About the Author
Gary D. Franc is an Associate Professor of Plant Pathology at the University of Wyoming, where he has statewide responsibilities for teaching research and extension programs related to plant pathology. He received his Ph.D. in Plant Pathology from Colorado State University in 1988, where he studied the epidemiology of potato blackleg. He has more than 18 years of research experience with potatoes and has published research results on diseases of potato, dry bean, and sugar beet. He has carried out numerous investigations on bacterial ring rot, late blight, the aerosol dissemination of bacterial pathogens, and the role contaminated irrigation water plays in the reinfection of healthy seed potatoes.
Potato Late Blight Management Through Cultural Practices
Gary D. Franc
Dept. of Plant, Soil and Insect Sciences
University of Wyoming
Introduction
Late blight is found in nearly all potato-producing
areas of the world and is most destructive when potatoes
are grown under cool, moist conditions. Late blight is
also destructive to tomatoes and several other species in
the family Solanaceae. Although late blight can cause
devastating losses, the impact of this disease can be
substantially reduced through the use of sound disease
management practices.
Cultural Practices for Disease Management
Cultural practices for disease management are
generally defined as those preventing the introduction of
inoculum (the pathogen or its parts that cause infection)
into the field, reducing inoculum survival and build up,
restricting build up of airborne inoculum in the field,
reducing infection rates, and creating conditions
unfavorable for pathogen development. The most effective
programs integrate multiple disease management practices
and do not rely on a single method. Potato producers can
readily integrate most of the cultural disease management
practices suggested below, as they progress through the
growing season.
Elimination of Primary Inoculum. In production areas where A1 and A2 fungal mating-types coexist, oospore formation is possible and soil-borne inocula may persist in the absence of a host. However, very little is known about the role that oospores play in disease development and the efficacy of strategies for the management of soil-borne inoculum. It is possible that oospores are, or will become, important sources of primary inoculum.
Asexual forms of the late blight fungus overwinter only within infected, living plant tissue. Infected seed tubers, tomato transplants, potato cull piles and volunteer potatoes are sources of primary inoculum, and their elimination greatly reduces late blight risk. Surveys in Ireland over a period of 50 years demonstrated that the most important sources of inoculum for late blight "outbreaks" were volunteer potatoes or cull piles, and were less frequently (2/76 outbreaks) associated with infected seed (21). Permitting tubers to freeze during the overwintering period is the most economical means for volunteer and cull management in many North American production areas. Burying, composting, mechanical cultivation, and herbicide treatments are other potential means for volunteer and cull management. Regardless of the method utilized, spore production and spore spread from tuber surfaces and volunteer plants must be prevented.
Berkely in 1846 (22) was probably the first to suggest that Phytophthora infestans overwinters as mycelia in the potato tuber. This "perennial-mycelium" theory was difficult to demonstrate experimentally since infected seed tubers usually decayed. De Bary (7) established that sprouts produced by infected tubers may be invaded by P. infestans and survive long enough to reach the soil surface and produce sporangia. Thus, these "infector" sprouts serve as infection foci from which the fungus is able to spread. In attempts to repeat De Bary’s work, other researchers observed that infected tubers rapidly decayed and that infected sprouts were rarely observed. Van Der Zaag (37) estimated that approximately 1 percent of the infected seed tubers give rise to infected plants. He also estimated that one infected plant per square kilometer (245 acres) was sufficient to initiate annual late blight epidemics in the Netherlands. However, development of the epidemic was dependent upon the number of infection foci, the percentage of the land area occupied by potatoes, cultivar susceptibility as well as environmental conditions (37). In small scale plots, disease spread from infection foci was estimated at 3.7 m (12 ft) per day (23). However, large scale estimates of disease spread, more likely to measure the effects of wind as a dispersal agent, were not made. In one example, infectious sporangia were believed to be carried by wind 11 km (7 miles) to healthy plants located on an island (37).
