THE POTATO BLIGHT IS BACK
Although we can never be completely certain, analysis of both nuclear and mitochondrial DNA fingerprints and of Phytophthora infestans allozyme argues strongly that the disease lived undisturbed, in the shadow of the Toluca Volcano, for perhaps thousands of years. As a fungus, it propagated clonally and gradually mutated in the cool, humid, forests that dominated the valleys of Mexico's central highlands. Sometime, possibly early in the 19th century, the relatively benign fungus expanded from its forest hosts to other species, especially the potato. What havoc it may have wrought among the Otomi, Huastec, and other agriculturalists is not recorded. The Huastec however, practised (as they do to this day) a highly-sophisticated form of forest management known as te'lom which allowed them to utilise as many as 300 different forest species including 81 species directly for food. Such a diversified production strategy would have kept P. infestans in check , at least up until the time the Spanish introduced crop monoculture.
From the forest to the field
Researcher William Fry at Cornell University theorises that an American biologist may have accidentally brought P. infestans home with him from an expedition to the volcano in the early 1840s, not long before American soldiers occupied the region during the Mexican-American War. What is known is that sometime in the autumn of 1843, the outbreak of a devastating new disease was reported in Philadelphia. Somewhere in the city's outskirts an epidemic was boiling, and no antidote was available. Yet, whether it was a change in the weather -- which had grown unseasonably cool and rainy -- or some other factor, the potato blight did not advance further. Worries subsided until the following year -- again in the autumn -- when the disease seems to have hopped to the maritime provinces of Canada and the American mid-west. It killed wherever it landed. The disease appeared to have been airborne - capable of moving as much as three or four miles a day. Wherever it landed, destruction occurred within 24 hours. But, once again, as quickly as it came, the disease faded into the background. Although it never truly disappeared and, indeed, returned from time to time to repeat its destruction, it never reaped the ruin in North America that it was about to visit upon Europe.
In June of 1845, Phytophthora infestans struck again. Belgian newspapers reported the first signs of the disease, and the country braced itself for disaster. Throughout the summer, P. infestans surfaced in the Netherlands and then Germany. Not long thereafter, it was on the fringes of Moscow, ravaging Spain out to the Canary Islands, and searing the Balkans.
On August 17, 1845, newspapers announced the arrival of the death fungus in Ireland. On October 15th, the British Prime Minister declared Ireland a disaster area. The disease swept from one shore to the other almost overnight and, for almost four years, held sway over the lives of millions. Before it faded -- but, as in America, never vanished -- more than a million (perhaps as many as 1.5 million) Irish were dead, and a quarter of the population had fled.
There were sporadic rumours of the fungus's continuing devastation. Stories from Spain and the Balkans, tales of destruction as far away as China, and in parts of Africa then hardly known to Europeans. Modern DNA probes now show these rumours to have been true. The disease even doubled back from Europe into Brazil where its impact was the same as everywhere else. By the 1860s, however, the rumours petered out and the world gradually forgot. All that was left were the unmarked mass graves and the continuing devastation to the psyche of the nations and the families who survived.
The second epidemic
The fungus remained a muted force among the poor for more than a century but it never again reached the heights of destruction felt in the 1840s. But then, in the mid-1970s, the disease broke free of the volcano's shadow once again. Epidemiologists know for a certainty that a more aggressive strain (dubbed genotype A2) of P. infestans was found in Switzerland in 1981 and that scientific evidence traces the pathogen back to the central highlands of Mexico. In the same year, 1981, the "new" P. infestans struck The Netherlands and Germany. The UK was hit in 1984, and the disease materialized in Poland in 1988 and Ireland in 1989. According to Dutch and American investigators pursuing the fungus, European traders -- likely Belgian and Dutch -- inadvertently carried the disease with them to Egypt in '84, Japan in '85, and then to points as diverse as Rwanda, Israel, and Brazil in the late 1980s. By the beginning of the 1990s, Korea, The Philippines, Taiwan, and Bolivia all reported outbreaks of the new A2 strain. In every encounter, the disease mysteriously presented itself only to fade, reappear, and fade again, causing limited but recurring destruction. Some claimed it was the cool, humid weather that brought it on. Others simply counted their blessings.
By 1992, epidemiologists noticed that P. infestans had changed. Evidence suggests that the two strains of the disease, types A1 and A2, converged sometime that year in a field in British Colombia on Canada's Pacific coast. Not only were there two distinct types of the same disease together, they were mutating rapidly and multiplying differently. Where the fungus had previously evolved, ponderously, through clonal reproduction, the convergence in Canada's far west meant the disease could now propagate, much more aggressively, sexually.
In 1994, like a tropical depression, the "new" sexually-reproducing P. infestans gained hurricane force and leapt through the United States and Canada. The scientific sleuths tracking it counted numerous different forms of the fungus --each more vicious than the last --and the last forms were resistant to every available chemical remedy.
