Notes to Chapter XII
The reader will find a summary of such fungi as are here concerned in Massee, A Text-Book of Plant Diseases, 1899, or Prillieux, Maladies des Plantes Agricoles.
For further details the student should consult the works of Frank and Sorauer referred to in the notes to Chapter IX., and Tubeuf, The Diseases of Plants, Engl. ed. 1897, pp. 104-539.
For experiments on the effects of grass on orchard trees, see Report of the Woburn Experimental Fruit Farm, 1900, p. 160.
For the further study of weeds, the interesting bulletins of the Kansas State Agricultural College, 1895-1898, will show the reader what may be done in the matter of classifying them according to their biological peculiarities.
In regard to insects, the reader will find the following list embraces the subject: Somerville, Farm and Garden Insects, 1897; Theobald, Insect Life, 1896; Ormerod, Manual of Injurious Insects, 1890, and Handbook of Insects Injurious to Orchards, etc., 1898.
The admirable series of publications of the U.S. Department of Agriculture under the editorship of Riley and Howard, and entitled Insect Life, 1888-1895, also abounds in information.
Further, Taschenberg's Praktische Insektenkunde, 1879-1880, and Judeich and Nietsche, Lehrbuch der Mitteleurop. Forst. Insektenkunde, 1889.
For an elementary introduction to the study of fungus diseases, see Marshall Ward, Diseases of Plants, Soc. for Promoting Christian Knowledge, London.
CHAPTER XIII.
NATURE OF DISEASE
General and local disease—General death owing to cutting-off supplies, etc.—Disease of organs—Tissue-diseases, e.g. timber—Root-diseases—Leaf-diseases, etc.—Diseases of Respiratory, Assimilatory, and other organs—Physiological and Parasitic diseases—Pathology of the cell—Cuts—Cork—Callus—Irritation—Stimulation by protoplasm—Hypertrophy.
On going more deeply into the nature of those changes in plants which we term pathological or diseased, it seems evident that we must at the outset distinguish between various cases. A plant may be diseased as a whole because all or practically all its tissues are in a morbid or pathological condition, such as occurs when some fungus invades all the parts or organs—e.g. seedlings when completely infested by Pythium, or a unicellular Alga when invaded by a minute parasite; or it may die throughout, because some organ with functions essential to its life is seriously affected—e.g. the roots are rotten and cannot absorb water with dissolved minerals and pass it up to the shoot, or all the leaves are infested with a parasite and cannot supply the rest of the plant with organic food materials, in consequence of which parts not directly affected by any malady become starved, dried-up, or poisoned or otherwise injured by the results or products of disease elsewhere.
In a large number of cases, however, the disease is purely local, and never extends into the rest of the organs or tissues—e.g. when an insect pierces a leaf at some minute point with its proboscis or its ovipositor, killing a few cells and irritating those around so that they grow and divide more rapidly than the rest of the leaf tissues and produce a swollen hump of tissue, or gall; or when a knife-cut wounds the cambium, which forthwith begins to cover up the dead cells with a similarly rapid growth of cells, the callus. Numerous minute spots due to fungi on leaves, cortex, etc., are further cases in point, the mycelium never extending far from the centre of infection.
Many attempts have been made to classify diseases on a basis which assumes the essential distinction of the above cases, and we read of diseases of the various organs—root-diseases, stem-diseases, leaf-diseases, and so forth; or of the various tissues—timber-diseases, diseases of the cambium, of the bark, of the parenchyma, and so on. Furthermore, attempts have been made to speak of general functional disease, of diseases of the respiratory organs, of the absorptive organs, and so forth, as opposed to local lesions.
Critical examination, however, shows that no such distinctions can be consistently maintained, partly because the organs and functions of plants are not so sharply marked off as they are in animals, the diseases of which have suggested the above classification, and partly because all disease originates in the cells and tissues, and it is a matter of detail only that in some cases—e.g. severe freezing or drought of seedlings, or when some ingredient is wanting in the soil—the diseased condition affects practically every cell alike from the first, while in others it spreads more or less rapidly from some one spot.
Even the distinction into physiological diseases versus parasitic diseases cannot be maintained from the standpoint of the nature of the disease itself. All disease is physiological in so far as it consists in disturbance of normal physiological function, for pathology is merely abnormal physiology, no matter how it is brought about. This is not saying that no importance is to be attached to the mode in which disease is incurred or induced: it is merely insisting on the truth that the disease itself consists in the living cell-substance—the protoplasm—not working normally as it does in health, and this, whether want of water, minerals, or organic food be the cause, or whether the presence of some poison or mechanical irritant be the disturbing agent, as also whether such want or irritation be due to some defect in soil or air, or to the ravages of a fungus or an insect.
