The fungus was first reported in Japan in It is one of the most destructive diseases of tomatoes 1, 2, 3. There is no distinguished physiological race of FORL. However, nine Vegetative Compatibility Groups VCGs have been identified, which indicates it has a high genetic diversity. There is no known teleomorph 4. Symptoms and Signs In general, symptoms include yellowing, wilting, stunted growth, and discolored internal stem tissue.
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Snyder and H. Hans, a soilborne plant pathogen in the class Hyphomycetes, causes Fusarium wilt specifically in tomato. This disease was first described by G. Massee in England in It is of worldwide importance where at least 32 countries had reported the disease, which is particularly severe in countries with warm climate.
At one time, the disease nearly destroyed tomato production in parts of Florida and the southeastern states of United States. However, the development and use of resistant cultivars have nearly eliminate the concern over this disease.
Host Range and Distribution Three physiological races of this pathogen have been reported. Race 1 is the most widely distributed and has been reported from most geographical areas. Although race 2 was first reported in Ohio in , it did not become widespread or of economic concern until its discovery in Florida in Since then, it was rapidly reported in several of the states and in several other countries, including Australia, Brazil, Great Britain, Israel, Mexico, Morocco, the Netherlands, and Iraq.
Race 3 was reported in in Brazil. Thereafter, it has been found in Australia and in Florida and California. Trim off all the leaves and secondary roots leaving only the main stem and the hypocotyls and main root. Dry the stem on paper towels. Place wedges on PDA plates. Incubate the plates under fluorescent lights. Once the fungus has grown sufficiently from the pieces, transfer isolates onto fresh PDA plates.
Incubate the plates for days. Colonies of F. The soil dilutions are plated on a selective medium. The plates are kept under fluorescent lights for incubation. Identification The mycelia Plate 1 of Fusarium oxysporum f. Hans are delicate white to pink, often with purple tinge, and are sparse to abundant.
The fungus produces three types of spores: microconidia Plate 2 , macroconidia Plate 3 , and chlamydospores Plate 4. Microconidia are borne on simple phialides arising laterally and are abundant, oval-ellipsoid, straight to curved, x 2. Macroconidia, sparse to abundant, are borne on branched conidiophores or on the surface of sporodochia and are thin walled, three- to five-septate, fusoid-subulate and pointed at both ends, have pedicellate base.
Three-septate conidia measure x mm while five-septate conidia measure x mm. Three-septate spores are more common. Chlamydospores, both smooth and rough walled, are abundant and form terminally or on an intercalary basis. They are generally solitary, but occasionally form in pairs or chains. No perfect stage is known. Pictures taken from Toussoun, T. Symptoms The first indication of this disease is a yellowing Plate 5 and drooping of the lower leaves.
This symptom often occurs on one side of the plant or on one shoot. Successive leaves yellow, wilt and die, often before the plant reaches maturity. As the disease progresses, growth is typically stunted, and little or no fruit develops. If the main stem is cut, dark brown streaks may be seen running lengthwise through the stem.
This discoloration Plate 6 often extends far up the stem and is especially noticeable in a petiole scar. The browning of the vascular system is characteristic of the disease and generally can be used for its identification. Plate 5. Yellowing and death of leaves on one side of the stem. Plate 6. Dark brown vascular discoloration. Ecology and Life Cycle Fusarium wilt is a warm-weather disease, most prevalent on acid, sandy soils.
The pathogen is soilborne and remains in infested soils for up to ten years. If soil temperatures are optimum but air temperatures below optimum, the pathogen will extend into the lower parts of the stem, but the plants will not exhibit external symptoms. Virulence of the pathogen is enhanced by micronutrients, phosphorus, and ammonium nitrogen and decreased by nitrate nitrogen. The pathogen enters the plant through the roots and is then spread throughout the plant by the vascular system.
Dissemination of the pathogen is via seed, tomato stakes, soil, and infected transplants or infested soil adhering to transplants. The pathogen could be disseminated long distance through seed and transplants. Local dissemination is by transplants, tomato stakes, windborne and waterborne infested soil, and farm machinery. Disease Control Control measure is mainly through the use of resistant cultivars. The control of races 1 and 2 utilizes both polygenic and monogenic resistance while monogenic resistance to race 3 has been developed.
Pasteurization of infested soil with steam or fumigants, raise the soil pH to 6. Links to other sites.
Snyder and H. Hans, a soilborne plant pathogen in the class Hyphomycetes, causes Fusarium wilt specifically in tomato. This disease was first described by G. Massee in England in It is of worldwide importance where at least 32 countries had reported the disease, which is particularly severe in countries with warm climate. At one time, the disease nearly destroyed tomato production in parts of Florida and the southeastern states of United States.
Fusarium oxysporum f. sp. radicis-lycopersici Related Abstracts
Paper Count: 4 Fusarium oxysporum f. Lakhdari , A. Dahliz , Y. Bouchikh , R. Hammi , A. Soud , A.
Fusarium oxysporum f. sp. radicis-lycopersici
Received Jun 22; Accepted Sep 7. This article has been cited by other articles in PMC. Abstract Benzo- 1,2,3 -thiadiazolecarbothioic acid S-methyl ester BTH , a synthetic chemical, was applied as a foliar spray to tomato Lycopersicon esculentum plants and evaluated for its potential to confer increased resistance against the soil-borne pathogen Fusarium oxysporum f. In nontreated tomato plants all root tissues were massively colonized by FORL hyphae. Pathogen ingress toward the vascular stele was accompanied by severe host cell alterations, including cell wall breakdown. In BTH-treated plants striking differences in the rate and extent of fungal colonization were observed.