Deahl recently proposed that sprouts become infected when healthy, sprouted seed tubers are commingled with infected tubers having surface sporulation (9). He observed that sprout infections could remain dormant during stem elongation and eventually served as inoculum sources several months later. The "time-delay" for symptom development associated with tuber-borne inoculum may explain Wallin and Polhemus’ (38) observation that late blight was sometimes traced to fields previously determined to be late blight "free." Boyd (4) observed that late blight developed 42-125 days after planting infected seed tubers. However, he demonstrated that infected seed tubers contaminated surrounding soil and that foliage was inoculated by rain-splash of inoculum from soil and by direct contact between foliage and contaminated soil. As the seed planting depth increased, foliar infection decreased, presumably because of the greater physical barrier provided by the soil. Platt (28) concluded that the response to foliar late blight was not appreciably affected by seed derived through either in vitro or clonal seed selection methods. Although the incidence of late blight tuber rot was generally not significantly different as well, clonally selected Kennebec tubers developed more disease than those originally derived through in vitro culture.
Although infected seed is known to be an important source of inoculum, the role that infected seed and its relative risk as an inoculum source are poorly defined. However, it is highly recommended that growers plant only certified seed from fields with no observable late blight. Although seed certification does not guarantee freedom from disease, planting non-certified "common" seed poses a needless risk.
Cultivar Selection. Most potato cultivars traditionally planted in North America are susceptible to varying degrees with none being totally resistant or immune. However, selectively planting resistant cultivars may slow disease development sufficiently to reduce the need for fungicide. The relative disease reaction of commonly planted cultivars did not change appreciably following infection by new isolates of P. infestans (18).
Environmental and Physiological Factors. Several environmental and physiological factors are known to affect late blight development, including plant nutrition, plant age, the presence of other pathogens and pests, day-length and others. A discussion of these and other factors is included in Thurston (35) and Erwin et al (13). Several factors are discussed below.
Environmental. Prior to the widespread availability of fungicides, potatoes were grown primarily when and where late blight was not likely to be a problem. Planting during the dry season, when enough rain is available to produce a crop yet not too much rain so that late blight is favored, is a method for avoiding late blight that is available to some producers (26). Early planted potatoes suffered less yield loss compared to later planted potatoes, because they were less likely to be exposed to late blight inoculum early in the growth cycle (12).
If leaf and stem tissue becomes infected during the growing season, shaping hills to keep developing tubers well below the soil surface reduces tuber infection, presumably, by diverting water away from the rows (5, 19). Zoospores are believed to swim effectively in many natural soils and are transported rapidly by water moving into soil (13). Avoid planting into heavier soils that are more likely to form cracks and channels for water movement, thus permitting movement of inoculum to tubers (5). Overhead irrigation can create environmental conditions more favorable for late blight development. On a natural substrate, sporulation by P. infestans was inhibited by radiation in the blue region of the spectrum (6). Therefore, time of planting, seed placement depth, soil type, irrigation practice, plant density, canopy architecture, and even planting direction may influence subsequent disease development.
Plant Nutrition. Late blight disease severity can be influenced by N, P, and K fertilization under some growing conditions. Increased N rates applied to soil increased the size of late blight lesions on potato leaves while increased P and K decreased lesion size (2). The amount of P applied was found to have the greatest effect on foliar lesion size. Phosphorus also had a pronounced effect on the percentage of blighted tubers recovered from infected plants (17). The incidence of blighted tubers was reduced by an average of 8 percent (by weight) through the addition of P (17). The addition of N increased the incidence of blighted tubers by approximately 4 percent (17).
In addition to N, P, and K effects, high general (balanced) fertility increased foliar late blight to levels sufficient to kill plants considered to possess general (multigenic) resistance (20). Under conditions of normal fertility, these plants survived greenhouse inoculation with P. infestans.
The mechanisms proposed for increased susceptibility to late blight are increased leaf growth and succulence which provide a greater number of sites favorable for infection (2, 20) and increased canopy growth which provides a more favorable environment for infection (16). Thus, increased disease severity could result even when apparently contradictory data showed individual lesion size was reduced. High N is believed to increase tuber blight by delaying maturity while P accelerates tuber maturity and decreases tuber blight (16).