This being understood I need not dwell on the common fallacy of confounding the fungus, insect, soil or other agent with the disease itself, or of making the same blunder in confusing symptoms with maladies. In this sense, wheat rust is not a disease: it is a symptom which betrays the presence of a disease-inducing fungus, the Rust fungus. Similarly, chlorosis is not a disease: it is a symptom of imperfect chlorophyll action, and the best proof of the truth of both statements is that in both cases the fundamental disease-action is the starvation of the cell-protoplasm of carbohydrates and other essential food matters—in the one case because the fungus steals the carbohydrates as fast as the leaves can make them, in the second because the leaf is unable to make them.
The foundation of a knowledge of disease in plants therefore centres in the understanding of the pathology of living cells.
If a suitable mass of living cells is neatly cut with a sharp razor the first perceptible change is one of colour: the white "flesh" of a potato or an apple, for instance, turns brown as the air enters the cut cells, and the microscope shows that this browning affects cell-walls and contents alike. The cut cells also die forthwith; and the oxygen of the air combining with some of their constituents forms the brown colouring matter which soaks into the cell-walls. The uninjured cells below them grow longer, pushing up the dead débris, and divide across by walls parallel to the plane of the wound, and so form series of tabular cells with thin walls, which also soon turn brown and die, the cell-walls meanwhile undergoing changes which convert them into cork. The living cells deeper down are now shut off from the outer world by a skin, of several layers, of cork-cells, which prevent the further free access of air or moisture. During the period of active cell-division which initiates the cork, the temperature of the growing cells rises: a sort of fever (wound-fever) is induced, evidently owing to the active respiration of the growing cells.
This healing by cork occurs in any tissue of living cells exposed by a cut—leaf-tissue, young stem or root, fruit, cambium, etc.; and the same applies to any other kind of cutting or tearing injury—such as a prick with a needle or the proboscis of an insect, a stripping, or even a bruise.
Such healing is prepared for and carried out very thoroughly in the case of falling leaves and cast branches, the plane of separation being covered by a cicatrix of cork.
If the cell-tissue under the wound is actually growing at the time, however, a further process is observed when the wound-cork has been formed. The uninjured cells below go on growing outwards more vigorously than ever, the pressure of the overlying tissues taken off by the cut having been removed, and, lifting up the cork-layer as they do so, they rapidly divide into a juicy mass of thin-walled cells which is of a cushion-like nature and is termed a Callus. This callus is at first a homogeneous tissue of cells which are all alike capable of growing and dividing, but in course of time it undergoes changes in different parts which result in the formation of tracheids, vessels, fibres and other tissue-elements, and even organs, just as the embryonic tissues of the growing points, cambium, etc., of the healthy plant give origin to new growths. Such wound-wood, however, is apt to differ considerably in the arrangement, constitution and hardness of its parts as compared with normal wood, and its peculiar density and cross-graining are often conspicuous.
If instead of a simple tissue, the cut or other wound lays bare a complex mass such as wood, the resultant changes are essentially the same to start with. The living cells bordering the wound form cork, and then those deeper down grow out and form a callus. The exposure of the wood however, entails alterations in its non-living elements also. The lignified walls of tracheids, fibres, etc., turn brown to a considerable depth, and this browning seems to be—like all such discolorations in wounds—due to oxidation changes in the tannins and other bodies present: the process is probably similar to what occurs in humification and in the conversion of sap-wood into heart-wood in trees. Such wood is not merely dead, but it is also incapable of conveying water in the lumina of its elements, which slowly fill with similarly dark-coloured, impervious masses of materials termed "wound-gum," the nature of which is obscure, but which slowly undergoes further changes into resin-like substances.
The exposure of wood by a wound results also in another mode of stopping up the vessels and so hindering the access of air, loss of water, etc., for the living cells of the medullary rays and wood-parenchyma grow into the lumina of the larger vessels through the pits, forming thyloses, again a phenomenon met with in heart-wood. In Conifers the stoppage of the lumina is increased by deposition of resin, which also soaks into the cell-walls and the wounded wood becomes semi-translucent owing to the infiltration.
