Fusarium vasinfectum G.F. Atkinson, Bull. Alabama agric. Exp. Stn. 41: 19, 1892. Teleomorph: None known.

The fungus causes a vascular wilt of cotton. Plants at all stages of maturity are potentially susceptible. The fungus infects via the roots, crosses the root cortex and enters the vascular tissues, from where it spreads upwards through the plant. Typical internal symptoms of continuous, dark, vascular discolouration are usually evident. Young plants may die very rapidly following infection. Infected older plants remain stunted in comparison with uninfected neighbours. Interveinal leaf yellowing and localised wilting occurs, followed by leaf browning, abscission and death. Lower leaves often display symptoms first. Affected patches of plants therefore appear stunted and defoliated. Crop losses can be very severe. For an illustration of this fungus see IMI Description 211.

DISEASE: Vascular wilt.

HOSTS: Cotton (Gossipium spp., including G. hirsutum, G. barbadense, G. arboreum, G. herbaceum), Chinese lantern (Physalis alkekengi), lucerne (alfalfa) (Medicago sativa), lupin (Lupinus luteus), okra (Abelmoschus esculentus), soyabean (Glycine max), tobacco (Nicotiana tabacum). A wide range of other plants may also be infected without external symptoms (51, 2512).

GEOGRAPHICAL DISTRIBUTION: Widespread (IMI map 362). Africa: Central African Republic, Congo, Egypt, Ethiopia, Israel, Madagascar, Republic of South Africa, Senegal, Somalia, Sudan, Tanzania, Uganda, Zimbabwe. America: Argentina, Brazil, Chile, Colombia, Guatemala, Mexico, Nicaragua, Paraguay, Peru, Puerto Rico, Salvador, St. Kitts-Nevis, St. Vincent, USA (south eastern states), Venezuela. Asia: Burma, China, India, Iran, Iraq, Pakistan, Taiwan, USSR. Europe: France, Greece, Italy, Romania, Yugoslavia.

PHYSIOLOGIC SPECIALIZATION: Six physiological races have been distinguished (58, 243). Race 1 is most widely distributed and causes serious disease of upland cotton (G. hirsutum). It is distinguished from other races by its inability to incite wilt in G. arboretum cv. Rozi, Glycine max cv. Yelredo and Nicotiana tabacum cv. Gold Dollar. It also causes wilt of okra (51, 3030; 56, 3372; 57, 1553; 58, 3600; 62, 2751; McLeod et al., 1983). Race 2 is thought to be closely related to race 1. It is unable to cause wilt in G. arboretum cv. Rozi but, unlike race 1, can do so in Yelredo soyabean and Gold Dollar tobacco. Race 2 was first described from S. Carolina, USA (37, 459), but is now known to occur more widely within USA (63, 3373). Both races 1 and 2 cause wilt of Burley 5 tobacco and Grimm lucerne. Race 3 causes wilt of G. barbadense cvs grown in the Nile valley region of Egypt and, possibly, Israel and the USSR. It causes a slow wilt of Tithonia rotundifolia (49, 422) but does not cause wilt of G. hirsutum cv. Acala, tobacco or okra (40, 416). Race 4 is reported to cause wilt of diploid cottons in India, but does not attack okra or tobacco (40, 416). Race 5, similar to race 3, was described from Sudan on G. barbadense (46, 334). Race 6, from Brazil and Paraguay (60, 2043), resembles races 1 and 2, but is non-pathogenic to Burley 5 and Gold Dollar tobacco, Yelredo soyabean, Weikko III lupin and Grimm lucerne (58, 243).

TRANSMISSION: The fungus is soil borne and may be transmitted by seed (11, 713; 32, 186) and in irrigation water (62, 4911).