It is important to recognize that reports of fertility effects on late blight development are not always consistent, and that several mechanisms are frequently proposed to explain the observed results. The effect of fertilizers on late blight development and tuber infection has been summarized (13). Even though many questions remain unanswered about the role plant nutrition plays in late blight development, optimal soil fertility required for producing the anticipated yield should be part of an integrated late blight management program.
Plant Age. Grainger (15) reported that plants were more susceptible to late blight when newly-emerged and during the tuber-forming stage, and that plants at intermediate growth stages, the period of most rapid growth, were less susceptible. Fry and Apple (14) also reported that late blight progressed more rapidly in older plants. The disease suppression afforded by intermediate-aged plants relative to older plants, was equivalent to the disease suppression achieved by weekly applications of 0.3 kg chlorothalonil per hectare. This age effect was more noticeable for late-season cultivars and was less noticeable for early-season cultivars. Van Der Plank (36) reported that some late-maturing cultivars, especially from continental Europe, had considerable resistance to late blight.
Disease Forecasting and Detection. Disease prediction models are based on the duration of temperature, rainfall and/or humidity. Although models are useful in areas where late blight is an annual threat, their use is not well documented for irrigated production areas where the amount of moisture applied to each field varies and inoculum availability is uncertain. Upper temperature limits for disease development appear to be poorly defined and may need to be redefined for new P. infestans strains. Inoculum survival in various plant tissues also needs to be defined for the purposes of debris management as well as for forecasting. Ideally, forecasts enable producers to apply fungicide at the optimal time(s) for disease management.
Careful field scouting is needed to detect late blight as early as possible. Weed control to eliminate alternate hosts will aid in late blight management. Surveys to identify potential hosts of P. infestans may be needed, because a wider host range may exist (1). If pockets of disease development are found, spot treatment with herbicide or tillage to quickly kill infected plants can reduce subsequent disease spread by eliminating inoculum sources. The articles pertaining to forecasting and late blight diagnosis provide additional information.
Fungicide Use. Fungicides are highly effective tools for late blight management when used properly. Thorough coverage is essential for effective disease management. Widespread use of some fungicides has selected for insensitive (resistant) fungal isolates. Label instructions must be carefully followed if fungicide efficacy is to be maintained. Fungicides applied with a low volume sprayer (controlled droplet application sprayers) were not as effective as fungicides applied in greater volumes of water with conventional sprayers (29). Reduced control was attributed to poorer fungicide penetration into the canopy and poorer coverage of foliage. A summary of fungicides and late blight management is provided in the accompanying article.
Harvest Preparation and Tuber Storage. Tuber infection before harvest results from inoculum washed into soil from infected foliage. Tuber infection during lifting results from tuber contact with blighted foliage and/or sporangia surviving in surface layers of the soil. Deahl (9) and others demonstrated that intact mature tubers are infected through eyes, lenticels and wounds and that mature periderm was not readily penetrated by P. infestans. Therefore, proper harvest preparation will reduce tuber infection and loss.
Complete vine kill prior to harvest is essential since the fungus does not sporulate on dead tissue. The immediate and complete killing of infected vines can sometimes prevent infection of daughter tubers (19). Delay harvest to promote pre-harvest tuber decay and to permit sporangia to die on the soil surface (5). When late blight is present, it is commonly recommended to apply protectant fungicides to dying vines to further minimize spore spread and tuber infection. However, pre-harvest intervals listed on fungicide labels must be followed. Misener et.al. (24) found (cv. Green Mountain) no differences between mechanical top pulling and vine desiccation with diquat. However, there was some indication that when both methods were used, increased tuber decay resulted. Do not allow blighted vines to be carried into storage as a general sanitation practice.
Infected tubers should not be stored and tubers from infested fields, if storage is necessary, should only be stored for a short time. Because infected tubers have a high decay potential, continuous storage monitoring for hot or wet spots is necessary. High air movement rates to dry tubers will reduce decay. Tuber storage at 38 F will retard decay significantly while storage at 48 F is likely to result in extensive decay. Dowley (11) demonstrated tuber to tuber spread occurred during in-storage handling when P. infestans was actively sporulating on the tuber surface.
