Epidemiology of Potato Black Dennis A. Johnson, Department of Plant Pathology, Washington State University, Pullman, WA 99164-6430 Black dot of potato, caused by the fungus Colletotrichum coccodes, was considered a minor diseased worldwide until the early 1990’s, when reports from South Africa (4), France (1), Israel (12,13), and Idaho (2) and Washington (7) states documented high disease incidences and significant impacts on potato production. Colletotrichum coccodes has been referred to as an elusive pathogen of potato because damage is not readily associated with symptoms unless careful and timely observations are made (11). Yield losses of potato have been documented with very little symptom expression (2). Symptoms may also be over looked because they are frequently expressed late in the growing season and confused with natural plant senescence and verticillium wilt (2,8). Latent infection in tomato by C. coccodes is common (3,10) and likely occurs in potato (5). Colletotrichum coccodes attacks crops within the family Solanaceae including potato, tomato, and pepper. It has been detected in on mint rhizomes (6), and roots of several weed species including velvetleaf (Abutilon theophrasti) and eastern black nightshade (Solanum ptycanthum). The fungus is a soil-, seed- and air-borne pathogen, and survives in soil for long periods as sclerotia. Infected plant debris and sclerotia can be wind blown within and between fields, and infected seed tubers distribute the fungus among potatoproduction areas (9). Significantly greater stem infections developed in plants grown from seed tubers in which C. coccodes had been detected than in plant grown from seed tubers from which C. coccodes had not been isolated (9). Disease symptoms in potato include yellowing and wilting of foliage; cortical rot of roots, stolons and belowground stems; surface lesions and periderm discoloration on daughter tubers; and eventually early death of plants. An amethyst color is common inside the vascular cylinder of stem. Black dot may be confused with symptoms caused by other wilt pathogens, and can be a component of potato early dying syndrome. Small black sclerotia develop externally and internally on senescent and dead plant tissue, on decaying roots, and stems, and on stolons and daughter tubers. On tubers the disease produces a brown-gray blemish, which detracts from their appearance. This is particularly noticeable on packaged tubers washed before sale and is often confused with silver scurf. Dark brown to black lesions may occur on leaves, petioles, and aboveground stems. Lesions on foliage are generally similar to those of early blight, but do not contain concentric rings. Two phases of the disease were identified in the field when isolations were made from below- and aboveground plant tissues. One phase is on belowground stems, roots, stolons, and tubers; the second phase is on aboveground stems and foliage. Infection of one phase is independent of the other. Recently, C. coccodes has been demonstrated to be a major pathogen of potato in the Columbia Basin of Washington and the Snake river Valley of southern Idaho. Observations from several experiments give supporting evidence. First, potato plants in commercial fields are infected early in the growing season, and by mid-season, C. coccodes is associated with a high proportion of plants in fields throughout central Washington. In 1990 and 1991, C. coccodes was isolated from plant stems 38 and 15 days, respectively, after plant emergence; by mid-July the fungus was isolated from over 70% of sampled plants stems in 10 fields in 1990 and 3 fields in 1991 (8). A weak pathogen is not likely to infect plant relatively early in the growing season nor a large proportion of plants by mid-season. Sclerotia of C. coccodes rapidly develop on a large proportion of senescent and dying potato stems, roots, and stolons near the end of each growing season. Such a rapid development of sclerotia on host tissue by a fungus that is not an aggressive saprophyte, such as C. coccodes, indicates that infections occurred much earlier and are latent until host tissue become senescent or stressed. This is called prior colonization. Second, inoculation of potato foliage in the greenhouse and field with several isolates of C. coccodes showed that most isolates were pathogenic and infections resulted in various combinations of foliar lesions, chlorosis, and wilting, Disease