ARTICLES

Will our national emblem vanish?

The green leaf that means Canada the world over is turning brown. Our graceful maples themselves may be doomed to extinction. The enemy is a mysterious affliction that baffles our forestry experts

FRED BODSWORTH August 15 1959
ARTICLES

Will our national emblem vanish?

The green leaf that means Canada the world over is turning brown. Our graceful maples themselves may be doomed to extinction. The enemy is a mysterious affliction that baffles our forestry experts

FRED BODSWORTH August 15 1959

Will our national emblem vanish?

The green leaf that means Canada the world over is turning brown. Our graceful maples themselves may be doomed to extinction. The enemy is a mysterious affliction that baffles our forestry experts

FRED BODSWORTH

ALEXANDER MUIR, the pious and patriotic schoolmaster who wrote The Maple Leaf Forever, could have been wrong. There is a danger that the maple leaf, “our emblem dear,” may not wave forever. But the foe is not an invading army as the fervently nationalistic Muir envisaged; it is an insidious and mysterious tree disease that has so far struck only in scattered, widely separated spots but may represent a threat to maples everywhere.

The disease, which is killing thousands of maples in various regions of eastern North America, is as yet undiagnosed and only vaguely understood. Some authorities expect it to disappear as mysteriously and quickly as it came. Others fear that it is spreading and that Canada’s national emblem may soon be facing a fight for its life.

Foresters call it a “dieback,” a term they use for a variety of diseases in which the tree “dies back” slowly from the outer twigs and leaves inward. A curious feature is that it seems to have appeared almost simultaneously in at least three widely separated regions — New England, southern Ontario and Wisconsin — and doesn’t seem to have spread from a single centre of infection. Despite an extensive scientific search, no diseasecausing organism has been found; the trees are just dying for no discernible cause. Scientists are not even certain yet that it is the same disease in each region, although the symptoms are the same.

Authorities disagree over whether it’s serious. Nurserymen, arborists, commercial tree surgeons and municipal officials responsible for city trees and parks are alarmed. At their National Shade Tree Conference in Ottawa this spring, some of them claimed that Canada’s proud and stalwart maple is in serious peril. They asked for an immediate large-scale research program to solve the maple dieback mystery.

Federal government forest pathologists, however, take a calmer view, even though the mysterious maple killer has covered thousands of acres in Wisconsin, Michigan and New England, has been found in nearly three hundred woodlots in Ontario and has appeared in city and roadside trees around Toronto and Hamilton.

“Until we find a specific causal organism involved, and until there is stronger evidence that it is spreading, we feel there is no cause for concern,” says Dr. Lewis White, director of the federal government's forest pathology laboratory at Maple, Ont.

“We hope they are right,” says Toronto commercial arborist F. E. Martin, president of the Shade Tree Conference of North America. “But we are getting worried.”

(The two groups have different academic backgrounds. Forest pathologists are university-trained scientists who have specialized in tree diseases, the undisputed experts in the field. The shade-tree people, on the other hand, are mostly horticulturists whose training and experience has been largely in the field of practical tree care and landscaping.)

The shade-tree authorities are well aware of diseases that can wipe out whole species of trees — the blight that made the sweet chestnut virtually extinct in eastern Canada and the United States thirty years ago; and Dutch elm disease, which now seems certain to destroy all eastern Canadian elms except those kept alive by costly annual spraying.

Does a fate like this await the maple?

Forest pathologists claim there is yet no basis for such hasty and gloomy comparisons. Both the chestnut blight and Dutch elm disease were recognized as contagious

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Will our national emblem vanish? continued from page 17

“Already alarmed, shade-tree experts fear an epidemic similar to the birch dieback of the 1930s”

and virulent killers from the Old World as soon as they appeared on this continent. But this is not true of the maple dieback.

Many shade-tree authorities believe, however, that there is already enough evidence to justify their alarm. They point to the similarity between maple dieback and the birch dieback that has killed large numbers of eastern Canadian birches since the 1930s and which still has forest pathologists arguing over its cause, even after twenty years of study. The present maple dieback, they say, could similarly develop into a severe killer, even though it does no* .ppear to be caused or spread by any living parasitic organism.

