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Disease Cycle and Epidemiology

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Disease process

Verticillium wilt is favored by moist soils and a temperature range of 21-27° C (70-81° F). Microsclerotia are stimulated to germinate by root exudates of both host and non-host plants (Figure 12). The fungus penetrates a root of a susceptible plant in the region of elongation and the cortex is colonized. From the cortex, the hyphae invade the xylem vessels where conidia are formed (Figure 13). Vascular colonization occurs as conidia are drawn up into the plant along with water. Due to fungal material and host reaction products, the vascular system becomes plugged, preventing water from reaching upper parts of the plant. Leaves and stems deprived of water soon begin to exhibit symptoms of wilting and foliar chlorosis. As the diseased plant senesceces, the fungus produces microsclerotia which are released into the soil with the decomposition of plant material. The fungus survives for many years in this dormant form or as mycelium or conidia in the vascular system of perennial plants.

Figure 12

Figure 13

Spread of the pathogen

The transport of infected planting stock can move the pathogen long distances. In bare root or vegetatively propagated plants such as ornamentals or peppermint, a nursery may spread the fungus by selling non-symptomatic, but infected, planting stock. Similarly, Verticillium can be spread in infected potato seed tubers. Once established in a field or landscape, spread of the pathogen occurs primarily by soil cultivation and movement of soil by wind or water. Verticillium propagules occur in highest concentration in the top 30 cm (12 inches) of the soil profile, but they have been recovered from depths as low as 41 cm (16 inches). Inoculum densities and disease severity tend to increase from year to year when susceptible crops are planted.

Nematode/Verticillium interactions

Symptoms of Verticillium wilt of potato and peppermint are often more severe in fields infested with the root-lesion nematode, Pratylenchus penetrans. This nematode may increase the severity of the disease by altering the host physiology, thus making the plant more susceptible to damage. Symptoms may develop even when population densities of Verticillium and P. penetrans individually are too low to cause significant disease.

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