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Disease Cycle and Epidemiology

Disease Cycle

The disease cycle for all cucurbit Fusarium wilts is similar. Initial infection of seedlings usually occurs from chlamydospores that have overwintered in the soil. Chlamydospores germinate and produce infection hyphae that penetrate the root cortex, often where the lateral roots emerge. Infection may be enhanced by wounds or damage to the roots. The fungus colonizes the root cortex and soon invades the xylem tissue, where it produces more mycelia and microconidia. Microconidia may be carried up the xylem (Figure 7) in the transpiration stream where they may become lodged against the vessel wall or perforation plate. Subsequent germination results in hyphae that penetrate and emerge on the other side where they repeat the process of mycelial growth and sporulation. Consequently, the fungus becomes systemic and often can be isolated from tissue well away from the roots. In response to the advance of the fungus within the xylem, the host plant typically produces tyloses, in an attempt to restrict pathogen movement. If the tyloses form quickly enough and sufficiently to completely plug the xylem vessel (Figures 8 & 12), before the fungus has proceeded up the plant, they may prevent systemic colonization of the xylem - the result being a resistant plant. In susceptible plants, however, tyloses form more slowly and do not completely block the vessel (Figures 10 & 11), ultimately allowing the fungus to pass through. As the fungus continues to colonize the xylem, more tyloses are formed, eventually restricting water flow and causing the vine to wilt. The formation of tyloses in some vessels and not in others partially explains the ‘one-sided’ wilt (Figure 2) often seen in watermelon and muskmelon. Further colonization of the tissue results in necrosis and cellular gums that hastens wilt and death of the plant and produces the characteristic brown discoloration of the vascular tissue (Figures 3a - b). Because the fungus is systemic in the xylem, it can be readily isolated from diseased plants by surface-sterilizing cross sections of the stem or root and plating them onto a growth medium. Mycelium of F. oxysporum will emerge directly from within the xylem within 24 - 48 hours (Figures 13 - 14).

The vascular wilt fusaria spend most of their time within the plant. In the very late stages of disease or upon plant death, the fungus begins to grow profusely along the outside of the decayed stem, producing thick mats of white mycelia (Figure 16) and abundant macroconidia. Macroconidia become incorporated into the soil and, along with the mycelium, convert into chlamydospores, which can remain dormant until next season. Chlamydospores formed within the mycelium may survive in a dormant state in the soil for 15 to 20 years.


Figure 13	Figure 14	Figure 16

Epidemiology

Fusarium wilts are generally presumed to be monocyclic - that is, the disease does not exhibit plant-to-plant spread during the season. This is primarily because there are no propagules capable of dissemination to other plants to cause secondary infections that form above ground until very late in the season. However, the time to appearance of symptoms and the rate of disease progression in plants may vary considerably within a field, giving the appearance of secondary spread. There is some evidence that suggests some Fusarium wilts i.e., Fusarium wilt of tomato, in fact, may be a polycyclic disease capable of significant secondary spread during the season. While the extent of secondary plant-to-plant spread of Fusarium wilt of watermelon is not entirely clear, the pathogen can be spread within a field over a period of several seasons and from field to field. Spread within a field can occur by the movement of infested soil. Tillage practices, flooding or heavy rain, contaminated farm equipment, and other cultural or environmental factors may be involved. Field-to-field spread can occur when equipment and infected plants are moved from one field to another. It is possible that macroconidia formed on the decaying vines on the soil surface could be blown short distances and aid in the spread. Watermelons typically are grown using commercially produced transplants and transport of infected transplants is likely responsible for most long distance spread.

Many Fusarium wilt pathogens, including F. oxysporum f. sp. niveum, are capable of being seedborne, although the extent of the contamination varies widely. There is little direct evidence as to how the seed becomes infected and/or contaminated but the likely means are either by direct infection of the developing seed by the fungus within the infected plant or by accidental contamination of the seed during harvesting and seed extraction. F. oxysporum f. sp. niveum has been isolated from both the external seed coat (Figures 17-19) and from within the seed (Figures 20 & 21) . The role of contaminated seed in the long distance dissemination of Fusarium wilt of watermelon is not entirely known, as seed contamination has been documented only sporadically. However, there are numerous anecdotal reports where Fusarium wilt has occurred in plants grown on land planted to melons for the first time or land that had just been cleared of its natural vegetation. How and when the pathogen gets to these fields is more than of just academic interest. Contaminated seed and infected transplants are obvious routes, but the low level of infection observed in commercial watermelon transplants and seed lots likely cannot account for all cases. Likewise, the use of contaminated farm implements (tractors, cultivators, etc.) probably plays a limited role. The question remains as to how and why the pathogen occurs in ‘virgin soil’. Clearly, the pathogen could be introduced during land preparation, but accidental introductions such as this would not be expected to cause wide spread disease. Thus, other mechanism might be operating. One hypothesis, although there is not much experimental evidence to support it, is that pathogenic forms somehow evolve from existing nonpathogenic forms. Nonpathogenic strains of F. oxysporum are ubiquitous in soil around the world and are excellent colonizers of plant roots. That they are incapable of causing disease may simply be a function of their inability to penetrate the cortex and enter the xylem. Perhaps in the presence of new hosts some saprophytic strains can develop the ability to penetrate root tissue and cause disease. For a detailed discussion of this and other aspects of the evolutionary biology of F. oxysporum, the reader is referred to the review by Gordon and Martyn (1997).


Figure 17	Figure 18

Figure 19	Figure 20

Figure 21

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