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Remarks (public):For a complete description including images see www.cababstractsplus.org/dfb 
Remarks (internal):Fusarium wilt of tomato is one of the most studied vascular diseases and many papers have been published on all aspects of the disease. Only recent literature and some important older papers are referred to here. For earlier literature see IMI Description Sheet 217, Booth (1971), Holliday (1980) and reviews by Walker (50, 3174), Jones & Woltz (1981). The disease occurs in warm climates and in glasshouse tomatoes grown in temperate regions. A temperature of 28°C is optimal for disease development, whilst below 20°C symptoms are much reduced (2, 428). Persistence of chlamydospores and microconidia of the pathogen in soil has been studied (64, 1481; 69, 517). The fungus may colonise non-susceptible weed hosts (57, 2280) and survive saprobically in root debris in soil. The ultrastructure of vascular colonization has been described (57, 5124; 58, 1954; 60, 4652; 61, 5218; 63, 1670, 4818; 70, 3465). Cellulolytic and pectolytic enzymes of the pathogen have been studied (58, 371, 4023; 59, 460; 60, 6293). The role of phenolic compounds in resistance has been discussed (67, 4672, 5574). Resistance has been correlated with high phenolic content of host tissues (57, 4139; 69, 1833). Inhibitory effects of some phenolics on the pathogen have been studied (60, 4654; 67, 1693). Treatment of plants with catechol was reported to reduce wilt (57, 3618). An ultrastructural and cytochemical study of phenolic metabolism demonstrated differences between susceptible and resistant plants and induction of activity in xylem parenchyma cells (69, 3238). Differential reponse of resistant and susceptible cultivars was seen in the reaction of secondary xylem parenchyma cells to infection and in subsequent callose deposition (68, 2818). Ultrastructure of callose deposition has been studied (67, 6188). Fusaric-acid-detoxifying bacteria were reported to protect tomatoes from wilt (68, 2816). Accumulation of phytoalexins, e.g. rishitin, tomatine and cis-tetradeca-6-ene-1,3-diyne-5, 8-diol have been studied (58, 1397, 2402; 60, 3950; 61, 5960; 65, 373; 66, 4469; 67, 3096; 69, 7434; Elgersma & Liem, 1987). Infection by root-knot nematode may interfere with rishitin production (Noguera, 1982). Degredation of medicarpin by the fungus has been studied (63, 1133). The relation between induced resistance to F. oxysporum f.sp. lycopersici, glycosidases and ethylene production has been discussed (66, 3960, 5310; 67, 6190; 68, 5820). Ultrastructural changes in leaves of infected plants have been studied (66, 4958). Extracts of xylem vessels have been shown to contain fungitoxic compounds (57, 295). Cultural variation in the pathogen has been described (65, 2976). Growth of the fungus on different C sources (57, 2415), phospholipid content of mycelium (59, 1881) and response to low temperatures have been studied (64, 1260). Extracellular enzymes produced by the pathogen in vitro have been tested (69, 2876). Properties of cholinephosphotransferase of the pathogen have been studied (64, 4763). Effect of phenolics on spore germination has been studied (70, 1720). The nitrate reductase gene of the pathogen has been transformed by the niaD gene of Aspergillus nidulans (69, 2880). Lectin agglutination reactions have been used to differentiate in vitro between F. oxysporum f.sp. lycopersici and F. oxysporum f.sp. radicis-lycopersici (68, 5311). Electroporation of fluorescein isothiocyanate-conjugated albumin into spores has been demonstrated (68, 3051). A simplified method of extracting nuclear and mitochindrial DNA from the pathogen has been described (67, 1721). 10% repetitive sequences were found in nuclear DNA. Restriction fragment length polymorphisms were studied in one isolate (66, 4704). Vegetative incompatibility (VC) between isolates of the pathogen has been studied. Three VC groups were represented by several strains, but numerous other isolates were incompatible with any others tested, thus representing a range of genotypes. No correlation was found between VC group and cultural morphology or pathogenic race designation. Isolates of different race may belong to the same VC group and isolate of different VC groups may be the same race (70, 3543). This may be due to the small number of genes involved in determining host resistance. It has the implication that heterokaryons are potentially