NOTES: For earlier references see IMI Description Sheet 28 and 50, 3783. The cotton wilt disease was reviewed by Smith et al. (1981). Accounts have been published for Brazil (58, 3308), China (65, 732), Egypt (50, 105), India (69, 2359; 70, 4158), Tanzania (50, 3779; 54, 1284, 2821; 55, 2248; 60, 5451; 62, 3530; 68, 2690), USSR (52, 747; 54, 2261; 56, 231; 57, 176, 4482). Crop losses may be significant (66, 1937).
The fungus may persist as chlamydospores and as a saprobe in soil debris for many years (50, 2976; 51, 4038; 52, 3704; 54, 4506; 56, 4918). A selective isolation medium containing bile salts, PCNB and streptomycin has been described (59, 6494). The pathogen enters cotton roots either via wounds or by direct penetration, invades intercellular spaces and then colonizes the vascular system (51, 2514; 52, 133, 3330; 55, 5208; 56, 3048; 57, 2952; 58, 796, 797). The fungus spreads widely throughout the host xylem as microconidia (51, 1519). Host-pathogen interactions have been modelled (62, 676; 70, 3465). A strain-specific fluorescent antibody reagent has been described, able to detect the pathogen in soil and host tissues (65, 4946).
Nematodes, particularly Meloidogyne incognita, may act synergistically with F. oxysporum (45, 2502; 51, 4037; Saadabi et al., 1986; 53, 561; 55, 5758; 56, 233, 3047; 60, 328; 62, 1052; 65, 4947; 67, 798; 69, 257). Rhizoctonia solani may also act in combination with F. oxysporum on some cultivars (67, 4535).
Cultures fall within the range of variation within F. oxysporum (50, 3784), but isolates vary in their morphological characteristics and pathogenic potential (51, 2519; 52, 134, 2949, 2950; 54, 2824; 58, 242; 59, 5206; 60, 5946; 61, 2298; 63, 2227; Sedova & Guseva, 1985; 68, 4807). Optimal growth conditions (51, 2510; 52, 2849, 3948), enzyme activities (49, 2152; 49, 2153; 55, 1262; 56, 4540; 69, 2876), vitamin requirements (59, 2608) and the effect of light (61, 2718) and pH on growth (50, 1803) of strains have been studied. Pathogenicity of isolates declines when grown in agar culture or stored under mineral oil, but may be retained if cultures are stored in sterile soil or in refrigerated cotton tissues (67, 1344). No correlation was found between dehydrogenase activity (57, 3311) or nystatin resistant mutations and virulence (52, 748). ATP activity was reportedly higher in pathogenic than in nonpathogenic strains and the latter less sensitive to 2,4-D (55, 1263). Virulent isolates were reported to have more electrophoretic protein bands (57, 3310). Serology and protein electrophoresis indicated some similarity to F. udum Butler, cause of pigeon pea wilt, and F. oxysporum f.sp. ciceris, cause of chickpea wilt (56, 1485). DNA G+C ratios of the pathogen and host cultivars have been studied (57, 616). Immunoelectrophoresis allowed distinction of races 1 and 4 (57, 3476). Infected plants have modified protein electrophoretic and antigenic profiles (58, 2805). Esterase isozyme patterns differentiated isolates from China into three groups, correlating with geographical origin (61, 6409).
Pathogenicity of heterokaryons forced between auxotrophic mutants has been studied (52, 3703). Heterokaryosis has been reported in strains from China (68, 5573). This requires substantiation in the light of recent work on vegetative compatibility (VC). However, isolates of race 3, collected from 5 sites in 2 regions in Israel were found to belong to a single VC type (68, 2231).
Pectolytic enzymes have been studied (49, 2486; 58, 5871; 59, 306) and a rapid method of quantifying polygalacturonase activity described (57, 2419). Purified polygalacturonase isozymes isolated from the pathogen were shown to induce wilt-like symptoms in cotton shoot cuttings (64, 2562). A correlation has been reported between wilt symptom development and production of polygalacturonases in vitro (63, 4945). Production of phytotoxins has been discussed (55, 5757; 64, 4338; 69, 1998). Virulence of different strains may (51, 1520; 63, 2892) or may not (49, 2486) correlate with levels of fusaric acid production. The influence of medium composition on in vitro production of fusaric acid (49, 1919; 49, 2486) and methods for screening strains for fusaric acid production have been reported (70, 1817; Paterson & Rutherford, 1991). In vitro production of ethylene by the fungus has been investigated (64, 943).
