Schumann, G.L. and C. J. D’Arcy. 2000. Late blight of potato and tomato. The Plant Health Instructor. DOI: 10.1094/PHI-I-2000-0724-01Updated 2005.
DISEASE: Late blight of potato and tomato
PATHOGEN: Phytophthora infestans
HOSTS: Potato, tomato (economically important hosts)
AuthorsGail L. Schumann, University of Massachusetts, AmherstCleora J. D'Arcy, University of Illinois
Fungicide-treated plants (background) and non-fungicide treated plants (foreground) in an experimental field trial. (Courtesy D. Inglis, copyright-free)
Late blight is the disease that triggered the Irish potato famine of the 1840s. It also was the first plant disease for which a microorganism was proved to be the causal agent, leading to the birth of plant pathology as a science.
Late blight of potato is identified by black/brown lesions (Figures 2,3) on leaves and stems that may be small at first and appear water-soaked or have chlorotic borders, but soon expand rapidly and become necrotic. In humid conditions, Phytophthora infestans produces sporangia and sporangiophores on the surface of infected tissue. This sporulation results in a visible white growth at the leading edge of lesions on abaxial (lower) surfaces of leaves (Figures 4,5,6). As many lesions accumulate, the entire plant can be destroyed in only a few days after the first lesions are observed (Figure 7).
Potato tubers become infected in the field when sporangia are washed from the foliage into the soil. Infections generally begin in tuber cracks, eyes or lenticels. Infected tuber tissues (Figures 8,9) are copper brown, reddish or purplish in color. Sporulation (Figure 10) may occur on the surface of infected tubers in storage or on cull piles. Infected tubers are often invaded by soft rot bacteria which rapidly convert adjoining healthy potatoes into a smelly, rotten mass that must be discarded (Figure 11).
Tomato plants are also susceptible to late blight, and the foliar symptoms are similar. Like potato, infected tomato plants (Figure 12) may be rapidly infected and destroyed by P. infestans. White sporulation (sporangia and sporangiophores) (Figure 13) may be visible in humid weather.
Late blight infections produce dark brown, firm lesions (Figure 14) which may enlarge and destroy the entire tomato fruit. Late blight lesions on tomato fruit are often followed by soft rot and disintegration as described for potato tubers.
Phytophthora infestans...was named by Anton deBary. The name is derived from the Greek: Phyto = plant, phthora = destroyer. P. infestans is a member of the oomycetes, a group of organisms sometimes referred to as the "water molds" which are related to brown algae. The mycelium is hyaline and coenocytic (few septa), and the nuclei are diploid. The formal name for this group of organisms is Oomycota which have been assigned to the Kingdom Stramenopila of the eukaryotes. Oomycetes are no longer considered members of the Kingdom Fungi although they share many biological, ecological, and epidemiological characteristics with fungal plant pathogens.
As is typical of this group, P. infestans produces sporangia on sporangiophores (Figure 15). The sporangiophores are indeterminate. (i.e., they grow and produce sporangia continuously). These stalk-like structures aid in air dispersal of the sporangia. P. infestans is one of the few species in the genus Phytophthora adapted to air dispersal. Sporangia may be dispersed to neighboring fields, but do not generally survive long-distance travel because of desiccation and exposure to solar radiation.
In cool, wet conditions, zoospores will form and emerge (Figure 16) from the sporangia after about two hours. In warmer conditions, sporangia may function as a single spore and germinate directly (Figure 17). Zoospores are biflagellate (have two flagella) (Figure 18), with one tinsel flagellum directed anteriorly and one whiplash flagellum directed posteriorly. After swimming on the surface of the host plant surface, zoospores encyst and infect the plant.
If both mating types (A1 and A2) come into contact with one another, sexual reproduction may occur. A nucleus from the antheridium enters the oogonium. Following karyogamy (the fusion of two nuclei), a thick-walled, diploid oospore (Figure 19) is formed. Before the 1990s, only mating type A1 was present in potato-growing areas outside Mexico (see Historical Importance), so sexual reproduction did not play a significant role in the disease cycle. Now, mating type A2 has migrated to most potato and tomato growing regions of the world, and sexual reproduction is believed to occur in some areas. However, for the past 150 years, survival of P. infestans in most parts of the world has been in infected tuber tissues (see Disease Cycle).
In the absence of the oospore stage, Phytophthora infestans survives between potato crops as mycelium in infected tubers (Figure 9).
If infected tubers are left behind at harvest or dumped (Figure 20) at the edges of fields, sporangia may be produced on the infected tubers or new sprouts the following spring. Air currents carry sporangia to healthy potato foliage. Sometimes seed potatoes can become infected (Figure 21); freshly cut seed tuber surfaces are especially susceptible to infections from airborne spores in contaminated storage facilities.