Interaction with Other Pathogens and Pests
The expression of resistance to P. infestans
in potato is affected by both virus and viroid infection.
Plants (cultivars Katahdin and New York 47) secondarily
infected with PVX, PVY, PLRV, and PSTV were more
resistant to P. infestans than were healthy
plants, when the size of lesions, time of sporulation,
amount of sporulation, number of lesions and percentage
of defoliation were used as criteria for determining
resistance (8). Similar results were found by other
researchers working with PLRV, PVX, PVY, PVS and PVM (27,
32). Pietkiewwicz (27) observed that plants infected with
PVY, PVS, PVM and PLRV were more resistant to penetration
by P. infestans while plants infected by PVY, PVX,
PVS, and PVM were more resistant to the spread of P.
infestans. He also observed that less sporulation
occurred on tubers infected with viruses. The increased
late blight resistance associated with virus-infected
plants was visually apparent, even during field
observations (25). Muller and Monro (25) positively
correlated late blight resistance with severity of virus
symptom expression, and concluded that the altered growth
habit of virus-infected plants did not account for the
increased resistance to late blight.
However, Dowley (10) found that infection with PVX increased the number of blighted tubers in the field. Richardson and Doling (32) observed that approximately twice as many tubers harvested from PLRV-infected plants were blighted compared to tubers harvested from asymptomatic plants. They concluded that the microenvironment created by rolled PLRV-infected leaflets was more conducive for late blight development. Apparently, the change in the microenvironment compensated for the increased late blight resistance associated with PLRV infection. This accounted for their field observations that late blight infection centers were associated with PLRV-symptomatic plants as well as the increased incidence of subsequent tuber decay.
Late blight tuber infection readily occurred through powdery scab (Spongospora subterranea) lesions (3, 33). Histological studies revealed that powdery scab sori failed to heal properly, and provided an avenue for infection similar to that provided by tuber injury (skinning and shatter bruise). Field observations suggest that P. infestans does not penetrate through common scab (Streptomyces scabies) lesions (3). Thus, pathogens able to disrupt the periderm or tuber injuries may explain the presence of extensive decay in tubers harvested from fields with a low incidence of foliar late blight.
The application of the insecticides malathion or resmethrin to potato foliage inhibited lesion development by P. infestans (30, 34). The inhibition persisted for at least several days to one week and the inhibitory effects were reduced when treated leaves were washed with tap water prior to inoculation (34). Radial growth of P. infestans was inhibited in vitro when the concentration of insecticides in agar was similar to those applied in foliar sprays. Although the mechanisms of inhibition were not determined, these effects may be particularly relevant when producing a minituber crop in the greenhouse or when conducting research.
The routine application of fungicide sprays for late blight management can increase green peach aphid populations and the incidence of net necrosis (31). Two mechanisms for the increase in aphid numbers and PLRV spread are believed to be involved. First, vines tend to be more difficult to kill later in the season when routinely protected by fungicide, thus, late-season aphid feeding and virus spread is more likely. Second, fungicides used to protect potatoes from foliar pathogens also affect populations of entomophthoran fungi that cause mycoses (fungal infections) that would otherwise kill the aphids. Field studies demonstrated that captafol, mancozeb and metalaxyl are particularly prone to enhancing green peach aphid populations, while chlorothalonil, copper hydroxide and triphenyltin hydroxide resulted in only moderate increases. Laboratory studies showed that captafol, mancozeb and metalaxyl were the least toxic to the green peach aphid and also severely inhibited germination of entomophthoran conidia. The fungicides most toxic to the green peach aphid were chlorothalonil and copper hydroxide and they also had little effect on conidial germination. Thus, the potential exists to upset natural aphid biological control mechanisms and to trigger outbreaks of the green peach aphid.