A few tree diseases are caused by bacteria and viruses, but the commonest and most prolific disease organisms in trees are minute fungi — relatives of mushrooms and toadstools. They spread by dust-like spores and most of them grow as a network of microscopic, thread-like strands which spread through the water-carrying pores of the wood. The killing process is not fully understood, but forest pathologists believe ihe fungi usually block off the water-carrying ducts, strangling the tree's circulatory system, or produce poisons which kill the tree.

First case seven years ago

Many disease-like conditions are actually caused by disturbances in the tree's natural environment. These disturbances may be slow' climatic changes, gradual alterations in soil composition or temperature, or long-term fluctuations in water supply. One theory for birch dieback is that it is caused by an increase of one degree in average soil temperatures through the year as a result of our warming climate.

Environmental disturbances or diseases can affect leaves through "wilts’' or "diebacks.” Wilts occur when water supply to the leaves is cut off by a blockage in a main branch or trunk. The leaves wither, curl and die. A wiltaffected tree thus dies from the inside out, whereas diebacks start in outer tw'igs and progress inward. In diebacks the leaves die in a manner that is more like the natural death of leaves in the fall.

The maples afflicted in the present outbreak show typical dieback symptoms. Leaves turn pale or yellow on a few outer and usually upper branches. Then they usually turn brown or, in a few cases, take on autumn colors. The following year the maple show's only dead naked tw'igs where the disease struck. Meanwhile the paling and browning of leaves has moved to a larger and more central portion of the tree and in another year whole branches die. The whole tree may die in two or three years, although it usually takes longer, and foresters are not certain yet that a maple afflicted with dieback is sure to die.

What now appears to have been the first report of maple dieback was made in 1952. Harold F. Wilson, of Markdale, Ont., had a hundred-acre woodlot, about half of w'hich was maple. He was proud of his bush, kept cattle out of it and cared for it well, because within ten years it could start providing him with

valuable, furniture-quality saw' logs.

He had cleaned all defective trees out of it two years previously but had not examined it carefully for about one year when, in the summer of 1952. he went back to pick w'ild berries. Wilson w'as

shocked to find that in a year a disease had swept through his maples and in sections of the bush half of the trees were already dead. Alarmed, he notified Ernest Danes, provincial zone forester at Ow'en Sound.

Danes examined the hush, expecting to find what is known as VerticiUium wilt, a fairly common disease of maples that never becomes epidemic or a serious killer. Danes recognized that this was something very different from Verticil-

lium and notified federal department of agriculture forest pathologists at Toronto.

Since it was an isolated occurrence, and since woodlot diebacks like this are not uncommon because of altering environmental factors, authorities decided on a wait-and-see policy. The decision seemed justified, because for four years there were no new developments. Wilson’s woodlot continued to die back, but no serious outbreaks of a maple dieback were reported elsewhere.

The next development was in Hamilton. In 1955 Hamilton arborist Gordon McNair launched a two-year tree cleanup program in which all dead wood was cut from the city’s trees. The following year McNair was surprised to discover that in his maples there were many new, freshly killed branches appearing.

"We don’t know how long it had been going on,” he says. "The fact we had a lot of new killing didn’t become apparent until after we had cut out all the old stuff and had a clean start.” McNair sent samples of dying branches to the forest pathology laboratory at Maple but scientists there were unable to find any known disease.

That fall, the staff at Maple got reports that something was killing roadside maples around Whitby, east of Toronto. Dr. James Reid investigated, found thirty-six trees dead and discovered dieback symptoms prevalent along roads throughout an extensive area east and north of Toronto.

Wisconsin’s alarming outbreak

The Hamilton and Whitby occurrences presented the forest pathologists with what is probably their toughest task — diagnosing troubles in city and roadside trees. It’s a tough job because such trees are always fighting for their lives against man’s encroachments. Pavements and sewers drain away their water supply; smoke, dust and fumes foul the air they breathe; compaction of soil by traffic and roadside fill cuts off air from the roots; gas leaks and the salt used on winter ice may ruin their soil; and they are always fighting wounds inflicted by traffic accidents, telephone and powercompany pruners, girdling fence wires, sewer diggers and boys with hatchets.

