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Disease Management

Control of MRR/VD has proven to be difficult. At present, there is no one method available that is both cost effective and long lasting that provides adequate control of the disease, although research using several different strategies is ongoing in several laboratories. Factors contributing to the difficulty in controlling MRR/VD include:

intensive and successive cropping of melons, allowing for the buildup of inoculum,
presence of numerous thick-walled ascospores that may reside in the soil for years and which are apparently tolerant to desiccation and chemicals,
the general difficulty in applying and incorporating pesticides into the soil environment,
the inherent buffering capacity of the soil and plant rhizosphere,
the apparent wide host range of the fungus and its ability to colonize and reproduce on several monocot and dicot plants,
cropping practices such as plastic mulch and buried drip irrigation that create a favorable soil environment for infection and survival of the fungus,
cultural practices that result in poorly developed and shallow root systems, and
lack of melon genotypes that are resistant or highly tolerant to infection and disease.

In spite of these obstacles, progress is being made in managing this disease. An integrated approach to the management of MRR/VD may be the best strategy. Integration increases the chance of developing effective management programs by combining partially effective methods, reducing the chances of negative side effects, and providing flexibility in adapting the control programs to different agricultural situations.

Chemical Soil Treatment. The most effective technique so far has been preplant soil fumigation with methyl bromide (Figure 13), chloropicrin, 1,3 dichloropropene, or metam sodium (VapamTM). However, the planned phase-out of methyl bromide and the increasing restrictions on fumigants, in general, make this a tenuous strategy. Other compounds have been applied experimentally via drip irrigation and have shown various degrees of control. A multi-phased strategy consisting of a preplant soil fumigation to reduce the resident inoculum in the soil, a postplant application of fungicide to inhibit root colonization during the season, and a postharvest cultivation of plants has been developed for control of MRR/VD in California.

Figure 13.

Soil solarization. Studies in both the U.S. and Israel using conventional soil solarization were ineffective in controlling MRR/VD, presumably due to the ability of the fungus to grow at high temperatures. However, a modified method of solarization and the combination of soil solarization with reduced rates of fumigation have shown good potential for control of MRR/VD, as well as other soilborne diseases in Israel.

Genetic resistance. Like most soilborne diseases, genetic resistance to MRR/VD is the method of choice for control; however, a good source of resistance to M. cannonballus has not been identified. Several laboratories are actively pursuing sources of resistance, and a few melon lines have been identified that exhibit tolerance to MRR/VD.

Grafting. Other attempts at controlling MRR/VD include grafting susceptible melons (muskmelon and watermelon) onto Cucurbita spp. or Lagenaria spp. (bottle gourd) rootstock. This practice is used most commonly in Asia and the Mediterranean basin for the control of several soilborne diseases, primarily Fusarium wilt. There is good rootstock-scion compatibility among many of the cucurbit species, and the large and extensive root systems of these winter squashes and gourds allow them to survive infection during the season. The use of these rootstocks should be approached with some caution, however as they are susceptible to infection by M. cannonballus and, therefore, could aid in the potential build-up of inoculum in the soil.

Biological control. The use of hypovirulent isolates of M. cannonballus is being investigated as a biological control for MRR/VD. Isolates infected with one or more double-stranded (ds) RNAs often result in cultures that are greatly reduced in virulence (hypovirulent) (Figure 9 ). These dsRNAs can be transmitted to normal, wild-type virulent isolates via hyphal anastomosis (fusion), rendering them hypovirulent. Subsequent "curing" of the infected isolates by extended growth at high temperature restores them to their wild-type pathogenicity. Thus far, transmissible hypovirulence has only been shown to have disease control potential in greenhouse experiments (Figure 14).


Figure 9.	Figure 14.