In that same year the new strains appear to have bridged the Atlantic and begun another march through Europe. It is also spreading from cargo shipments to Rwanda and other parts of central Africa, and back to Latin America via Bolivia and Ecuador. In the closing quarter of 1995, investigators know they were dealing with one of the most dangerous plant diseases the world has ever seen. The economic interests at stake are huge. Just the hint of a new potato famine has doubled potato prices in some parts of the United Kingdom. Last year, farmers in New York State, hit by the blight, had $100 million in crop losses added to another $100 million in extraordinary expenses trying to contain the disease. With more virulent forms of the disease cropping up in the US state of Idaho, farmers are braced for an assault on their $587 million potato harvest, and the government is alarmed that their $2.6 billion potato-processing industry is in jeopardy. This pales in comparison to the world-wide implications of a new pandemic: in 1992 the farmgate value of the global potato market was $40 billion and the world potato industry -- including processing -- was valued at $160 billion.
The real threat, however, lies neither in western Europe nor in North America. From a crop originally domesticated in the Andes and, later, cultivated in Central America, the potato has risen to become -- after rice and wheat -- one of the world's most critical sources of carbohydrates and a farm product for 129 countries. Since the 1970s, international agricultural research programmes have evangelised the undoubted merits of the bountiful tuber throughout Africa and Asia. According to one study the nutritional value of the potato ranks second only to eggs and is well-ahead of wheat or beans. A strong case was made that the potato produces more food -- of higher dietary value -- per hectare than any other crop.
Yet, in retrospect, the evangelism seems a little overblown. Even as the A2 strain began its latest march across Europe, the International Potato Centre (CIP) in Lima, Peru, released an epistle from one of its economists arguing that policy-makers in the South "grossly underestimates" the economic and nutritional merits of the potato. Decrying the fact that farmers in the South "account for only 15%" of the world's cultivated potatoes, CIP identified the barriers to increasing potato production as unfounded historic biases and high production costs (commercial tuber seed in the late seventies could cost as much as US$1,000 per hectare). There was not a word about P. infestans and the ongoing ravages of even the original A1 strain.
Belgian and Dutch seed potato companies were quick to follow public research programmes selling their own varieties throughout the Third World. Seed companies created markets in the Middle East, and East Asia. The trade also looped back from the Benelux countries to the crop's centre of genetic diversity in the Andes. The fungus tagged along. Outbreaks of the more aggressive disease genotype have been identified in Bolivia, Ecuador, Colombia, and Brazil. Seed company interest in the Third World market grew as the potato acreage in the North declined. Between 1961 and 1991, land sown to the crop in industrialized countries was almost halved. During the same period, acreage doubled in Asia, and almost tripled in Africa, making the South the growth market for commercial varieties.
As it was 150 years ago, potatoes continue to be the crop of the poor. Some of the world's poorest countries have been encouraged to plant potatoes as a new staple. Researchers now speculate that the original strain of P. infestans spread accidentally from Belgian missionaries into east and central Africa (Zaire, Rwanda, Burundi, Uganda) many decades ago. Today, about 110,000 hectares of this highland area --on both sides of the Zaire-Nile Divide --are seeded, by small farmers with half-hectare plots, to the new crop. Three-quarters of their harvest goes for home consumption.In this region, potatoes can mean the difference between survival and starvation.
Back in Europe, the people likely to suffer most from a new blight, are the Poles, Russians, Ukrainians and (east) Germans who eat as much as two or three times the quantity of potatoes consumed in Western Europe. Russia is the world's number one potato producer. A crop failure in eastern Europe or the republics of former USSR could have disastrous human consequences.
Despite the alarm for the African highlands and eastern Europe, perhaps the greatest danger lies back in the Andes. If the sexually-mutating strains of P. infestans, reach the shores of Lake Titicaca --where potatoes have been grown for almost 6,000 years --then the genetic diversity of the crop could be wiped out. The entire world depends upon the unique Aymara and Quechua-bred cultivars (and their associated species) sown throughout the region. There is a real risk that the fungus could eat away the genetic resources we will need to defeat it.
If potato breeders were unduly complacent about late potato blight in the sixties and seventies, they were properly alarmed by the mid-eighties. By 1992, CIP estimated that the disease was cutting Third World yields by 30% and that fungicide control campaigns, related to late potato blight, were costing the Third World $600 million each year. Global fungicide costs are estimated to be $1.8 billion -- making potatoes the most chemically--intensive food crop in the world. In a frantic effort to outbreed the fast-mutating fungus, CIP released more than 250 new potato clones to 27 countries around the world. Among the hardest hit locations are Rubengeri in Rwanda and Rio Negro in Colombia. Scientists recognize, however, that nothing offers farmers or consumers true security.
At least in part, the present threat is the product of over-enthusiastic potato evangelism, backstopped by aggressive company marketing, foolish breeding strategies, and reliance on a single commercial fungicide. The only widely-used fungicide effective against the disease was, Metalaxyl, developed by Ciba-Geigy, the giant Swiss Pharmaceutical house. It had proven effective against the original strain, but Metalaxyl was impotent in the face of later forms of the Type A1 fungus as well as Type A2 strains. Some international researchers maintain that Metalaxyl, sold under the trade names Rindomil, Apron, Subdue and Acylon, accidentally but inevitably, created the more aggressive disease by forcing the fungus to mutate around the chemical for its own survival. The worry now is that fear of the new strains will push governments to accept still more potent chemicals contributing to a cycle of toxics and disease that will only threaten humanity further.