Because of these hazards, forest pathologists rarely get alarmed about disease signs in city and roadside trees unless there is evidence that the same disease is present in woodlot trees growing under natural and more favorable conditions.

Thus, by the end of 1956, there was a good deal of dieback known to be present in maples around Toronto and Hamilton, and something similar in a single, isolated woodlot near Owen Sound a hundred miles away. It seemed insignificant; Ontario had a dozen treedisease problems that looked much more serious. But before the year ended Canadian foresters learned that during the summer a maple dieback had appeared in Wisconsin, but nobody in the U. S. was alarmed about it.

And then, in the summer of 1957, maple dieback in Wisconsin suddenly exploded to alarming proportions. Almost overnight, Wisconsin maples were dying by the thousands. Dieback there was undergoing a spread so rapid that it could be detected week by week. In one ten-thousand-acre tract almost every maple was infected. Lumber companies, universities, state and federal government departments joined forces in a gigantic research program to find a cause and methods of control. But no causal fungi or bacteria could be detected.

In light of the Wisconsin development, Ontario’s scattered dieback reports suddenly assumed serious significance. Late in the summer of 1957 provincial foresters and rangers were instructed to check carefully for maple dieback in natural forest stands. It was found in several new localities in Grey and Bruce counties south of Georgian Bay — the same general area where Harold Wilson had reported maple dieback five years before. And much of it was in natural woodlots. It seemed to have the same symptoms as in Wisconsin, but it wasn’t killing trees as rapidly.

That winter U. S. foresters reported

that their routine forest-disease surveys the previous summer had turned up much maple dieback in scattered regions from Pennsylvania to Maine. It w'as most serious in Vermont and New Hampshire. It was similar to Wisconsin’s, yet a thousand miles separated the outbreaks, with Ontario about midway between.

As soon as leaves began to unfold in the spring of 1958, the Ontario survey was resumed. It soon became apparent that maple dieback was now fairly widespread in southern Ontario but didn’t exist in the hardwood forests from Muskoka northward. The survey covered three hundred and thirty-nine woodlots

“Searching for maple dieback, forest pathologists found it in 272 out of 339 Ontario woodlots”

in southern Ontario and maple dieback was found in two hundred and seventytwo of them.

Dr. Reid who directed the survey cautioned: “This doesn't mean that two hundred and seventy-two out of every three hundred and thirty-nine woodlots in the province have maple dieback. We wanted to find maple dieback for study purposes and we looked only at woodlots where we had reason to believe that dieback might be present.”

But the dieback was found from Toronto and Lake Simcoe westward to Lake Huron, and from Georgian Bay southward to Lake Erie. It was most severe in two regions — in Grey and Bruce counties, where they had found it the year before, and in a small area south of Lake Simcoe. There seemed to be no link with the Wisconsin outbreak, because five hundred miles and two of the Great Lakes stood between.

Reid and his staff now began tedious and complicated testing to find any attacking organism that might be causing the disease. The culprit might be any one of a great many fungi and bacteria — or none of them.

Samples of affected branches, twigs, leaves or leaf stems were taken from some four hundred maples. At the forest pathology .lab at Maple the samples w'ere surface-sterilized by dipping them in alcohol to kill any fungi or bacteria present as surface contaminants. Then quarter-inch wood chips or leaf fragments were placed on small trays of agar, a gelatin-like culture medium containing chemical nutrients which induce growth of micro-organisms. Any organism present begins growing out on the surface of the agar in a small circular, widening mat. These mats, resembling growths of mold, produce a variety of halo-like concentric patterns and colors, often very beautiful, and microscopic examination will usually identify for the expert the species of organism producing them.

Reid and his staff studied their cultures week after week, but the tiny, spreading, mold-iike mats on the agar plates had no conclusive story to tell.

"We found some VerticiUium wilt,” Reid said, “and all the usual fungi species that produce rot in wood, but nothing turned up often and consistently enough to be the cause of the maple dieback.”

Meanwhile, during the summer of 1958, there was a puzzling but encouraging change in Wisconsin. The dieback there was as prevalent as the year before, but it had lost the deadly virulence it had in 1957. No longer were whole trees dying suddenly as they had the previous year. Wisconsin authorities were so encouraged that several phases of the big research project launched in 1957 were halted.

