON toxicosis are much better understood in livestock than in humans. DON levels of greater than 2 mg/kg cause reduced feeding in swine stemming from palatability problems. Levels greater than 20 mg/kg in feed will prompt livestock to either refuse their food or vomit after eating (thus the common name). FDA advisory levels for feed barley are 5 ppm for swine and 10 ppm for cattle and chickens.

Most of the information on human toxicosis from this class of mycotoxins is based upon empirical information from underdeveloped or remote parts of the world, where the identified population had been consuming heavily infected grain. There are no reports involving mycotoxicoses from beer in the developed world.