There are also grounds for questioning the breeding strategies of both public and private institutions. Some years ago, in order to fend off the A1 fungus strain, breeders opted for a strategy of single-gene vertical disease resistance, creating a series of short-lived fungus resistant potato varieties. Breeders put up one resistance gene after another until a succession of 16 different resistance-genes had been thrown into commercial potatoes --each outgunned by a fungus that only grew meaner and leaner with each fight. The first resistance gene stayed in the ring 6 years but by the time breeders released the sixth resistance gene the crop could barely survive a season. Breeders now agree that single-gene resistance was a bad idea. The only real beneficiary was Ciba-Geigy -- still selling metalaxyl to ever more desperate farmers.
The political disease
But then, the problem was, and still is, only in part caused by P. infestans. When the British were criticised in the 1840s for not buying enough food to feed the starving Irish, the government's famine coordinator replied, "Our purchases, as I have more than once informed you, have been carried out to the utmost limit short of seriously raising the price in the London market" The London rulers were clearly more concerned about market prices at home than about the inhabitants of the other island far away. Historians could well argue that the havoc wrecked in the 1840s was not caused so much by P. infestans as by private investment and the marketplace. Historians concur that there was never a food shortage in Ireland. For every shipload of (usually indigestible) food aid that reached Irish docks, six or more shiploads of cereal crops left the same ports for markets in England and Europe. The hungry had no control over this haemorrhaging of food stocks abroad. The land tenure system, taxation, and the mercantile theories of the time were what killed people
Remarkable little seems to have changed over time. On the 16th of October 1995, Agriculture Ministers from 165 nations convened at the Chateau Frontenac in Quebec City to mark FAO's fiftieth anniversary with a special conference on world food security. One of the tasks of this conference was to look at a draft declaration that will be signed by Heads of State at the Food Summit next year. To date, the draft being considered reads more like a stockholders' report than a campaign to vanquish starvation. The word "farmer" arises only once in the brief document. "Investment" or "investor", on the other hand, appears 22 times -- more often than FAO refers to "government". Exchange or interest rates and discussion of GATT's Uruguay Round are more common than the word "hunger". There are more references to the economic or investment "environment" than to the ecological "environment". On the only occasion in the draft Declaration where the word "sanctity" arises, it is in the context of the "sanctity of contracts". The solution to world hunger, it would seem, lies in private investment and the marketplace. This is the language of the IMF, the World Bank and the World Trade Organisation -- not of a United Nations agency dedicated to a war against hunger.
We seem to be turning full circle. One hundred and fifty years ago, a fungus slipped out of the Toluca Valley through the USA and Canada to decimate Ireland and terrorise Europe. Today, more virulent forms of the same fungus have again escaped the eroded forests of Toluca to sweep across North America into Europe and, propelled by international trade, to the Third World. In 1845, the solution to hunger was a free market. In 1995, the answer is said to be the same. Farmers are left to place their faith in the weather and hope for the best.
This article was taken from RAFI Occasional Paper Series, Vol .2, No 6, August 1995. It was edited by GRAIN to fit into a Seedling article format. The original text was prepared by RAFI staffers Pat Mooney, Hope Shand, and Edward Hammond with assistance from Beverly Cross and Jean Christie. The full paper is available from RAFI, 110 Osborne St., Suite 202; WINNIPEG, MB R3L 1Y5; CANADA; Phone: (1-204) 453 52 59, Fax: (1-204) 925 80 34, E-mail: [email protected]. Cost: $US 10, free for Third World NGOs
* Cecil Woodham-Smith, The Great Hunger, Harper and Row Publishers, New York and Evanston, 1962.
* CIP, "Economic Impact of High-Yielding Late Blight Resistant Varieties in the East and Central African Highlands", in CIP, Case Studies of the Economic Impact of CIP-related Technologies, (First Draft), January, 1995.
* Fry, William E. et. al., "Historical and Recent Migrations of Phytophthora Infestans: Chronology, Pathways, and Implications", Plant Diseases, July, 1993, p.653.
* Alcorn, J.B. "Development policy, forests, and peasant farms: Reflections on Haustec-managed forest contribution to commercial and resource conservation" Economic Botany, 38(4), 1984, 389-406.
* "Potato blight mystery: DNA traces fungus to Mexican tomato", Biotechnology Newswatch, July 3, 1995
* Fry, William E. et. al., "Historical and Recent Migrations of Phytophthora Infestans: Chronology, Pathways, and Implications", Plant Diseases, July, 1993, .
* Goodwin, Stephen B. and William E. Fry, "The Genetic Composition of Phytophthora infestans Population in the United States During 1994: A Preliminary Report", (unpublished manuscript), December 19, 1994,
* Sahm, Phil, "Blight Threatens Idaho Economy", The Idaho Statesman, July 25, 1995, p.1B.