Selected Literature
1. Abad, Z.G., J.A. Abad and C. Ochoa. 1995. Historical and scientific evidences that support the modern theory of Peruvian Andes as the center of origin of Phytophthora infestans. Phytopathology 85:1127 (abst.).
2. Awan, A.B., and R.A. Struchtemeyer. 1957. The effect of fertilization on the susceptibility of potatoes to late blight. Am Potato J 34:315-319.
3. Bonde, R. 1955. The effect of powdery scab on the resistance of potato tubers to late blight rot. Maine Agricultural Experiment Station Bulletin 538, Orono, ME.
4. Boyd, A.E.W. 1980. Development of potato blight (Phytophthora infestans) after planting infected seed tubers. Ann. Appl. Biol. 95:301-309.
5. Callbeck, L.C. 1950. Late blight of potatoes and its control. Publication 837, Canada Department of Agriculture, Ottawa, Canada.
6. Cohen, Y., H. Eyal, and T. Sadon. 1975. Light-induced inhibition of sporangial formation of Phytophthora infestans on potato leaves. Can. J. Bot. 53:2680-2686.
7. De Bary, A. 1876. Researches into the nature of the potato fungus Phytophthora infestans. J. Royal Agr. Soc., England, Series 2, 12:239-269.
8. de Cubillos, C.F., and H.D. Thurston. 1975. The effect of viruses on infection by Phytophthora infestans (Mont.) De Bary in potatoes. Am Potato J 52 221-226.
9. Deahl, K.L. 1995. Potato Tubers Role in the Late Blight Complex. In: Proc. National Potato Council Seed Seminar 14:10-16.
10. Dowley, L.J. 1973. Effects of primary and secondary infection with potato virus X (PVX) on yield, size, chemical composition, blight resistance and cooking quality of potato variety Kerr’s pink. Potato Res. 16:3-9.
11. Dowley, L.J., and E. O’Sullivan. 1991. Sporulation of Phytophthora infestans (Mont.) de Bary on the surface of diseased tubers and tuber to tuber spread during handling. Potato Research 34:295-296.
12. Erwin, A.T. 1916. Late blight in Iowa. Bulletin No. 163, Agricultural Experiment Station, Iowa State College of Agriculture and Mechanic Arts, Ames, IA.
13. Erwin, D.C., S. Bartnicki-Garcia, and P.H. Tsao. (Eds). 1983. Pp 189-196 In: Phytophthora Its Biology, Taxonomy, Ecology, and Pathology. APS Press, St. Paul, MN.
14. Fry, W.E., and A.E. Apple. 1986. Disease management implications of age-related changes in susceptibility of potato foliage to Phytophthora infestans. Am Potato J 63:47-56.
15. Grainger, J. 1956. Host nutrition and attack by fungal parasites. Phytopathology 46:445-456.
16. Herlihy, M. 1970. Contrasting effects of nitrogen and phosphorous on potato tuber blight. Plant Pathol. 1965-68.
17. Herlihy, M., and P.J. Carroll. 1969. Effects of N, P, and K and their interactions on yield, tuber blight and quality of potatoes. J. Sci. Fd Agric. 20:513-517.
18. Inglis, D.A., D.A. Johnson, D.E. Legard, W.E. Fry and P.B. Hamm. 1996. Relative resistances of potato clones in response to new and old populations of Phytophthora infestans. Plant Dis. 80:575-578.
19. Johnson, H.G. 1959. Late blight of potatoes. University of Minnesota Agricultural Extension Service, St. Paul, MN.
20. Main, C.E. and M.E. Gallegly. 1964. The disease cycle in relation to multigenic resistance of potato to late blight. Am Potato J 41:387-400.
21. McKay, R. 1957. A retrospect of fifty years outbreaks of potato blight in Ireland 1907-1956. The Department’s Journal Vol. LIII 5-10, University College, Dublin, Ireland.
22. Melhus, I.E. 1915. Hibernation of Phytophthora infestans in the Irish potato. J.A.R. 5:71-102.
23. Minogue, K.P., and W.E. Fry. 1983. Models for spread of plant disease: some experimental results. Phytopathology 73:1173-1176.
