Phytophthora infestans, cause of late blight of potato and the Irish potato Famine, Tom Volk's Fungus of the Month for March 2001, alternate page Tom Volk's Fungus of the Month for March 2001 This month's fungus is Phytophthora infestans, cause of late blight of potato and the Irish potato Famine For the rest of my pages on fungi, please click This is the alternate version of the Fungus of the month for March 2001 that lacks the QuickTime video of swimming zoospores. The Oomycota are now placed in the kingdom Stramenopila, which you may have never heard of. This kingdom was erected to include the Oomycota, the brown algae (giant kelps), the diatoms the yellow-green algae, and the golden-brown algae. Some researchers place everything that's not a plant, animal, fungus, or bacterium in a "dumping ground" kingdom called the Protista. It's likely the Protista will be split into a few dozen kingdoms in the coming years. The slime molds are another group that's put in the Protista.

Most mycologists still include these non-fungal groups in their mycology courses, and researchers who work on these groups form a significant part of any Mycology or Plant Pathology meeting. Ecologically, many of these organisms behave like fungi, especially those that are plant pathogens. We're glad to still have them in our mycology fold. Phytophthora infestans (pronounced fy-TOF-thor-uh in-FEST-ans) is a rather common pathogen of potatoes wherever they are grown, but it is usually not a problem unless the weather is unusually cool and wet. The water is necessary for the spores to swim to infect the leaves of the potatoes; the tubers and roots of the potato are more resistant to the pathogen. The name, meaning "infesting plant destroyer" is especially appropriate, because under the right conditions and with the correct susceptibility genes in the host, Phytophthora can kill off a field of potatoes in just a few days! Phytophthora infestans is so virulent in wet weather because it produces enormous numbers of swimming spores called zoospores in zoosporangia, shown to the left.

The red structures are the sporangiophores poking out of the stomata of an infected potato leaf. The oval-shaped sporangia have fallen off, although a few are still visible in the field of view. The zoosporangia crack open and release dozens of zoospores, as shown in the above video. These zoospores have two flagella; a whiplash flagellum faces the back and pushes the spore through the water and a tinsel flagellum points forward and pulls the spores through the water. The flagella are shown on the scanning electron micrograph above and to the right. I'm sorry I don't know the source of this picture; it was given to me in a set of slides by Dr. Bill Whittingham, with whom I was first a TA in Mycology in 1981. A bit of history of the Irish Potato Famine Late blight of potato is an example par excellence of the impact that a "fungal" disease has had on the political, economic and social atmosphere of several nations.

Although this disease is best known as being responsible for the Irish potato famine in the 1840's we have to go back 3.5 centuries to look at a some of the history of the potato. Before 1500, the potato was unknown except in a few regions of Central and South America, where its native habitat was in mountainous regions. It was cultivated by the Incas in the Andes Mountains and served as a main food staple. There were (and still are) many varieties, none of which resemble the modern Irish potato. The other varieties are not just big bags of starch, but are smaller and very tasty. Spanish seamen carried the potato to Europe, where it was a curiosity in private horticultural gardens for two centuries. It was not often eaten because gardeners knew it was in the same family (Solanaceae) as deadly nightshade. In fact all parts of the potato plants, except the tubers, are poisonous to people. The tubers may become poisonous on exposure to light when they begin to turn green.

Sometime after 1800, Europeans found the potato tuber (really an underground stem anatomically) was edible, and it was quickly adapted as a staple crop-the climate and soil in Europe was similar to that of the Andes and thus ideal for cultivation. The potato was especially attractive to Irish peasants. Why should this be so? Most of the land in Ireland was owned as large estates by absentee English landlords, who made long-term leases to English middlemen. They, in turn, subdivided the estates into small parcels and rented them at high rates to Irish tenants (often to the same people whose families had historically owned the land). Although the Irish peasants were poor, they could pay the high rent in the form of produce, grains, and sometimes pigs. Thus the main problem for tenants was to have a crop to sustain the family for almost a year while growing conditions were adverse. The potato provided the perfect solution. It gave a good yield and satisfied their hunger-- because of its bulk, stomachs were distended from 8-14 pounds (4- 6 kg) of potatoes per person per day!! Think about a 10 pound bag of potatoes; that's a lot of potatoes!

