The easiest way to minimize certain root diseases is to utilize sound cultural practices.

Agronomy

Fusarium

Description

Fusarium Yellows (also called Fusarium Wilt) is a soil-borne disease caused by a fungus called fusarium oxysporum. Fusarium oxysporum occurs in most agricultural soils throughout the world. Most frequently, the fungus occurs as a form that is not pathogenic to plants. This common form of the fungus lives on the surface of plant roots, but does not cause harm. But with fusarium oxysporum the situation can be different. Special forms of this fungus are capable of causing severe disease, usually on a single or a few closely related plant species. There are Fusarium Wilt or Fusarium Yellows diseases that occur on cotton, pea, tomato, bean, melons, banana, cabbage, spinach, and more than 60 other plant hosts, as well as sugarbeet. Each of these diseases is caused by a different special form of the fungus. The fungus penetrates the roots and invades the vascular system where it produces toxins which cause the symptoms. The disease is favored by alternating wet and dry periods, poor soil structure and waterlogging.

Symptoms

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Image 1

The older leaves become greyish-yellow between the veins (image 1) then die and fall to the ground though still attached to the plant; the heart leaves curl inwards. A transverse section of the root shows some brown vascular rings. Mature plants are seldom killed but yield loss can nevertheless be considerable. Seed plants may be killed by the disease.

Development

The development of this disease is somewhat different than the other root diseases of sugarbeets. The pathogen survives as non-motile resting spores in the soil. These resting spores remain viable for several years. As the sugarbeet feeder roots grow through the soil, they will pass in close proximity to some of these spores. Nutrients exuding from the feeder roots will stimulate some of these spores to germinate. A vegetative filament, called a hypha, will emerge from the spore and grow toward the passing root. The fungus will contact the root and colonize its surface, growing and branching, forming a network of hyphae. The pathogen will penetrate the surface of the root tissue and will grow through or between the root cells to reach the vascular system of the root. The fungus then enters and colonizes the root's vascular system.

The pathogen can grow in the plant's vascular system as hyphae, but it can also sporulate in these tissues. Small spores called conidia are produced in the water conducting tissues of the plant. These conidia are passively carried up the plant in the water stream of the vascular tissue. These conidia will germinate and produce new hyphae and spores to invade roots or other tissues more removed from the initial site of infection. In this way the fungus can quickly colonize the entire sugarbeet plant.

As the pathogen colonizes the vascular tissues, many of the plant's cells will become necrotic and die. The vascular elements will become clogged and unable to efficiently transport water to the leaves. The fungus also produces toxins which are carried up the plant's water stream. These toxins are responsible for some of the foliar symptoms which are observed with this disease.

As the plant's tissues die, Fusarium oxysporum will begin to form more resting spores. These resting spores are produced in the dead and dying tissues. As these tissues are spread through the field by cultivation they will decay, and additional inoculum of the pathogen is added to the soil.

Disease symptoms seem to become most severe as the temperature rises during the summer. Increased transpiration, caused by higher temperatures, will move the pathogen rapidly within the plant. Because of this fast movement of the pathogen, the plant is unable to respond with its normal defense mechanisms. This situation results in very fast symptom development and eventual collapse of the plant.

Spread

An aspect of this disease that is different from other soil-borne disease of sugarbeet is the effect of soil moisture. The non-motile spores do not require free water to infect the roots, as opposed to the motile zoospores of phytophthora drechsleri or polymyxa betae. Infested fields should be irrigated at optimal levels to avoid undue stress on the sugarbeet crop.

The disease can be spread by the movement of infected plant tissue or infested soil. Infestations have occurred by returning tare dirt back to a field that will be planted with sugarbeets. Collecting beet tops and moving them to another field is another possible means of spread.

Control

Control of Fusarium Yellows is difficult, especially when inoculum levels are high. Control measures should concentrate on limiting the amount of inoculum in a field. Unlike the other soilborne sugarbeet pathogens, Fusarium oxysporum does not produce additional inoculum during the growing season. The severity of disease will be directly proportional to the amount of inoculum in the soil.

One of the best ways to reduce the amount of inoculum in a field is through crop rotation. The special form of fusarium oxysporum which causes disease on sugarbeet is host specific. Inoculum of this pathogen will not increase on other crop species such as alfalfa, barley, beans, cotton, corn, or wheat. Cultivation of the alternate crops will allow the inoculum of the pathogen to decline to lower levels. The longer the time between sugarbeet crops, the more the inoculum level will decline. Rotations out of sugarbeets for 3 or more years should be beneficial.

High plant populations are also useful for disease management. Increasing the number of plants in a field will effectively dilute the amount of inoculum available per plant and will result in lower disease incidence.

Early planting will also help with disease control. Getting as much growth as possible before temperatures rise in the summer will result in a vigorously growing crop better able to resist infection.

Probably the best method for control of fusarium yellows is host resistance. Variety development by Holly Hybrids involves screening germplasm through the fusarium nursery in Sheridan, WY. This has resulted in sugarbeet hybrids that are better adapted to produce under fusarium conditions. Major gene resistance is available for fusarium diseases of other crops. This type of resistance should also exist for sugarbeet. The Holly Sugar Plant Pathology Department, in cooperation with Holly Hybrids, is developing procedures to screen large quantities of sugarbeet germplasm in order to search for a source of this type of resistance. If this endeavor is successful, it will be the ultimate solution of this problem.