24. Misener, G.C., H.W. Platt, and W.A. Hodgson. 1990. Effect of mechanical top pulling and chemical top desiccation on the incidence of late blight tuber rot. Am Potato J 67:859-863.
25. Muller, K.O., and J. Munro. 1951. The reaction of virus-infected potato plants to Phytophthora infestans. Ann. Appl. Biol. 38:765-773.
26. Niederhauser, J.S., J. Cervantes, and L. Servin. 1954. Late blight in Mexico and its implications. Phytopathology 44:406-408.
27. Pietkiewicz, J. 1974. Effects of viruses on the reaction of potato to Phytophthora infestans. I. Characteristics of the reaction to Ph. infestans of plants infected with potato viruses X, Y, S, M and leafroll. Phytopath. Z., 81:364-372.
28. Platt, H.W. 1992. Potato cultivar response to late blight as affected by clonal selection and in vitro culture. Am Potato J 69:187-193.
29. Platt, H.W., and J.A. Ivany. 1983. Potato late blight control and top desiccation when pesticides are applied with a controlled droplet and a conventional sprayer. Am Potato J 60:939-947.
30. Populer, C. 1972. Infection of potato leaves by Phytophthora infestans (Mont.) De Bary inhibited by malathion sprays. Meded. Fac. Landbouwwet. Rijksuniv. Gent 37:507-510.
31. Radcliffe, T., D. Ragsdale, and A. Lagnaoui. 1996. Late Blight Fungicides have an Impact on Aphid Control In: Valley Potato Grower (July), Grand Forks, ND.
32. Richardson, D.E., and D.A. Doling. 1957. Potato blight and leaf-roll virus. Nature 180:866-867.
33. Schultz, E.S. 1952. Powdery scab, a precursor for the late blight infection of blight-immune potato tubers. Phytopathology 42:343 (abstr.).
34. Schumann, G., and H.D. Thurston. 1976. Foliar infection of potato by Phytophthora infestans inhibited by two insecticides. Plant Dis. Reptr. 60:734-735.
35. Thurston, H.D. 1971. Relationship of general resistance: late blight of potato. Phytopathology 61:620-626.
36. Van Der Plank, J.E. 1957. A note on three sorts of resistance to late blight. Am Potato J 34:72-75.
37. Van Der Zaag, D.E. 1956. Overwintering an epidemiologie van Phytophthora infestans, tevens enige nieve bestrijdingsmogelijkheden. Tijdschrift over plantenziekien 62:89-156.
38. Wallin, J.R., and D.N. Polhemus. 1956. The growth and development of Phytophthora infestans from potato tubers in steamed soil. Plant Dis. Reptr. 40:534-537.
Tizon tardio es encontrado en casi todas las areas productoras de papa en el mundo y es muy destructivo cuando la papa es cultivado en condiciones de humedad y frio. Tizon tardio es tambien destructivo al cultivo de tomate y otras especies de la misma familia de las Solanaceas. Aunque tizon tardio puede causar perdidad desvastadoras, el impacto de esta enfermedad puede ser reducido con el uso de algunas practicas culturales.
PRACTICAS CULTURALES PARA EL MANEJO DE LA ENFERMEDAD. Las practicas culturales para el manejo de esta enfermedad pueden ser generalmente definidos como preventivos a la introduccion del inoculo (del patogeno o de sus partes que causa infeccion) dentro del campo, reduciendo la sobrevivencia del inoculo y su multiplicacion, restringiendo la multiplicacion del inoculo transportado por aire a los campos, reduciendo la tasa de infeccion y creanado condiciones no favorables al patogeno para su desarrollo. El mas efectivo, es un programa integrado multiple de practicas de manejo y no solamente un simple metodo. Los productores de papa pueden facilmente integrar las practicas culturales de manejo de esta enfermedad que se sugiere lineas abajo.