possible between isolates of different race (58, 5506; 61, 6581). Losses may be severe, so effective means of control are essential (57, 4624; 63, 866). Control is through a combination of growing resistant cultivars, soil fumigation where appropriate, avoidance of infected seed or planting material, careful management of soil conditions, fallowing and crop rotation (Besri, 1984). Breeding and selection of resistant cultivars is an important aspect of disease control (57, 4138; 58, 373; 59, 456a; 59, 908; Pugacheva, 1982; Jordanov & Stamova, 1983; Scott et al., 1983; 64, 3190; 65, 2975; 66, 1132; Gomez et al., 1985; Horie, 1985; 67, 1474; Babaev, 1986; Berry & Gould, 1986; Henderson, 1986; Honma & Murakishi, 1986; 68, 351, 2598; 69, 2959, 3236, 5182, 7420; 70, 4373, 4375; Volin & Jones, 1982; Jones & Scott, 1987; Berry & Gould, 1988; Nandpuri et al., 1988; Gavrish et al., 1988; McFerran et al., 1989; Nguyen, 1989; Scott et al., 1989; Bosch et al., 1990; Gardner, 1990). Since 1940's, highly resistant cultivars have been available. Dominant genes I1, I2 and I3 confer vertical resistance to races 1, 2 and 3 (56, 2662; 57, 5686; Miller et al., 1985; Shahin & Spivey, 1986; 67, 1475; 70, 4373; McGrath et al., 1987; Scott & Jones, 1989). An RFLP marker for resistance to race 2 (69, 1245) and an isozyme marker for resistance to race 3 have been reported (69, 7436). Resistant lines may be selected in vitro by testing for reaction to toxins (63, 1953; 64, 2720; Shahin & Spivey, 1986; 69, 5633, 5935). Resistance reactions may sometimes be overcome due to interactions with root-knot nematodes (57, 5685; 60, 5556; Suhardi et al., 1980; 61, 1922, 4346, 5221; Kleineke-Borchers & Wyss 1982; 63, 1392, 2489, 4560, 5552; 64, 778). The role of amino acids in the nematode-wilt complex has been discussed (57, 1413). Where economic, soil fumigation with methyl bromide, Ditrapex (1,2-dichloropropane with 1,3-dichloropropene), DD-MENCS, methyl-isothiocyanate, metham-sodium, phenylphosphinic acids or chloropicrin reduces wilt incidence and improves yields (58, 372; 65, 2977; 67, 566; 68, 1916; 69, 47, 6629; Overman et al., 1987). Soil solarisation may be effective in reducing population levels of the pathogen (65, 1112; 67, 4373). Fumigation combined with solarisation may also be effective (Overman & Jones, 1986). Of different fungicides tested, difolatan gave best control of wilt (58, 1584). Soil drench with benomyl or thiophanate-methyl has been reported to give good control in glasshouse tomatoes (57, 783). Inheritance of benomyl resistance in the pathogen has been studied (63, 864; 65, 4697; 66, 4658). MBC resistant mutants retain their pathogenicity (60, 690). Extracts from garlic bulbs have been shown to be inhibitory to the pathogen (69, 6164). Inhibitory effects of the herbicides prometryn, fluometuron, simazine and bromophenoxim on growth and metabolic activity of the pathogen have been studied (63, 5338; 68, 394). Nitralin was reported to have a stimulatory effect on the fungus (67, 6189). Treatment with trifluralin may induce resistance in genetically susceptible host cultivars (63, 4819). Use of nematicides to control root-knot nematode may also reduce Fusarium wilt (57, 2651). Noguera & Smits, 1982; Noguera, 1983; Mangat & Bhatti, 1986). Non-pathogenic strains of F. oxysporum may provide cross-protection against the pathogen (57, 296; 58, 4194; 63, 4943; 64, 2721; 66, 67; 67, 403; 70, 3959). Antagonistic soil or rhizosphere microorganisms have been proposed for biological control of wilt (60, 2441; 61, 1389; 63, 360, 862, 868; 65, 3149; 66, 2278; 67, 108, 950, 3620; 69, 2549, 5306, 6233). Suppressiveness of soils may not correlate with antagonistic activity of their microbial populations (65, 3172). The influence of soil texture, pH and salinity on wilt incidence have been studied (63, 861, 863). Liming to raise the soil pH may reduce Fusarium wilt, but can increase losses due to Verticillium wilt and root-knot nematode (63, 865; 66, 2507). Use of nitrate-N, rather than ammonium-N, reduces disease levels (52, 3072; 61, 4348, 4349; 63, 1953). The effects of micronutrients on the pathogen, host and disease levels have been studied (68, 4948). Increasing the organic matter content of soil can reduce disease levels (60, 1077, 1078). Use of ozone to disinfect water used in hydroponic culture has been tested (70, 1571). Microwaves have been used to sterilise synthetic horticultural growth substrates (67, 2758) and soil (63, 5319).