Control measures include crop rotation, especially with lucerne, use of fungicides and breeding for host resistance (60, 925). Breeding and screening cultivars for wilt resistance is an important means of control (50, 104; 51, 1517; 51, 1518; 53, 563; 54, 161, 2259, 3328, 4942; 55, 1806, 3191; 56, 4061, 4062, 4543; 58, 1772, 3855; 59, 2769, 2770, 5779; 60, 327, 4468; 61, 265, 1742, 4160; 62, 213; 63, 653; Hande et al., 1983; 64, 3079; 65, 1913; Gridi-Papp et al., 1984; 66, 2387; Gridi-Papp et al., 1985; Jeffers et al., 1985; Sappenfield, 1987; Smith, 1987; Bourland, 1988; Bourland & Waddle, 1988; Jones et al., 1988; Roberts et al., 1988; Bourland & White 1989; Johnson, 1989; 69, 1100; 69, 2361; 69, 6446; 70, 4161; El-Zik & Thaxton, 1990; Johnson, 1990; Tan & Liu, 1990). Resistant cotton lines have been produced by direct injection of DNA from a resistant cultivar into the ovaries of a susceptible cultivar (Huang et al., 1986). Breeding strategies should also take into account resistance to M. incognita otherwise wilt resistance may be overcome by nematode infection (54, 4507; 59, 5780; 61, 266; 62, 2500; Shepherd, 1986; 65, 6056). A rapid method for screening for wilt resistance in field plots has been described (65, 5544). After several years continuous cropping with resistant cultivars, wilt incidence may decline (65, 3935) or more virulent strains be selected for (53, 3033). The genetics of host resistance to wilt has been studied in G. hirsutum (52, 4085; 64, 3079; 69, 2363), G. arboreum (Singh et al., 1988), G. barbadense (56, 4542; 64, 3080; 69, 5781) and in interspecific hybrids (62, 4647; 64, 4339).
Resistance in different cultivars correlated with accumulation of phenolic compounds and free gossypol (55, 251; 58, 707; 62, 1987; 64, 4337; Kertykova et al., 1982; 70, 1378). The role of phytoalexins in wilt resistance has been discussed (61, 2895). The significance of lectins in host-pathogen interaction has been studied (67, 4537; 69, 2362). A correlation was reported between host susceptibility and number of cross-reactive antigens against F. oxysporum antisera (54, 3944; 60, 5945; 61, 264; 67, 4538). However, pathogenic and nonpathogenic strains do not necessarily show serological differences (49, 2486; 49, 3082a). Cultures of different ages may have different antigenic properties (62, 1820). A correlation has been reported between the peroxidase and polyphenoloxidase contents of healthy seedlings and their resistance to wilt (64, 2045). Resistant and susceptible cultivars have different peroxidase isozyme activities following infection (57, 5516).
Control by hot water treatment of seed followed by dressing with fungicide can be effective (54, 864). Seed treatment or pre-sowing drench with carbendazim or carboxin reduced seedling mortality (68, 3793). In field conditions, carbendazim followed by Agallol has been reported to give good control (65, 5542). The fungus is able to degrade the fungicide metalaxyl in vitro (67, 3296). Some substituted tetronimides and butyrolactones have been reported to be more effective than carbendazim in vitro and as seed treatments (64, 3446). Herbicides are reported to have an inhibitory effect upon spore germination, growth of the pathogen and the rhizosphere mycofloras of treated cotton plants (49, 1918; 49, 3130; 52, 344; 53, 3811; 62, 2498, 2499, 3811; 63, 5338; Youssef & Heitefuss, 1983; 64, 203; 64, 1133; 64, 3857; 64, 4336; 70, 4161). The inhibitory effect of the herbicide prometryn on metabolic activity of race 3 has been studied (68, 394). Conversely, herbicides may stimulate release of sugars from roots, so increasing rhizosphere population levels (62, 3880; 67, 3239; 70, 1378). Herbicides may also influence cell-wall degrading abilities of the pathogen (68, 3682) and stimulate phytoalexin production by the host (63, 4819). Nematicides may also inhibit the fungus (56, 5422). Soil fumigants may cause a significant reduction in wilt losses (58, 3309) by reducing soil populations of the fungus and/or nematodes. Caffeic acid was reported to inhibit the pathogen and reduce wilt (59, 2771).
Cross-protection using non-pathogenic strains of F. oxysporum has been investigated (59, 3776; 63, 4943; 66, 3387). Antagonistic bacteria and actinomycetes are common in soil and the rhizosphere of cotton plants (51, 1522, 1523, 1524, 2516, 2517, 4039; 52, 1437 53, 4295; 56, 5467; 57, 3477; 60, 2041, 5453; 65, 4255; 66, 619). Antagonistic isolates of Trichoderma harzianum were reported to be able to reduce incidence of wilt in glasshouse conditions (56, 232; 65, 5926). Interactions between F. oxysporum, Trichoderma harzianum, seed exudates and nutrient levels in the rhizosphere have been investigated (68, 2533). Soil solarization has been used either singly (63, 1810; 67, 2825) or in combination with fungicide (68, 51) to reduce population levels of the pathogen. Pinus litter extract promoted germination of F. oxysporum chlamydospores in soil but caused lysis of germ tubes (49, 959). Peppermint (Mentha piperita) has been reported as a possible means of wilt control (69, 256). Oils, especially eugenol, from sweet basil (Ocimum basilicum) were inhibitory to the pathogen in vitro (63, 5290). Crop rotation has been shown to reduce wilt incidence (51, 2513). Planting date may have a significant effect on disease severity (Jeffers et al., 1986). Wilt of G. hirsutum is often more severe in acid, sandy soils (55, 2736). Fertilisers may influence wilt levels (55, 1264, 253, 2735). Wilt may be lessened by adding lucerne compost plus ammonium nitrate to soils low in organic matter (53, 3494), or with calcium ammonium nitrate fertilizer as compared to urea or ammonium sulphate (70, 836). Mineral uptake by the fungus in vitro has been studied (49, 1917; 49, 2765).

