| Crop Knowledge Master | Fungi | |
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Fusarium oxysporum f.s.p. niveum |
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| wilt of watermelon (Plant Disease Pathogen) | ||
| Hosts | Distribution | Symptoms | Biology | Epidemiology | Management | Reference | |
Author
Stephen A. Ferreira, Extension Plant Pathologist
Rebecca A. Boley, Educational Specialist
Department of Plant Pathology,CTAHR
University of Hawaii at Manoa
Watermelon, Citrullus lanatus (Thumb.) Matsum. & Nakai or Citrullus vulgaris Schrad., is the principle host that this fungus attacks. Citron and the closely related bitter apple are also susceptible to this particular pathogen, although other hosts, especially muskmelons, are affected by a closely related species. Citrons have a high degree of resistance to the disease and many commercial watermelon cultivars are crosses of Citrullus and citron.
Documentation of Fusarium wilt in watermelon was first recorded in 1894 in Georgia and South Carolina. It is now well-established throughout all watermelon growing regions in the United States and the world. Race 0 is believed to occur only in Florida; it is only pathogenic on cultivars with no wilt-resistance genes and, consequently, is not considered a significant economical concern since most cultivars need wilt-resistant genes in order to produce fruit.
Watermelons are susceptible to Fusarium wilt at all growing stages. When seedlings are infected at a very young stage, the result is serious damping-off and/or stunting. Adult plants show a true wilting followed by death or are stunted in resistant cultivars. In advanced stages of the disease the roots begin to decompose and eventually die. Wilt symptoms usually start at runner tips and continue to the base of the plant. Stems and vines of diseased plants will have discolored vascular tissue, usually yellow or brown in color, instead of clear. A white mold growth may develop on vines or at the base of the plant.
Fusarium lives from season to season on decaying organic matter and is able to survive in the soil for as long as 16 years, though its abundance declines over time. The pathogen lives in the soil and enters through small root tips, nematode stings, and other injuries or openings. It then advances through the xylem causing vascular plugging followed by wilted vines.
Fusarium grows at most any degree of soil moisture, except that very wet conditions reduces infection. The fungus is sensitive to temperature: culture range 41 to 100 F (5 to 37 C), optimum is 75 to 90 F (24 to 32 C); infection range 60 to 95 F (15 to 35 C), optimum 75 to 83 F (24 to 28 C).
Fusarium has been subdivided into pathogenic races. Originally two races were described, race 0 and 1. Race 0 does not cause wilt in resistant cultivars, while race 1 causes slight to moderate wilt on most cultivars that are classified as resistant to Fusarium wilt. Another race is now recognized as race 2, which is very aggressive and causes severe wilt in all known cultivars. This third, more aggressive race 2 pathogen occurs in Texas and Oklahoma.
Fusarium is a soilborne fungus with races 1 and 2 capable of being seedborne also. Once a field is infested, the pathogen may survive in the soil for many years. The fungus can be transported by farm equipment, drainage water, wind, or animals, including humans.
NON-CHEMICAL CONTROL
Use of resistance:
Use of resistant watermelon varieties is the most practical means of control of watermelon wilt. There is variation in susceptibility to the disease of different strains and varieties of watermelons, none of which are completely immune. Some of the more resistant varieties are likely to succumb to wilt over the years due to the formation or introduction of new pathogenic races.
Cultural practices:
Watermelons should not be planted in the same field two years in a row if wilt has occurred. Rotation with nonsusceptible crops is recommended. Rotating watermelons back to a previously used field will depend on the degree of Fusarium infestation, and rotation could range from two or three to 12 years.
Control of drainage water:
Watermelons should not be planted in areas that may receive drainage water from infested fields.
CHEMICAL CONTROL
In China, carbendazim, thiophanate and thiophanate-methyl are fungicides that have been used to control Fusarium wilt (at least in China). However, the pathogen is able to develop resistance to the fungicides. An organo-copper fungicide called Homodemycine (HDE) has been developed in China. Field trial results indicate that a chemical treatment for Fusarium wilt may now exist. Field trials comparing HDE and carbendazim (1988) and HDE and thiophanate (1986) show that HDE was significantly more effective in curbing Fusarium wilt. Results also indicate that HDE may be useful as a plant-growth regulator.
Chupp, C., and A.F. Sherf. 1960. Vegetable diseases and their control. Ronald Press, New York, NY. 693 pp.
Larkin, R.P., D.L. Hopkins, and F.N. Martin. 1990. Vegetative compatibility within Fusarium oxysporum f.sp. niveum and its relationship to virulence, aggressiveness, and race. Can. J. Microbiol. 36:352-358.
Li, Z., and C. Liu. 1990. A new fungicide - HDE and its application in controlling wilt disease of cucurbits. Pest. Sci. 28: 413-418.
MacNab, A.A.. A.F. Sherf, and J.K. Springer. 1983. Identifying diseases of vegetables. Pennsylvania State University, University Park, PA. 62 pp.
Martyn, R.D., and B.D. Bruton. 1989. An initial survey of the United States for races of Fusarium oxysporum f.sp. niveum. HortScience 24(4):696-698.
Orton, W.A. 1922. Diseases of Watermelons. Farmers' Bulletin No. 1277. US Dept. of Agriculture. 31 pp.
Walker, M.N., and G.F. Weber. 1931. Diseases of Watermelons in Florida. Univ. Fla. Ag. Exp. Stn. Bull. 225. 52 pp.
NOVEMBER 1991
3A-FOXNI
