Could the English elm, so sadly laid low by Dutch elm disease, make a comeback? Paul King, who breeds trees at Raine in Essex, is on the case. Nearly 25 years ago he acquired cuttings from a few mature trees. He has now multiplied the tissues to produce a whole new generation of young elms that seem to be resistant (and are on sale for £120 apiece). Scientists at the Forestry Commission’s research centre in Surrey welcome his initiative – they are on the case, too – but are cautious. Resistance, they point out, is a tricky business.
The English elm, Ulmus procera, is probably not a “true” native – Britain has only 39 “truly” native trees – and was most likely introduced by Neolithic farmers from south-east Europe, via Spain. But it is an honorary citizen, treasured for its usefulness and its looks, favourite of landscape painters, notably of Constable; a tree of open woodland but just as happy in hedgerows where, if it was left alone, it flourished by the tens of millions. In the West Country it was known as “the Wiltshire weed”.
The first sign of trouble came in 1910 when the fungus Ophiostoma ulmi, a distant and degenerate cousin of the truffle, started killing trees in mainland Europe. It acquired its name, Dutch elm disease, in 1921 because it was first properly researched in Holland. It arrived in Britain by 1927 and looked very nasty. Happily, the disease died down by the Forties, after killing 10 to 40 per cent of our elms. Dr Tom Pearce of the Forestry Commission predicted, in 1960, that such a thing should not happen again – unless, he added, “the fungus completely changes its present trend of behaviour”.
Which it duly did. A new, closely related species of Ophiostoma appeared in North America – Ophiostoma novo-ulmi. It arrived in Britain in 1967 on imported logs, and throughout the Seventies and into the Eighties it killed about 25 million out of about 30 million elms, including most of the particular English species, Ulmus procera.
Dutch elm disease has all the biological attributes needed to be thoroughly nasty. It is one of the many “wilt diseases” of trees, which spread through the vessels of the xylem and block them. The spores are carried passively with wonderful efficiency in the sap, through the whole tree, and spread via the roots of separate trees that are often joined underground. The spores don’t live long once the tree has died and so should die out as their host succumbs – but they have a trump card: they are carried from tree to tree and from forest to forest by flying bark beetles of the genus Scolytus.
There is some innate resistance among the world’s many species of elm. The Ophiostoma fungus probably arose in Asia, so the Asian elms have evolved in its presence – and have developed considerable resistance. Breeding programmes are afoot in Europe to introduce genes from Asian species into European types by various means – and may yet succeed. Meanwhile, as Paul King has found, even within susceptible species, such as Ulmus procera, there will usually be some resistant strains. If they can be bred, perhaps we will have a new resistant strain.
So why the caution? Well, for one thing, it depends what the tree is really resistant to: the fungus or its insect vector? Paul King’s new trees are probably not resistant to the fungus itself, but are simply less palatable to the beetle. Of course, the fungus can’t usually infest the tree without the beetles – but it surely would be better to be specifically equipped with genes that would protect it even if beetles did get in.
The sad tale of Britain’s elms parallels that of the American chestnut, Castanea dentata – with some intriguing contrasts. For the American Indians and for the first immigrant Europeans, the American chestnut was a wonder tree. Its nuts were a food staple – and supported 40 million wild turkeys for good measure – and its trunks provided timber. There were so many that a squirrel could travel from chestnut to chestnut from Maine to Georgia without setting foot on the ground, or so the story went.
But the overconfident forestry “improvers” of the 19th century were still not content. They began to import Asian species with bigger nuts, to crossbreed. Inevitably, the newcomers came with their own diseases. And the American chestnuts, beset by novel pathogens, succumbed. By the end of the Twenties, the American chestnut, once perhaps the commonest North American broadleaf, was all but gone.
Again, through too much zeal, the Americans felled great swathes of chestnuts to create a firewall against the spread of infection. This failed to contain the disease – but it did, so some biologists suggest, remove the myriad genetic variations from among the wild trees, which might have included some that would have conferred resistance.
By leaving our own beleaguered elms to live on in the hedges, and nurturing the few survivors, as Paul King and others have been doing, we may avoid that final fate. (In truth, the American chestnut might not quite be dead. At least, George W Bush planted one outside the White House on Arbor Day in 2005 – but it is a hybrid: 15 per cent of its genes are from resistant Asian species. It is a sad relic, like an exhumed dodo).
Overall, the message is mixed. We could see the heroic efforts of a few growers and scientists as a triumph of human ingenuity over natural adversity – the continuing tale of “man’s conquest of nature”. Or we could see this endeavour as a desperate, last-ditch attempt to ward off the consequences of our own folly. For these are tales of hubris. We thought we could do what we liked in the name of commerce. But actually, life is more complicated than we ever supposed – and in the end, it is beyond our ken. Cause and effect relationships in nature are non-linear, which means it is intrinsically impossible to predict the outcome, beyond saying it won’t be good.