 
Description type:Non-original description 
Description:Fusarium oxysporum Schlecht. f.sp. lycopersici (Sacc.) Snyder & H.N. Hansen, Amer. J. Bot., 27: 66, 1940.
Fusarium oxysporum Schlecht. subsp. lycopersici Sacc., Syll. Fung. 4: 705, 1886.
Fusarium lycopersici Bruschi, Atti del Reale Accad. de Lincei 21: 227, 1912.
Fusarium bulbigenum var. lycopersici (Bruschi) Wollenw. & Reink., Die Fusarien: 114, 1935.
Teleomorph: None known.
The fungus causes a vascular wilt of tomato. Both field and glasshouse crops are affected and losses may be severe unless control is effective. Infection occurs from soil borne inoculum via the roots. The fungus spreads rapidly through the host xylem and induces dark brown vascular discolouration extending from the roots up to the leaf petioles. Leaves turn yellow and wilt, curling downwards towards the stem. Infected plants are often stunted and may bear small, prematurely ripe fruit. Eventually the plant dies.
Hosts: Lycopersicon esculentum (tomato). May also infect other species of Lycopersicon.
Disease: Vascular wilt. The fungus may also cause tomato fruit rot.
Geographical distribution: Widespread in tomato growing regions of the world. Africa: Kenya, Morocco, Nigeria, Republic of South Africa, Senegal, Tanzania, Tunisia. America: Argentina, Brazil, Canada, Cuba, Mexico, USA. Asia: China, India, Iran, Iraq, Israel, Japan, Korea, Pakistan. Australasia: Australia. Europe: Albania, Belgium, Bulgaria, France, Germany, Great Britain, Italy, The Netherlands, Spain, USSR.
Physiological specialization: Three pathogenic races are known. Races 1 and 2 have been distinguished since 1945 (24, 434). A third race was described from Brazil (Tokeshi et al., 1966) and another from Tunisia (El-Mahjoub, 1974), but these have not yet been confirmed. A similar race was reported from Australia in 1978 (61, 5222). The Australian race has since been recognised in Florida (Volin & Jones, 1982) and California (67, 5161), and is now widely accepted as race 3.
Transmission: The fungus is soil borne and may also be transmitted by seed (58, 3447; 67, 1486), planting material and locally by water flow.