This was virtually all the peasants had to eat during the winter months--the average family consumed up to a ton of potatoes per month. The potato did well for the Irish, for the population of Ireland exploded from 4.5 million in 1800 to about 8 million in 1845. This is particularly amazing because most of the population was dependent on the potato for their nutrition for 10 months of the year. But then came the late blight of potato. People noticed localized outbreaks of the disease during the early 1800's, although they didn't know the cause. There was always a background level of the disease, but it didn't become a problem until 1845. An ominous warning appeared in the Gardener's Chronicle and Agricultural Gazette: "A fatal malady has broken out amongst the potato crop. On all sides we hear of destruction. In Belgium the fields are said to have been completely desolated." The disease struck down plants like a hard frost in summer. It was said to spread faster than cholera does in humans.

It reduced the foliage to a putrid mass in a few days, and the tubers were affected to various degrees in a similar way, although they did not rot as rapidly. One amateur mycologist, the Rev. M.J. Berkeley, noticed the mycelium on the leaves and proposed that it was a fungal disease. This was not widely accepted-- scientific thinking at the time dictated that a fungus couldn't be the cause of a disease, so it must be a secondary invader. Of course Rev. Berkeley was right. In September 1845, the journal announced that the disease had become established in Ireland. The weather was unusually cool and wet that year allowing easy distribution of the zoospores of the pathogen. With the tremendous destruction it wrought, famine was inevitable, and (according to some sources) the English realized this. To stave off starvation, they considered importing cereal grains such as wheat, barley, and corn, but at the time the English had Corn Laws (for those of you on this side of the pond, grains in England were called corn, while what we call corn here is called maize in Britain).

The Corn Laws imposed a high tariff on imported grains, but not corn (maize), so they couldn't import enough wheat or barley to sell cheaply to the peasants. The winter of 1845 was disastrous. The stored potatoes were rotting because they had been harvested too early. So desperate were they that many of the stored seed potatoes were eaten, and many rotted. Thus the following year was critical. According to some reports, the English tried importing maize to ward off starvation for the Irish. However, the Irish refused to eat the corn-- it was not as filling as the potato, and they considered it chicken feed. As the growing season of 1846 progressed, those that had salvaged seed potatoes were optimistic, since the new plants seemed very healthy. It seems their prayers had been answered. BUT---. In July 1846 the disease struck again; there was a cool, wet period, just like the year before, allowing the Phytophthora's zoospores to multiply and spread. From that time on the disease was there to stay. In some years (warm and dry), the disease was localized; in wet years, the disease became epidemic.

The corn laws were repealed, but it was too late. Between 1845 and 1860 over a million Irish people died as a consequence of the blight; another 1.5 million emigrated, mostly to the east coast of the United States, where many became New York or Boston policemen (some shown to the right in the 2000 St. Patrick's Day parade in NYC) or workers on the transcontinental railroad (remember that the Irish laid track from the east and the Chinese from the west.) Nearly 150 years later, the Irish population has still not recovered from the disaster caused by the late blight of potato. Only in the past 25 years or so has there been increased fervent study of the history of the potato famine. Many would like to have forgotten the whole thing, but many Irish feel it is important to confront the sociological and political reasons for the famine, which is still responsible for some of the tension and animosity toward the English in Ireland today.

There are many web pages on the subject, and rather than list them all, I recommend you do a web search for "late blight of potato" or "Irish potato famine" and you'll find dozens of sites, many of which deal with the controversial role of the English in the famine. There is certainly no consensus on historical details, and 150 years has really muddied the waters. Interestingly, after many decades of its not being much of a problem, late blight of potato is a re-emerging disease, especially in the United States. The disease had been brought under control by the use of chemical pesticides (fungicides) and other agricultural control practices. Phytophthora was not able to quickly develop resistance because it was primarily reproducing only asexually, through mitosis. This was because there was only one mating type present in North America. However about 15 years ago, the second mating type of Phytophthora (which happens to be a more virulent pathogen) was first noticed in Wisconsin, and had probably by that time already spread throughout much of North America. The presence of the second mating type allows sexual reproduction (meiosis), which allows for quicker recombination of genes.