Las formas asexuales del tizon tardio pasan el invierno solo en tejido infectado, de plantas vivas. Porque semilla de tuberculos de papa, plantulas de tomate, deshechos de papa apilados, y plantas voluntarias de papa son fuentes de inoculo, su eliminacion enormente reduce el riesgo a tizon tardio. En zonas productoras donde los dos tipos de apareamiento coexisten, el inoculo en el suelo (oosporas) pueden persistir en ausencia del hospedero. Sin embargo, muy poco es conocido acerca del rol que las oosporas puedan jugar en el desarrollo y la eficacia de varias estrategias de manejo del inoculo que es transportado en el suelo.
El rol de la semilla infectada en el desarrolo del tizon tardio es pobremente definido. Sin embargo, es muy recomendable sembrar con semilla certificada provenientes de campos donde no ha sido observado infectiones de tizon tardio. Aunque la certificacion de semilla no es una garantia de que sea libre de enfermedad, sembrar con una semilla "comun" no certificada es un riesgo innecesario. Muchas de las variedades de papa tradicionalmente sembrados en Norte America son suceptibles con ningun grado de resistencia o immunidad. Sin embargo, cultivar con variedades resistentes pueden bajar la incidencia del desarrollo de la enfermedad suficientemente hasta reducir la no aplicacion de fungicidas. Si las hojas y los tallos se infectan durante el desarrolo de la planta, arrimando tierra a las plantas permite el desarrolo de los tuberculos debajo de la superficie del suelo reduce la infeccion de los tuberculos.
Los modelos de prediccion de la enfermedad estan basados en el tiempo de duracion de la temperatura, lluvias y humedad. Aunque los modelos son muy usuales en muchas areas donde tizon tardio anualmente esta presente, su uso no esta muy bien documentado en areas productoras bajo riego donde la cantidad de agua que se aplica en cada campo varia y la disponibilidad or presencia del inoculo no es conocido. Idealmente, las predicciones permiten a los productores aplicar fungicidas en la epoca optima para el control de la enfermedad. Cuidadosos reconocimientos de campo es necesario para detectar infecciones de tizon tardio tan pronto como sea posible. Si manchones de la enfermedad en desarrolo son encontrados, deberan ser tratados con herbicidas o enterrar con disco lo mas rapido las plantas infectadas dando lugar a reducir el esparcimiento de subsecunte infecciones, eliminando las fuentes de inoculo.
Aunque el uso de practicas culturales como control no es considerado generalmente, los fungicidas son herramientas muy efectivos para el manejo del tizon tardio cuando son utilizados apropiadamente. Completa cobertura es esencial para un manejo efectivo de la enfermedad. Un uso extenso de algunos fungicidas en el pasado a creado insensibilidad (resistencia) a los aislamientos del hongo. Las instrucciones de las etiquetas deben ser seguidas cuidadosamente si se quiere mantener la eficacia de los fungicidas.
Una preparacion cuidadosa de la cosecha reduce significativamente la infeccion de los tuberculos y perdidas. La destruccion completa de la parte aerea de la planta antes de la cosecha es esencial, debido a que el hongo no puede esporular en tejido muerto. Cuando el tizon tardio esta presente, fungicidas protectivos deberan ser aplicados a los residuos de tejido que quedan a fin de minimizar diseminaciones futuras de de las esporas y infecciones de tuberculos. Los intervalos de precosecha que figuran en las etiquetas de los fungicidas deben ser seguidos. Retrasar la cosecha si la infeccion de los tuberculos ha ocurrido para provocar la decaimiento de la precosecha. Los tuberculos infectados asi como los provenientes de campos infectados no deberian ser almacanados, si fuera necesario recurrir a esta practica solamente deberian ser almacenados por un periodo corto. Porque los tuberculos infectados tienen un poder alto de deteriorarse, un seguimiento constante es necesario para zonas calientes y humedos. Movimiento de aire caliente va ha secar los tuberculos y reducir deterioramiento. Tuberculos almacenados a 38 F retardan significativamente el deterioamiento mientras que tuberculos almacenados a 48 F provocan un extensivo deterioramiento.
