August 6, 1997 EMBARGOED UNTIL AUGUST 12
Terence L. Day - 509/335-2806 (office)
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Sidebar: Late Blight, The Disease
PULLMAN, Wash. -- A hundred and fifty years ago a fungus dramatically changed history.
The fungus, Phytophthora infestans, caused the late blight that devastated world potato fields between 1845 and 1850. The most severe consequences were in Ireland where 1 million-1.5 million peasants starved to death and another 1.5 million - 2 million fled Ireland during the great famine. Emigrant included ancestors of John F. Kennedy, 35th president of the United States.
The fungus releases enzymes that dissolve plant tissue and fungus then absorbs it. Leaves and stems die and tubers rot in the ground or in storage.
Dennis Johnson, a Washington State University plant pathologist who specializes in potato diseases, says late blight can be remarkably rapid and destructive. Fields that appear healthy, but containing low levels of disease can be wiped out within days. Importantly, low levels of disease are very difficult to detect. This gives the fungus a head start.
Each lesion in a leaf can produce as many as 300,000 spores per day. Soft-rot diseases often invade potato tubers infected with P. infestans, resulting in "meltdown" of stored tubers. Entire storages must be discarded.
Scientists believe the fungus originated in Mexico, coming to the United States around 1840. The disease was first reported in the Northeastern United States in 1843.
Late blight first appeared in Europe in June 1845 when it was discovered in Belgium. By August it was reported throughout northwestern Europe and southern England. Soon after it was introduced to Asia, Africa and South America.
The disease resulted in the Irish famine for several reasons:
Potatoes (introduced to the British Isles from America in 1586, by Sir Walter Raleigh) had become the basic subsistence food of Irish peasants.
Crops were swiftly and utterly devastated by the disease.
Relief measures were inadequate.
Late blight in potatoes has been difficult at times to control since the Irish Potato Famine, but genetic changes in the population of the late blight fungus recently has made control many times more difficult, Johnson says.
A dramatic increase in late blight in potatoes was observed in the early 1980s in Europe, and subsequently in the Middle and Far East. By March 1996, the problem was so bad that the International Potato Center in Lima, Peru, called for a global initiative to combat late blight.
Johnson says two reasons apparently explain the late blight comeback. Strains of the fungus are more aggressive than previous ones that have migrated into Washington. They also have developed resistence to metalaxyl, a fungicide that potato growers have relied on to stop the fungus in its tracks. At the same time, the fungus has "discovered" sexual reproduction. A second type of P. infestans known as A-2 also has recently migrated to Washington. It is compatible for sexual reproduction with the older type, A-1.
Resistance to drugs is a growing problem throughout the biological world. Until recently late blight in potatoes has been caused by a mode of asexual reproduction. But, beginning in 1995, European scientists confirmed P. infestans is reproducing sexually in the Netherlands and in Poland.
Johnson is convinced that the fungus is reproducing sexually in Northwest potato fields as well.
"We haven't seen sexual spores yet," Johnson says, "but we have DNA fingerprinting data that says P. infestans is reproducing sexually here."
That's bad news for potato growers because sexual reproduction introduces new gene combinations from sexual spores. This introduces more genetic variety in the fungus and that makes it more difficult to control late blight.
Developing resistant potato cultivars becomes more difficult and more aggressive strains of the fungus may result from sexual reproduction.
Spores created by sexual reproduction also help the organism survive adverse conditions such as freezing and drying, and to survive without a host of living plant material.
New strains are colonizing rapidly. One new strain, called US-8, was detected only in New York in 1992 and in Maine in 1993. In 1994 and 1995 it was found in 23 states, including Washington, Johnson says.
Even with the tools of modern science at hand, late blight can be devastating. In 1993 a farmer in the Northeastern United States saw his production fall from 79 tons per acre in 1993 to 14.8 tons in 1994. The value of his crop dropped from $1.2 million to $212,000 while his production costs went from $762,954 to $835,940.
Late blight was first reported in south central Washington during the 1947 growing season, which was unusually cool, cloudy and wet. The next report was 27 years later, in 1974. It has been observed in fields seven of the 16 years between 1974 and 1989.
From 1947 to 1990 the population of P. infestans in this area was composed of old clonal US-1 lineage. Resistance to metalazyl appeared in 1991 and A2 compatibility was detected in 1993.
Johnson believes metalaxyl-resistant strains of the fungus likely were introduced via infected potato seed brought to the Columbia Basin at the beginning of each growing season.
The scientist said 163,000 acres of potatoes in Washington's Columbia Basin and north-central Oregon were affected by late blight in 1995. That was virtually every potato field in the region. Johnson estimated increased costs associated with coping with the problem at $30 million. Costs could run in the $20 million neighborhood this year.
Computer simulations predict 15 percent to 25 percent increased use of prophylactic fungicides may be necessary to control late blight in the U.S. and Canada.
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