This in turn leads to quicker development of resistance to pesticides. Late Blight is a much bigger problem today than anyone ever anticipated. Other members of the potato family (Solanaceae), such as tomatoes and eggplant are also affected by late blight, although usually to lesser degrees. I hope you enjoyed hearing the story of this month's fungus. One of the lessons you should get from this is that planting of genetically identical plants throughout the fields is a very bad agricultural practice. When a pathogen gets into the fields it can destroy the crop much more easily if the plants are all genetically identical. We must conserve the genetic diversity of crop plants, much of which lies in the wild relatives of cultivated plants. Plant breeders and plant pathologists still have much work to do. Another lesson you should learn is that diseases have had a great impact on history. This is but one example. There are LOTS of fungi, and each one has an interesting story. For more information about fungi that produce swimming zoospores, please see Zoosporic Fungi Online from the University of Georgia.

If you have anything to add, or if you have corrections or comments, please write to me at volk.thom@uwlax.edu This page and other pages are © Copyright 2001 by Thomas J. Volk, University of Wisconsin-La Crosse. Late blight of potato and tomato APS > Education > Introductory > Plant Disease Lessons > Fungi and Fungus-like Organisms > Oomycetes Late blight of potato and tomato Schumann, G.L. and C. J. D’Arcy. 2000. Late blight of potato and tomato. The Plant Health Instructor. DOI: 10.1094/PHI-I-2000-0724-01 Updated 2005. DISEASE: Late blight of potato and tomato PATHOGEN: Phytophthora infestans HOSTS: Potato, tomato (economically important hosts) Authors Gail L. Schumann, University of Massachusetts, Amherst Cleora 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. Symptoms and Signs Potato stems and leaves 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). Figure 2 Figure 11 Tomato stems and leaves 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. Figure 12 Figure 14 Tomato fruit 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. Pathogen Biology 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. Asexual reproduction 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. Figure 15 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. Figure 16 Figure 19 Sexual reproduction 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). Disease Cycle and Epidemiology Disease Cycle 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. Figure 20 Figure 21 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). Figure 22 Epidemiology 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. Disease Management Preplanting management options 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. Figure 23 Figure 24 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. Figure 25 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.

Management in established potato fields 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. Figure 26 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. Figure 27 Figure 28 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. Figure 29 Figure 30 Management at harvest and in storage 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. Historical Significance 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." Figure 31 Figure 32 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. Figure 33 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. Selected References 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. Eastburn, D.M. and C.J. d’Arcy 1996. Late Blight and the Irish Potato Famine DVS. APS Press (available for purchase at ) 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.

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. Teaching Materials “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 Phytophthora Blight - Biology Crown of summer squash plant covered with spores of Phytophthora capsici (under a microscope) Biology Below you will find answers to some basic questions about how Phytophthora blight infects plants. Click on a question to read the answer, or simply scroll through all of the answers. How does Phytophthora blight spread? What causes Phytophthora blight? Phytophthora blight is caused by an organism called a “water mold.” Water molds look very similar to fungi, but they are actually more closely related to brown algae. The particular water mold that causes Phytophthora blight is called Phytophthora capsici (sometimes abbreviated as P.

capsici). P. capsici is related to another water mold – Phytophthora infestans – which causes late blight on potatoes and tomatoes and destroyed potato crops during the Irish Potato Famine. What vegetables are susceptible to Phytophthora blight? All cucurbits (squash, pumpkins, melons, and cucumbers) are very susceptible to Phytophthora blight, as are sweet and hot peppers. In addition, Phytophthora blight affects tomatoes, eggplants, snap beans, and lima beans, and can survive on some weed species (see list of susceptible crops and weeds ). Infected fruits turn soft and “melt,” while whole plants wilt and die. Check out the Photo Gallery to see what this disease looks like on each of these hosts. How does Phytophthora capsici reproduce? P. capsici reproduces most rapidly in warm and wet or humid weather by producing millions of short-lived, lemon-shaped spores on the surface of infected plants (see some pictures here!). These spores can be splashed from the soil to plants, or between plants, and they can also be carried by moving water in a field.

Each one can also release 20-40 motile spores that can swim short distances through standing water or saturated soil towards plant roots. Both of these spores can be produced very rapidly, and only require the presence of a single isolate of P. capsici. A second type of spore with much thicker walls is produced inside infected plant tissue, and requires the presence of at least two isolates of P. capsici. All P. capsici isolates can be classified as either A1 or A2 isolates, and these thick-walled spores are only produced when A1 and A2 isolates grow close to each other. Although these spores are produced more slowly, they are very important to the life cycle of Phytophthora blight because they can survive for years in the soil until a susceptible crop is planted. For this reason, once these thick-walled spores are in the soil Phytophthora blight is there to stay. More images of spores of the Phytophthora blight pathogen can be found here . Late Blight of Potatoes and Tomatoes Fact sheet Figure 16.