In the presence of water and at cooler temperatures, sporangia germinate indirectly (Figure 16) by the production of zoospores (Figure 18). At warmer temperatures, the sporangia germinate directly (Figure 17) by the production of a germ tube.
Several days after infection, new sporangia are produced on sporangiophores (Figure 15) which emerge from stomata. The deciduous sporangia may be dispersed by wind or water to new parts of the same potato plant or new plants.
Sporangia may also be washed through the soil to infect tubers. If both mating types come into contact with each other, thick-walled oospores (Figure 19) may be produced to persist in soil or plant tissues. Oospores usually germinate by producing a sporangium (Figure 22).
Temperature and moisture are the most important environmental factors affecting late blight development. Sporangia are formed on the lower leaf surfaces (Figure 4) and infected stems (Figure 5) when relative humidity is < 90%. Sporulation can occur from 3-26°C (37-79°F), but the optimum range is 18-22°C (64-72°F). Sporangia germinate directly via a germ tube at 21-26°C (70-79°F). Below 18° C (65°F), sporangia produce 6 to 8 zoospores which require water for swimming.
Each zoospore is capable of initiating an infection, which explains why disease is more severe in cool, wet conditions. Cool nights, warm days, and extended wet conditions from rain and fog can result in late blight epidemics in which entire potato fields are destroyed in less than two weeks. Infected tubers can sporulate in poorly controlled storage areas (Figure 11) where conditions are too humid. Condensation produces water droplets on the surface of infected tubers which may then cause the pathogen to sporulate and contaminate neighboring tubers, leading to destruction of the entire pile by soft rot bacteria.
Cultivars: No potato cultivar is immune to all strains of P. infestans, but some cultivars are more resistant than others (Figure 23). If the climate in which the potatoes are grown is relatively dry, even low levels of resistance may significantly reduce disease severity. Likewise improved host resistance can be combined with timely foliar fungicide sprays to enhance effective disease management.
Site selection: Good drainage and good air movement will help reduce moisture levels in the canopy. Fields bordered by trees (Figure 24) and dense vegetation should be avoided. The shape of the field may affect the ease and frequency of fungicide applications.
Crop rotation: Rotations of two to three years to non-host crops are recommended. Besides potato and tomato, several weeds and ornamental plants in the Solanaceae family are known to be susceptible to late blight. If oospore production becomes widespread, rotation plans may need to be modified to accommodate this new source of inoculum. The pathogen survives in infected tubers which decay relatively quickly, but oospores may survive in soil for many years.
Elimination of overwintering inoculum: In the absence of oospores, tubers infected during the previous season are the most important source of initial inoculum. Surviving tubers may be found in cull piles (Figure 20) and tubers left in the field at harvest. Culled potatoes should be left on the soil surface to freeze, trucked to a landfill, or buried at least 1 m (3 feet) deep. They also may be fed to livestock provided steps are taken to secure them during transport and dump them only on impervious surfaces. Volunteer plants in the spring should be destroyed to minimize initial inoculum.
Planting of pathogen-free tubers: Only certified seed tubers (Figure 25) should be planted. However, currently (2005), even certified seed tubers may be allowed to have up to 1% incidence of late blight. Fungicide treatments are available for protecting freshly cut seed tuber surfaces.
Hilling: Soil can be made deeper around the base of the plants after emergence of the young potato plants. Hilling helps in early weed control and minimizes tuber infections from sporangia that wash off the leaves of infected plants into the soil.
Irrigation: It is important to minimize the time that leaves are wet to help prevent foliar infection (Figure 26). Irrigation should be timed so that length of the night dew period is not extended- i.e., no late afternoon, early evening, or morning irrigation in order to allow plants time for drying. Excessive irrigation can wash some of the "hilled" soil away from the base of the plants, exposing tubers to greater potential infection.
Fertilization: Excessive nitrogen fertilization increases canopy cover, delays maturity and may reduce yield. Delayed maturity results in more foliage exposed to potential infection for a longer time, increasing the risk of late blight.
Scouting for disease: Field scouting alerts growers that the potential for a severe disease outbreak exists. Scout where moisture is likely to persist (low areas, near hedges and trees) and where fungicide applications may be difficult because of obstructions (corners, trees, utility poles). Infected plants should be burned or plowed under if found in an isolated "hot spot." Current season temperature, relative humidity and rainfall data are used to predict disease outbreaks, based on historical patterns. Some growers apply fungicides when the forecast indicates disease development is likely, which may be more risky than routine preventive fungicide applications. Forecasting systems (Figure 27) for late blight include the Hyre system, the Wallin system, and BLITECAST which incorporates both systems. Some commercial microcomputer units are available to provide forecasts.