symptoms developed when foliage was lightly wounded with sterile sand and then inoculated with either conidia (spores) or sclerotia and then placed in a moist environment for 3 to 12 hours. Lesions and sclerotia developed on roots, roots were discolored, and root growth was reduced when conidia washed off leaves or were applied directly to soil. C. coccodes was consistently reisolated from symptomatic plants. Third, tuber yield is reduced from infections of roots and below ground stems and of foliage. Yield of Russet Burbank was reduced after foliage was wounded with sterile sand and inoculated with C. coccodes. In the greenhouse, total yield was significantly reduced in two tests by 32 % and 19%, respectively. Mean tuber weight was significantly reduced by 29% and 43 %, respectively. In the field, total yield was significantly reduced by 7%, 11%, and 12%, and weight of No.’s was significantly reduced by 12%, 16% and 18% in trials over three years (5). Yields were decrease more in growth chambers at daily temperatures of 73-82 F than at 64 C from infections of roots and below ground stems of Russet Burbank and Norkotah Russet. Yields were reduced by 22 to 30% from below ground infections in Israel (12). Currently, black dot is not satisfactorily managed in commercial fields. Plant stress from heat and other factors increase disease severity. Soil fumigation has not been show to reduce disease severity. The fungicide, Azoxystrobin (Quadris) significantly reduced incidence of C. coccodes on seed-tubers (unpublished data) and has reduced black dot incidence in the field, but an economical disease control program in commercial fields has not been demonstrated with the material. Timing and frequency of applications need to be defined. Cultural practices will be key factors for black dot management in the future. The following practices will aid in reducing the severity of black dot: plant seed tubers with relatively low levels of C. coccodes, rotate out of potatoes for at least three years between potato crops, manage weeds in all rotation crops, manage soil fertility and irrigation water to maintain plant vigor, and manage soil to protect the crop, especially early in the season, from blowing sand. Literature Cited 1. Andrivon, D., Ramage, K., Guerin, C., Lucas, J.M. and Jouan, B. 1997. Distribution and fungicide sensitivity of Colletotrichum coccodes in French potato-producing areas. Plant Pathology 46:722-728. 2. Barkdoll, A.W., and Davis, J.R. 1992. Distribution of Colletotrichum coccodes in Idaho and variation in pathogenicity on potato. Plant Dis. 76:131-135. 3. Cerkauskas, R.F. 1988. Latent colonization by Colletotrichum spp.: Epidemiological considerations and implications for mycoherbicides. Can J. Plant Pathol. 10:297-310. 4. Denner, F.D.N., Millard, C.P., Geldenhuys, A., and Wehner, F.C. 1997. Treatment of seed potatoes with prochloraz for simultaneous control of silver scurf and black dot on daughter tubers. Potato Res 40:221-227. 5. Johnson, D.A. 1994. Effect of foliar infection caused by Colletotrichum coccodes on yield of Russet Burbank potato. Plant Dis. 78:1075-1078. 6. Johnson, D.A., Douhan, L.I., and Geary, B. 2002. Report of Colletotrichum coccodes associated with Mentha. Plant Dis. 86:695. 7. Johnson, D.A., and Miliczky, E.R. 1993. Effects of wounding and wetting duration on infection of potato foliage by Colletotrichum coccodes. Plant Dis. 77:13-17. 8. Johnson, D.A., and Miliczky, E.R. 1993. Distribution and development of black dot, Verticillium wilt, and powdery scab on Russet Burbank potatoes in Washington State. Plant Dis. 77:74-49. 9. Johnson, D.A., Rowe, R.C., and Cummings, T.F. 1997. Incidence of Colletotrichum coccodes in certified potato seed tubers planted in Washington state. Plant Dis. 81:11991202. 10. Pantidou, M.E., and Schroeder, W.T. 1955. Foliage as a source of secondary inoculum for tomato anthracnose. Phytopathology 45:338-345. 11. Thirumalachar, N.S. 1967. Pathogenicity of Colletotrichum atramentarium on some potato varieties. Am. Potato J. 44:241-244. 12. Tsror (Lahkim), L., Erlich, O., Hazanovsky, M. and Peretz, I. 1994. Colletotrichum on potato in Israel, is it a new disease: Phytoparasitica 22:88. 13. Tsror (Lahkim), L., and Johnson, D.A. 2000. Colletotrichum coccodes on potato. Pages 362-373 In: Colletotrichum – Host specificity, pathology and host-pathogen interaction. Prusky, D., Freeman, S., and Dickman, M.B. APS Press. St. Paul, MN.