Tomato plants completely defoliated by late blight Control Use of integrated management practices is necessary for successful suppression of potato or tomato late blight. In the absence of sexual reproduction P. infestans requires a living host to survive between seasons. Therefore, sanitation (elimination or exclusion of infected plant parts from a farm) is important in the overall management strategy. Ideally, no infected potatoes should be present in the vicinity of the crop. Volunteer plants that might be infected should be destroyed. Cull potatoes should be frozen, crushed, fed to livestock, or buried under at least 2 feet of soil. Only tubers that are free of P. infestans should be planted. The "Certified" grade for seed potatoes allows up to 1 percent late blight infection. Growers should request information from the seed potato producer as to whether late blight was observed during field or harvest inspections. After planting, additional precautions will reduce the chances of successful inoculations and can suppress development and reproduction of the pathogen. Using resistant cultivars (Figure 17) will reduce the chances of infection and slow the pathogen growth rate if some infections develop.

Early in the season, the lowest labeled rate of protectant fungicide will provide protection and thus prevent a rapid epidemic. Fungicide should be applied either at an appropriate regular interval for the production area or adjusted on the basis of weather. Several forecasting systems that identify favorable weather conditions are available (e.g., Blitecast, Tomcast) and can be used to adjust the intensity of scouting as well as the frequency of fungicide applications. Hilling of potatoes increases the amount of soil between tubers and the soil surface and thus helps protect tubers from sporangia that land on the soil surface. Scouting. Regular inspections of growing crops are important to the overall management of late blight. Because topography and crop growth can influence the microclimate encountered by the pathogen, late blight may be detectable earlier in some areas than in others. It is likely to appear first in wet areas (low spots in the field, areas adjacent to woods and hedgerows, dense crops, or areas adjacent to other features that might shade crops), especially when the macroclimate has been less than optimal for pathogen development. Protectant fungicides are often needed from mid- to late season when plants are growing actively and have a dense canopy.

Applications should be repeated regularly to replace fungicide that has been washed or abraded away and to protect foliage produced since the last application. It is during this time that the more effective fungicides are needed. (Consult current Cooperative Extension recommendations for specific information.) Applications should be more frequent during weather that is favorable to late blight (wet with moderate temperatures) than in unfavorable weather (dry foliage and very cool [<50°F] or very hot temperatures). Applying fungicides. Protectant fungicides are most effective if applied more frequently at low labeled dosages than less frequently at high dosages. This is partly because more frequent applications ensure better coverage. Coverage can be poor when applications are made using very low volumes of water (less than 15 to 20 gallons/acre). Some application systems such as electrostatic sprayers can achieve good coverage with very low volumes of water (5 gallons/acre), but most systems that produce large droplets and small volumes will achieve poorer coverage than those that use smaller droplets and larger volumes of water. Treating a crop exposed to inoculum.

Fungicides that have systemic activity (penetrate into plant tissues) are necessary if a crop has been exposed to sporangia within the last 24 hours. Even if the first infections occurred more than 24 hours earlier, if lesions are visible in the crop and a systemic has not been applied, an effective systemic will probably provide some benefit that is not possible from a protectant. Protectant fungicides (those that are not systemic and cannot penetrate tissue) are ineffective against the pathogen once it has penetrated the cuticle (sometimes within two hours of germination). Thus applications of a protectant fungicide will have no visible effect on disease suppression until six to nine days after application because it takes that long for lesions to be easily visible. Unfortunately, even systemic fungicides (at least those available in 1998) do not suppress all infections and will have little effect on infections that are more than 24 to 48 hours old. Effects from systemic fungicides may be visible within three to four days. Treating "hotspots." A hotspot is a group of infected plants located amid relatively healthy ones.

If very little disease is present in the crop and there are only a few hotspots, the latter should be destroyed as quickly as possible by flaming, disking, and burying the infected foliage or killing the plants with a rapidly acting herbicide. Plants immediately surrounding the hotspot should also be destroyed because they are very likely infected even though the infections are not yet visible. If fungicides are being used, the remainder of the held should be treated with a fungicide that has some systemic activity, and subsequently, applications of a protectant fungicide should be applied on a tight (frequent) schedule. Treating established infections. Once 5 to 10 percent of the foliage is infected it is usually not possible to halt the development or progress of the disease. Currently available (1998) systemic fungicides are inadequate to halt an epidemic at this stage. Only weather that is very dry and hot, both day and night, might temporarily stop the epidemic. Stem infections are very resistant to drying, however, and will sporulate when sufficient moisture is available. Growers can attempt to salvage apparently uninfected tomato fruit but should be aware that some fruit infections will not become visible for several days.