Fungicide applications: Fungicide applications (Figures 1, 28) are an important means of late blight management, particularly in humid areas. Contact fungicides are effective and have not resulted in pathogen resistance after many years of use. They coat the leaves to prevent infection, but cannot stop infections once they occur. Therefore, they must be applied before plants are exposed to spores. Systemic fungicides can offer some post-infection control.
Most of the newly introduced strains of P. infestans are of special concern because of their resistance to metalaxyl/mefenoxam. In the early 1990s, some growers lost entire potato crops (Figure 29) to them. Special emergency permits were granted for the use of fungicides not yet registered in the U.S. but available in Europe and other areas. Some new systemic fungicides, such as Acrobat (dimethomorph) and Curzate (cymoxanil), were recently registered. In addition, growers have been encouraged to concentrate on the prophylactic use of contact fungicides. Some growers routinely use contact fungicides early in the season, but then rely on forecasting systems after plants mature and the canopy is established.
At the time of harvest, it is possible that some late blight infections are present in the foliage. To prevent inoculation of the tubers during harvesting, foliage needs to be destroyed so that no green tissue remains. In the past, vines were killed with flames (Figure 30). Herbicides are currently used to assure that plants have died completely before harvest. Infected tubers should be removed before going into storage, and disposed of properly. Blighted tubers do not generally store well under typical storage conditions.
The late blight epidemics of the 1840s triggered the Irish potato famine, but the history of the potato as a food crop is much older. The potato (Solanum tuberosum) originated in the highlands of the Andes in the Lake Titicaca area between Bolivia and Peru, where native people had selected hundreds of different cultivars (Figure 31) for centuries. Most scientists agree that P. infestans originated in Mexico where both mating types of the fungus are commonplace. Where and how the plant and the pathogen first came together is not certain, but late blight epidemics seem to be described in the northeastern U.S. in about 1843 and Europe in 1845. Potato crops failed for a number of years during the cool and rainy "hungry '40s."
Although poor people who were dependent on potatoes for food suffered in many areas, the disaster was greatest in Ireland (Figure 32). One and one-half million people starved and a similar number emigrated during the famine, resulting in a large Irish diaspora in many parts of North America. As with many famines, politics enhanced the suffering. Many Irish peasants grew cereal crops to pay their rent. Although the grain was harvested, it could not be eaten, and was exported to the English landlords throughout the famine. In the 1990s, many exhibits and gatherings in North America and Ireland commemorated the 150th anniversary of the famine.
One reason that the early history of late blight is unclear is that the germ theory of disease had not yet been accepted. Many preliminary studies of various plant diseases had been conducted, but Anton deBary's (Figure 33) (the "father of plant pathology") conclusive studies finally convinced the scientific community that the white sporulation of P. infestans on infected plants was the causal agent of the disease and not the result of spontaneous generation from the decaying vegetation. Thus, late blight signifies the official beginning of the science of plant pathology. These early studies also contributed to Louis Pasteur's germ theory which was proposed 15 years later.
Andrivon, D. 1996. The origin of Phytophthora infestans populations present in Europe in the 1840s: A critical review of historical and scientific evidence. Plant Pathology 45:1027-1035.
D'Arcy, C.J. and D.M. Eastburn. 2000. Late blight. Plants, Pathogens, and People website. http://www.ppp.uiuc.edu/
Eastburn, D.M. and C.J. d’Arcy 1996. Late Blight and the Irish Potato Famine DVS. APS Press (available for purchase at http://admin.apsnet.org/apsstore/shopapspress/Pages/43372.aspx)
Fry, W.E., and S.B. Goodwin. 1997. Re-emergence of potato and tomato late blight in the United States. Plant Dis. 81:1349-1357.
Fry, W.E. and S.B. Goodwin. 1997. Resurgence of the Irish potato famine fungus. BioScience 47:363-371.
Powelson, M.L. and D.A. Inglis. 1998. Potato late blight: Live on the internet. APSnet feature article. http://admin.apsnet.org/publications/apsnetfeatures/Pages/LateBlight.aspx
Stevenson, W.R. 1993. Management of early blight and late blight. Pages 141-147 in: Potato Health Management. R.C. Rowe, ed. American Phytopathological Society Press, St. Paul, MN.
“Tracking Phytophthora infestans, the Irish Potato Famine Pathogen Kit”, a hands-on PCR kit for experienced high school and college classes. Available from Carolina Biological Supply Company, please click here