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Remarks (public):For a complete description including images see 
Remarks (internal):Infection is mainly through vascular wounds and not via uninjured stems or roots or through callus of healed wounds (18: 498; 29: 285; 30: 137). Infection over a wide soil moisture range with an opt. temp. for infection about 30°C (6: 749), 32°C reported from Japan (13: 123). Chlamydospores are formed within the central cell of the macroconidia (opt. temp. 28°C) and these occur in the parenchyma. After 11 months storage, 91% germinated when immersed in water (46, 417, 1085). Storage at 13°C prevents growth in root tubers (44, 819; 48, 2694). Physiological and in vitro studies have been done in Japan (14: 25; 19: 191). A toxin and a bacteriostatic and bactericidal substance have been reported (28: 193, 410; 44, 2866). Control is through certified healthy plant material (15: 681), fungicides and resistance. Fungicides (22: 510; 23: 374) are only partly effective (generally as dip treatment of propagating material), since they are affected by the relative host resistance and field conditions. They probably increase yields (21: 360; 35: 632; 48: 2694). Resistant varieties of sweet potato are available in U.S.A. and the var. Tinian is widely used in breeding (28: 418; 34: 103; 41: 249). Back crosses to var. Tinian using moderately resistant Fl material gave field immune progeny. Resistance is multifactorial (43: 2037; 46: 1086).
Description type:Non-original description 
Description:Fusarium oxysporum Schltdl.: Fr. f.sp. batatas (Wollenw.) Snyder & Hansen, Am. J. Bot. 27: 66, 1940.
= Fusarium batatatis Wollenw., J. agric. Res. 2: 268, 1914.
= Fusarium bulbigenum var. batatas Wollenw., 1931.
Hosts: Ipomoea batatas.
Disease: An important wilt disease of sweet potato in U.S.A. but apparently of little importance in the tropics. Interveinal yellowing of the leaves is followed by distortion and stunting and the old leaves fall. There is extensive vascular necrosis which may appear purplish below soil level; the cortex may rupture. Infected tubers may rot in storage. Fusaria that cause surface rots are probably different (41: 329). The fungus infects the roots of many plants without causing any external symptoms, viz. cabbage, cotton, cowpea, maize, okra potato, sage, snap bean, soybean, tobacco, tomato and water melon (28: 189; 37: 593). But race 2 causes wilt in Burley and flue cured tobacco (38: 421).
Geographical distribution: General in U.S.A., especially in the northern range of sweet potato production, including the Pacific coast and western states (40: 511). Also reported from Africa (Malawi); Asia (China, Formosa, India, Japan) Australasia & Oceania (Hawaii, New Zealand).
Physiological specialization: A complex relationship exists not only between this forma specialis and its hosts, as carriers or in which it can cause wilt, but possibly also with some other formae speciales of F. oxysporum (22: 456; 38: 421). Two races attacking sweet potato have been reported: R1 which also causes disease in Burley tobacco and R2 which attacks both Burley and flue cured tobacco. Isolates of both races may vary in virulence depending on the host.
Transmission: Through plant material and by any means through soil.
Literature: Harter & Field, Phytopathology 4: 279-304, 1914 (general); Smith & Shaw, Phytopathology 33: 469-483, 1943 (hosts & pathogenicity); Armstrong & Armstrong, Phytopathology 38: 808-826, 1948 (hosts as carriers); McClure, Phytopathology 39: 876-886, 1949, 40: 769-775, 1950 (infection and anatomy); Diener, Pl. Dis. Rept. 39: 918-921, 1955 (fungicides); Armstrong & Armstrong, Pl. Dis. Reptr. 42, 1319-1329, 1958 (physiologic specialization); Hendrix & Nielsen, Phytopathology 48: 224-227, 1948 (other hosts); Nielsen, Phytopathology 59: 508-510, 1959 (storage temps., fungicides and resistance); Jones, Proc. Am. hors. Soc. 94: 207-208, 1969 (inheritance of resistance).

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