Foliage in such fields should be promptly destroyed to prevent spread to nearby fields or farms. Forecasting. Forecasting schemes and fungicide registrations are constantly changing. Consult Cooperative Extension for the latest information on fungicide registrations, efficacy, and forecasting information. Using fungicides at planting. At the time of this writing, it appears that some systemic oomycete-specific fungicides can protect healthy seed tubers during the seed cutting process. If there is a chance that some seed tubers are infected, use of an effective fungicide will lower the chances that late blight will develop in the subsequent crop. Consult Cooperative Extension recommendations for the most current information. The Future Late blight in the United States may need to be managed very differently in the future than in the past. Before exotic strains were introduced in the early 1990s, the late blight pathogen could only reproduce asexually via sporangia. Sexual reproduction requires two individuals of different mating type (Al and A2), and before the 1990s all strains were of the same mating type. Both mating types of P.

infestans (A1 and A2) are now present in the United States and Canada, however, and have sometimes come into contact. Thus sexual reproduction is now theoretically possible. The spores resulting from sexual reproduction are called oospores. Oospores are thick-walled dormant structures (Fig. 18) that can survive in the absence of living plant tissue. The occurrence of oospores could change the epidemiology of the disease because they can survive in soil over winter or summer (if soil temperatures do not exceed 40°C [= 102°F]). If oospores are produced, the soil may become a source of this pathogen, therefore adding an entirely new dimension to the epidemiology of P. infestans and the control of late blight. The result will be new "sources" of the pathogen. At the time of this writing (1998), there is no evidence that oospores are contributing to the epidemiology of late blight of potatoes or tomatoes in the United States. Nonetheless, the possibility of sexual reproduction exists and growers and scientists need to be alert to this development.

Sexual reproduction will also yield recombinant individuals, thus providing a supply of "new" genotypes among the progeny. Whereas the majority of recombinant progeny are expected to be less problematic than parental strains, it is possible that some progeny could be more problematic. Summary Successful management of late blight relies on an integration of the following tactics: removing sources of the pathogen by eliminating cull potatoes and volunteers and planting only healthy seed tubers; using resistant cultivars when possible and as they become available; scouting locations where late blight might appear first; using a forecasting scheme to gain early warning of weather that is favorable to disease and to adjust frequency of fungicide application or the intensity of scouting; and using appropriate protectant or systemic fungicides. After harvest, store potato tubers at cool temperatures under conditions sufficiently dry that there is no free moisture on tuber surfaces. Control tactics are constantly modified as new information and technology become available, so consult the latest Cooperative Extension publications for the best recent specific recommendations. Useful References Bouma, E., and H. T. A. M. Schepers, eds. 1997.

Proceedings of the workshop on the European network for development of an integrated control strategy of potato late blight. NL8200 AK Lelystad (the Netherlands), Applied Research for Arable Farming and Field Production of Vegetables. Cornell University. (annually). Pest Management Recommendations-Commercial Vegetable and Potato Production. Ithaca, N.Y.: Cornell Cooperative Extension. Fry, W E., and S. B. Goodwin. 1997a. Re-emergence of potato and tomato late blight in the United States. Plant Disease 81:1349-5 7. Fry, W E., and S. B. Goodwin. 1997b. Resurgence of the Irish Potato Famine Fungus. Bioscience 47:363-71. Fry, W E., arid D. Shtienberg. 1990. Integration of host resistance and fungicide to manage potato diseases. Canadian Journal of Plant Pathology 12:111-16. 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 Disease 80:575-78. Ingram, D. S., and P H. Williams. 1991. Phytophthora infestans, the Cause of Late Blight of Potato. London: Academic Press. 273 pages NOT CURRENTLY AVAILABLE: Figure 17. Relative resistances of potato cultivars. Cultivars that are feast resistant are shown on the left-hand side and most resistant ones are shown on the right-hand side. This ranking is derived from a series of experiments in different locations (see Inglis et al. 1996.) This ranking considers foliage reactions only and not tuber reactions (which may be different from foliage reactions).

Question: Which catastrophe was caused by phytophtora infestans?
Answer: Potato Famine