LITERATURE: Bourland, F. M. (1988) Crop Science 28: 200-201. Bourland, F. M. & Waddle, B. A. (1988) Arkansas Farm Research 37: 7. Bourland, F. M. & White, B. W. (1989) Crop Science 29: 242-243. El-Zik, K. M. & Thaxton, P. M. (1990) Crop Science 30: 1359-1360. Gridi-Papp, I. L., Fuzatto, M. G., Cavaleri, P. A., Cia, E., Silva, N. M. da, Ferraz, C. A. M., Schmidt, W., Neves, O. da S., Rodrigues Filho, F. S. O., Chiavegato, E. J., Sabino, N. P. Martinelli, E. S., Lazzarini, J. F., Correa, F. A. & Grossi, J. M. M. (1984) Bragantia 43: 405-423. Gridi-Papp, I. L., Cia, E., Fuzatto, M. G., Cavaleri, P. A., Chiavegato, E. J., Ferraz, C. A. M., Sabino, N. P., Kondo, J. I., Soave, J. & Bortoletto, N. (1985) Bragantia 44: 645-658. Hande, Y. K., Padule, D. N. & Lokhande, S. B. (1983) Journal of Maharashtra Agricultural Universities 8: 191-192. Huang, J. Q., Qian, S. Y., Liu, G. L., Xue, D. Y., Ying, M. C., Hong, A. H., Zhou, G. Y., Weng, J., Zhen, Y. S., Gong, Z. Z., Wang, Z. F. & Yang, W. X. (1986) Scientia Agricultura Sinica 3: 32-36. Jeffers, D. P., Garber, R. H. & Roberts, P. A. (1985) Phytopathology 75: 1347. Jeffers, D. P., Hyer, A. H. & Roberts, P. A. (1986) Phytopathology 76: 844. Johnson, W. C. (1989) Agronomy and Soils Departmental Series - Alabama Agricultural Experiment Station 130: 1-20. Johnson, W. C. (1990) Agronomy and Soils Departmental Series - Alabama Agricultural Experiment Station 143: 1-20. Jones, J. E., Beasley, J. P., Dickson, J. I. & Caldwell, W. D. (1988) Crop Science 28: 199-200. Kertykova, E. Kh., Babaev, D. & Agakishiev, D. (1982) Turkmenistan SSR Ylymlar Akademijasynyn Habarlary, Biologik Ylymlaryn 3: 9-13. McLeod, J. M., Witcher, W. & Epps, W. M. (1983) HortScience 18: 249-250. Roberts, C. L., Malm, N. R., Davis, D. D. & Barnes, C. E. (1988) Crop Science 28: 190-191. Saadabi, A. M., Yassin, A. M. & El Tayeb, Y. M. (1986) International Nematology Network Newsletter 3: 28-29. Sappenfield, W. P. (1987) Crop Science 27: 150. Sedova, S. & Guseva, N. (1985) Khlopkovodstvo 9: 23-24. Shepherd, R. L. (1986) Crop Science 26: 233-237. Singh, T. H., Randhawa, L. S. & Chopra, B. L. (1988) Genetica Agraria 42: 141-150. Smith, C. W. (1987) Arkansas Farm Research 36: 7. Smith, S. N., Ebbels, D. L., Garber, R. H. & Kappelman, A. J. (1981) In Fusarium: diseases, biology and taxonomy. Eds P.E. Nelson, T.A. Toussoun & R.J. Cook, Pennsylvania State Univ. Press, Univ. Park & London, pp. 29-38. Tan, L. W. & Liu, Z. D. (1990) Scientia Agricultura Sinica 23: 12-19. Youssef, B. A. & Heitefuss, R. (1983) Zeitschrift für Pflanzenkrankheiten und Pflanzenschutz 90: 160-172.

AUTHOR: D. Brayford

[Numbers in brackets, e.g. (62, 5055), refer to abstracts in the Review of Plant Pathology]

Issued by the International Mycological Institute, Bakeham Lane, Egham, Surrey TW20 9TY, England

© CAB International, 1992, 1997. All rights reserved