Fig. 33.—Vertical section through a very young Æcidium of Peridermium Pini (var. acicola), with part of the subjacent tissue of the leaf, h, the mycelium of the parasitic fungus running between the cells of the leaf; immediately beneath the epidermis of the leaf, the ends of the hyphæ give rise to the vertical rows of spores (b), the outermost of which (p) remain barren, and form the membrane of the blister-like body. The epidermis is already ruptured at p by the pressure of the young Æcidium. (After K. Hartig: highly magnified.)
Much more disastrous results can be traced directly to the action of the mycelium in the cortex. The hyphæ grow and branch between the green cells of the true cortex, as well as in the vast tissues beneath, and even make their way into the medullary rays and resin canals in the wood, though not very deep. Short branches of the hyphæ pierce the cells, and consume their starch and other contents, causing a large outflow of resin, which soaks into the wood or exudes from the bark. It is probable that this effusion of turpentine into the tissues of the wood, cambium, and cortex has much to do with the drying up of the parts above the attacked portion of the stem: the tissues shrivel up and die, the turpentine in the canals slowly sinking down into the injured region. The drying up would of course occur if the conducting portions are steeped in turpentine, preventing the conduction of water from below.
The mycelium lives for years in the cortex, and may be found killing the young tissues just formed from the cambium during the early summer: of course the annual ring of wood, etc., is here impoverished. If the mycelium is confined to one side of the stem, a flat or depressed spreading wound arises; if this extends all round, the parts above must die.
When fairly thick stems or branches have the mycelium on one side only, the cambium is injured locally, and the thickening is of course partial. The annual rings are formed as usual on the opposite side of the stem, where the cambium is still intact, or they are even thicker than usual, because the cambium there diverts to itself more than the usual share of food substances; where the mycelium exists, however, the cambium is destroyed, and no thickening layer is formed. From this cause arise cancerous malformations which are very common in pine woods (Fig. 34).
Fig. 34.—Section across an old pine stem in the cancerous region injured by Peridermium Pini (var. corticola). As shown by the figures, the stem was fifteen years old when the ravages of the fungus began to affect the cambium near a. The mycelium, spreading in the cortex and cambium on all sides, gradually restricted the action of the latter more and more; at thirty years old, the still sound cambium only extended half way round the stem—no wood being developed on the opposite side. By the time the tree was eighty years old, only the small area of cambium indicated by the thin line marked 80 was still alive; and soon afterward the stem was completely "ringed," and dead, all the tissues being suffused with resin. (After Hartig.)
Putting everything together, it is not difficult to explain the symptoms of the disease. The struggle between the mycelium on the one hand, which tries to extend all round in the cortex, and the tree itself, on the other, as it tries to repair the mischief, will end in the triumph of the fungus as soon as its ravages extend so far as to cut off the water supply to the parts above: this will occur as soon as the mycelium extends all round the cortex, or even sooner if the effusion of turpentine hastens the blocking up of the channels. This may take many years to accomplish.
So far, and taking into account the enormous spread of this disastrous disease, the obvious remedial measures seem to be, to cut down the diseased trees—of course this should be done in the winter, or at least before the spores come—and use the timber as best may be; but we must first see whether such a suggestion needs modifying, after learning more about the fungus and its habits. It appears clear, at any rate, however, that every diseased tree removed means a source of Æcidiospores the less.
Probably every one knows the common groundsel, which abounds all over Britain and the Continent, and no doubt many of my readers are acquainted with other species of the same genus (Senecio) to which the groundsel belongs, and especially with the ragwort (Senecio Jacobæa). It has long been known that the leaves of these plants, and of several allied species, are attacked by a fungus, the mycelium of which spreads in the leaf passages, and gives rise to powdery masses of orange yellow spores, arranged in vertical rows beneath the stomata: these powdery masses of spores burst forth through the epidermis, but are not clothed by any covering, such as the Æcidia of Peridermium Pini, for instance. These groups of yellow spores burst forth in irregular powdery patches, scattered over the under sides of the leaves in July and August: toward the end of the summer a slightly different form of spore, but similarly arranged, springs from the same mycelium on the same patches. From the differences in their form, time of appearance, and (as we shall see) functions, these two kinds of spores have received different names. Those first produced have numerous papillæ on them, and were called Uredospores, from their analogies with the uredospore of the rust of wheat; the second kind of spore is smooth, and is called the Teleutospore, also from analogies with the spores produced in the late summer by the wheat rust. The fungus which produces these uredospores and teleutospores was named and has been long distinguished as Coleosporium Senecionis (Pers.) We are not immediately interested in the damage done by this parasite to the weeds which it infests, and at any rate we might well be tempted to rejoice in its destructive action on these garden pests. It is sufficient to point out that the influence of the mycelium is to shorten the lives of the leaves, and to rob the plant of food material in the way referred to generally in my last article.