So 1958 ended with a confusing picture: Maple dieback was known now to be widespread in Ontario: the Wisconsin scare had ended as dramatically and inexplicably as it began; there was no

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change in the New England situation; and nowhere had a cause or explanation been discovered.

There was another question now that needed careful study: is there a definite and demonstrable spread of the dieback from tree to tree, indicating that an organism is involved, or is it turning up haphazardly, suggesting that some widespread environmental influence such as

climate is responsible? This is the problem that Ontario scientists are tackling in 1959.

They are doing it by keeping a detailed, month-by-month and branch-bybranch record of the dieback's progress on some fifteen hundred individual trees. Last spring about seventy plots, each one tenth of an acre, were staked out in diseased woodlots throughout southern

Ontario, most of them at the edge of diseased tracts so that each plot would contain some healthy as well as sick trees. The average plot has around twenty mature trees on it. Every tree has been numbered with yellow paint and its initial condition recorded by placing it in one of seventeen different health categories, from "completely healthy" to “completely dead." Each plot

is being revisited periodically to check on spread within individual trees or to adjacent healthy trees. And other factors such as soil type, moisture content and exposure to wind and sunlight are being studied to determine whether any of these are influencing the dieback and its spread.

It may he many months before anything conclusive has emerged from these studies. Meanwhile, the forest pathologists refuse to get alarmed.

“We have no good evidence that it is spreading seriously, if at all." says Dr. Reid. “It exists over a large region, but it is spotty, and in actual total no great area is involved. It is not nearly as virulent as what Wisconsin had in 1957. What we are doing is purely precautionary so that we’ll be equipped with some basic knowledge about it if it does break out suddenly into something serious.”

Reid doesn’t expect their plot studies to show any significant spreading, nor does he expect now to find that any fungus or bacterial parasite is causing the disease, although sampling and laboratory culturing is still continuing. The fact that it seems to have sprung up independently in several widely separated parts of the continent suggests strongly, he believes, that some general and widespread environmental change may be producing it.

Since the climate of temperate North America has been slowly warming over the past couple of decades, the cause could be something associated with this, such as shortened winter rest periods, diminishing groundwater tables, increasing soil temperatures, an increase in leaf evaporation, or a combination of these. If so. the maple dieback would be an example of nature applying its old law of survival of the fittest, the less adaptable members of the species dying out. the adaptable ones surviving, producing in the process a new maple race adapted to the altered environmental conditions.

Meanwhile city and roadside maples in many areas continue showing severe

deterioration. Hamilton, four years after the tree clean-up. now has another sixty or seventy maples in advanced stages of dieback. At least half the maples on the Queen Elizabeth Way. the super-highway between Toronto and the Niagara Peninsula, are diseased and a number have recently died, and some disease has begun killing maples in Ottawa.

Dr. Reid says it is impossible to tell yet whether the trouble in these city and roadside trees is the same as the dieback in forest trees. "It all looks the same." he says, "but there may be no connection. We don’t know enough about factors affecting shade trees in various areas to be able to say.”

Hamilton arborist Gordon McNair believes it is an infectious disease. “We agree that city trees live in a pretty inhospitable environment,” he said, “but they have always had that environment; it hasn’t changed.”

And the shade-tree authorities are not mollified when government scientists claim that the factors affecting health and vigor of shade trees are too complex to unravel with current knowledge of the subject. The National Shade Tree Conference was critical of the way all present federal government research into tree diseases is concentrated only on trees of timber value.

"A good shade tree in a park, or by a street or highway is as valuable as half a dozen like it back in the bush somewhere." McNair says. “You can’t measure the value of every tree by how many board feet it will provide a sawmill. If scientists don’t understand our shade tree diseases and problems, as they claim, it's time we started finding, out before it is too late."

Is it too late now for the maple? The mystery of the maple dieback seems no nearer an answer, and while its mystery remains there is always a threat. Is it merely Darwin’s evolution remolding a species to fit a changing environment? Or is Canada’s national emblem in dire peril from an unknown and invisible foe? ★