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Remarks (public):For a complete description including images see 
Remarks (internal):The fungus causes a typical vascular wilt. The factors favouring disease development are: soil temperature of 28°C, low soil moisture, short day length, low light intensity, nutrients low in N and P and high in K and a low pH. The physiology of the disease has been studied intensively notably by Gaumann, Walker, Dimond, Davis and Ludwig (see Dimond, 1955; Wood, 1960; Sadasivan, 1961; Beckman, 1964; Gaumann, 1957a, b). Gaumann attributes wilting to the polypeptide lycomarasmin produced by the pathogen, other workers consider that blocking of the vessels is the main cause and in this fungal enzymes (PME, DP) are involved. Epinasty of leaves (one of the symptoms) is attributed to ethylene produced during pathogenesis. Like other formae speciales of Fusarium oxysporum, the fungus also produces fusaric acid in vitro and, although presence in vivo has been established, this perhaps plays only a secondary role in wilt (Kuo & Scheffer, 1964). The chief method of control is by resistant varieties, of which many have been developed in U.S.A. following the pioneering effort of Essary, Edgerton, Pritchard and Walker. These varieties are resistaot to Race 1 alone. In the case of Race I the resistance factor is believed to be linked with the metabolism of the resistant plant in which a transient substance inhibitory to the pathogen was being produced or in which substances required for growth and developmant of the pathogen were absent (Gothoskar et al., 1955).
Description type:Non-original description 
Description:Fusarium oxysporum Schltdl.: Fr. f.sp. lycopersici (Sacc.) Snyder & Hansen, Am. J. Bot. 27: 66, 1940.
= Fusarium oxysporum Schltdl. subsp. lycopersici Sacc., Syll. Fung. 4: 705, 1886.
= Fusarium lycopersici Bruschi, 1912.
= Fusarium bulbigenum var. lycopersici (Bruschi) Wollenw. & Reinking, 1935.
Hosts: On Lycopersicon esculentum (tomato), L. pimpinellifolium (red currant tomato) and other species of Lycopersicon.
Disease: Vascular wilt of tomato.
Geographical distribution: Africa, Asia, N. and S. America, Australasia, Europe, W. Indies and C. America.
Physiological specialization: Isolates differing in morphology, cultural characters and pathogenicity are known. Two races, Race 1 and Race 2, have been described (Alexander & Tucker, 1945; Gerdemann & Finley, 1951), the latter is rarely found in nature and is pathogenic on strains of the host highly resistant to other isolates (Race 1).
Transmission: Soil-borne and seed-borne. Long distance spread by infected seed and transplants. Local dissemination by transplants, wind-borne and water-borne infested soil, surface-drainage water.
Literature: Wollenweber & Reinking, Die Fusarien, pp. 219-223, 1935; Walker, Plant Pathology, 2nd ed., pp. 261- 269, 1957 (general); Alexander & Tucker, J. agric. Res. 70: 305-313, 1945; Gerdemann & Finley, Phytopathology 41: 238-244, 1951 (races); Beckman, Ann. Rev. Phytopath. 2: 231-252, 1964; Dimond, Ann. Rev. Pl. Physiol. 6: 329-350, 1955; Gaumann, Phytopathology 47: 342-357, 1957a; Phytopath. Z. 29: 1-44, 1957b; Sadasivan, Ann. Rev. Pl. Physiol. 12: 449-469, 1961; Wood, Ann. Rev. Pl. Physiol. 11: 299-322, 1960 (physiology); Gothoskar, Scheffa, Stahmann & Walker, Phytopathology 45: 303-307, 1955 (resistance); Kuo & Scheffer, Phytopathology 54: 1041-1044, 1964 (fusaric acid).
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