Literature: Babaev, A.G. (1986) Selektsiya i Semenovodstvo, USSR 4: 27-28. Berry, S.Z. & Gould, W.A. (1986) HortScience 21: 334. Berry, S.Z. & Gould, W.A. (1988) HortScience 23: 930. Besri, M. (1984) Cahiers de la Recherche Agronomique 40: 19-26. Booth, C. (1971) The genus Fusarium. International Mycological Institute, Kew, 237pp. Kleineke-Borchers, A. & Wyss, U. (1982) Zeitschrift für Pflanzenkrankheiten und Pflanzenschutz 89: 67-78. Bosch, S.E., Boelema, B.H., Serfontein, J.J. & Swanepoel, A.E. (1990) HortScience 25: 1313-1314. Elgersma, D.M. & Liem, J.I. (1987) Canadian Journal of Plant Pathology 9: 80. El-Mahjoub, M. (1974) Annales de l'Institut National de la Recherche agronomique, Tunis 47: 1-17. Gardner, R.G. (1990) HortScience 25: 989-
990. Gavrish, S.F., Sysina, E.A., Amcheslavskaya, E.V. & Shmorgunov, G.T. (1988) Kartofel' i Ovoshchi 6: 45-
46. Gomez, O., Depestre, T., Hernandez, J.C. & Baldy, B. (1985) Ciencia y Tecnica en la Agricultura, Hortalizas, Papa, Granos y Fibras 4: 63-70. Henderson, W.R. (1986) HortScience 21: 1247-1248. Holliday, P. (1980) Fungus diseases of tropical crops. pp. 175-178, Cambridge Univ. Press, Cambridge, UK. Honma, S. & Murakishi, H.H. (1986) HortScience 21: 1244-1245. Horie, Y. (1985) Japanese Journal of Breeding 35: 87-88. Jones, J.P. & Scott, J.W. (1987) Proceedings of the Florida State Horticultural Society 100: 240-241. Jones, J.P. & Woltz, S.S. (1981) In Fusarium: diseases, biology and taxonomy. pp. 157-168, Eds P.E. Nelson, T.A. Toussoun & R.J. Cook, Pennsylvania State Univ. Press, Univ. Park & London. Jordanov, M. & Stamova, L. (1983) Tagungsbericht, Akademie der Landwirtschaftswissenschaften der Deutschen Demokratischen Republik 216: 617-622. Mangat, B.P.S. & Bhatti, D.S. (1986) International Nematology Network Newsletter 3: 21-23. McFerran, J., Goode, M.J., Scott, S.J. & Montgomery, F.W. (1989) HortScience 24: 712-713. McGrath, D.J. (1988) HortScience 23: 1093-1094. McGrath, D.J., Gillespie, D. & Vawdrey, L. (1987) Australian Journal of Agricultural Research 38: 729-733. Miller, S.A., Williams, G.R., Medina Filho, H. & Evans, D.A. (1985) Phytopathology 75: 1354. Nandpuri, K.S., Surjan Singh & Mahajan, R. (1988) Indian Journal of Nematology 18: 121-122. Nguyen, V.Q. (1989) Rural Newsletter (NSW, Australia) 107: 26-27. Noguera, R. (1982) Agronomia Tropical 32: 303-308. Noguera, R. (1983) Agronomia Tropical 33: 103-109. Noguera, R. & Smits B., G. (1982) Agronomia Tropical 32: 147-154. Overman, A.J., Csizinszky, A.A., Jones, J.P. & Stanley, C.D. (1987) Proceedings, Soil and Crop Science Society of Florida 46: 4-7. Overman, A.J. & Jones, J.P. (1986) Proceedings of the Florida State Horticultural Society 99: 315-318. Pugacheva, T.I. (1982) Trudy po Prikladnoi Botanike, Genetike i Selektsii 71: 117-119. Scott, J.W. & Harbaugh, B.K. (1989) Circular - Agricultural Experiment Station, University of Florida S-370: 6 pp. Scott, J.W. & Jones, J.P. (1989) Euphytica 40: 49-53. Scott, J.W., Jones, J.P. & Volin, R.B. (1983) Proceedings of the Florida State Horticultural Society 96: 120-122. Scott, J.W., Olson, S.M., Bryan, H.H., Howe, T.K., Stoffella, P.J. & Bartz, J.A. (1989) Circular - Agricultural Experiment Station, University of Florida S-359: 10 pp. Shahin, E.A. & Spivey, R. (1986) Theoretical and Applied Genetics 73: 164-169. Suhardi, Dede Rohana & Lukman Hutagalung (1982) Buletin Penelitian Hortikultura 8: 19-27. Tokeshi, H., Galli, F. & Kurozawa, C. (1966) Anais da Escola superior de agricultura 'Luiz de Queiroz' 23: 217-227. Vlasova, E.A. (1982) Trudy po Prikladnoi Botanike, Genetike i Selektsii 71: 100-106. Volin, R.B. & Jones, J.P. (1982) Proceedings of the Florida State Horticultural Society 95: 268-270.

 
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