Every living cell in an active condition is irritable, and one of the commonest physiological reactions of growing tissues is that of responding to the touch of a resistant body, as is vividly shown by the movements of the Sensitive plant, Dionaea, etc., and by those of tendrils, growing root tips, etc., on careful observation. We have reason for stating that if a minute insect, too feeble to pierce the cuticle, cling on to one side of the dome-shaped growing point of any shoot, the irritation of contact of its claws, hairs, etc., would at once cause the protoplasm of the delicate cells to respond by some abnormal behaviour; and, as matter of experiment, Darwin showed long ago that if a minute piece of glass or other hard body is kept in contact with one side of the tip of a root, the growth on the side in contact is interfered with. Moreover we know from experiments on heliotropism, thermotropism, etc., that even intangible stimuli such as rays of light, etc., impinging unsymmetrically on these delicate cells cause alterations in their behaviour—e.g. arrest or acceleration of growth.
Perhaps the most remarkable class of stimulations, however, is that due to the presence of the entire protoplasmic body of one organism in the cell of another, each living its own life for the time being, but the protoplasm of the host cell showing clearly, by its abnormal behaviour, that the presence of the foreign protoplasm is affecting its physiology. A simple example is afforded by Zopfs' Pleotrachelus, the amoeboid protoplasmic body of which lives in the hypha of Pilobolus, causing it to swell up like an inflated bladder, in which the parasite then forms its sporangia. The Pleotrachelus does not kill the Pilobolus, but that its protoplasm alters the metabolic physiology of the latter is shown by the hypertrophy of the cells, and by the curious fact that it stimulates the Pilobolus to form its sexual conjugating cells, otherwise rare, an indication of very far-reaching interference with the life-actions of the host.
An equally remarkable example is that of Plasmodiophora, the amoeboid naked protoplasm of which lives and creeps about in the protoplasm of a cell of the root of a turnip, to which it gains access through the root-hairs. It does not kill the cell, but stimulates its protoplasm to increased activity and growth and division, itself dividing also and passing new amoebae into each new daughter-cell of the host. Here the processes of stimulation, hypertrophy and further division are repeated, until hundreds or thousands of the turnip root-cells are infected. The externally visible result is the formation of distorted swellings on the root (Finger and Toe), most of the cells of which are abnormally large and filled with amoeboid Plasmodiophora protoplasm, which finally devours the turnip-protoplasm and itself passes over into spores. Here we have most convincing proof of the stimulation of protoplasm by other protoplasm in direct contact with it; and that the metabolism of the host-cells is profoundly altered is shown not only by the abnormal growth of the cells, but also by the starvation of the rest of the turnip plant as the Plasmodiophora gets the upper hand. We have here, in fact, a local intracellular parasitic disease, gradually invading large tracts of tissue and eventually inducing general disease resulting in death—a state of affairs reminding us of cancer in animals.
Irritation and hypertrophy of cells, however, may be induced by parasites which never bring their protoplasm into direct contact with that of the host. Many Chytridiaceae penetrate the cells of plants, and grow inside them as short tubes, vesicles, etc., the protoplasm of which is separated by their own cell-walls from that of the host-cell; nevertheless hypertrophy and abnormal cell-divisions and secretions are induced, and the effect even extends to neighbouring cells—e.g. Synchytrium—showing that some influence is exerted through cells themselves not directly affected. This latter point need not surprise us now we know that the cells of plant-tissues are connected by fine protoplasmic strands passing through the separating cell-walls.
But the invading plant need not actually enter the cells, and may still stimulate them through both its own and their own cell-walls to abnormal growth. This is well shown by the intercellular mycelium of Exoacus and Exobasidium, and the latter affords an excellent illustration of the far-reaching effects of hyphae on the cells (of Vaccinium) into which they do not penetrate. Not only are the cells stimulated to grow larger and divide oftener than normally, thus producing large gall-like swellings, but the chlorophyll disappears, the cell sap changes colour to red, the numerous compound crystals normally found in the tissues diminish in number and are different in shape, large quantities of starch are stored up, and even the vascular bundles are altered in character. All these changes indicate very profound alterations in the physiological working of the protoplasm of the cells of the host, and yet the fungus has done its work through both its own cell-walls and those of the host.
Even harmless endophytic algae in the intercellular spaces of plants may stimulate the cells in their immediate neighbourhood to increased growth, e.g. Anabaena in the roots of Cycads.
Notes to Chapter XIII
With reference to cork-healing and wound-fever the student may consult Shattock "On the Reparative processes which occur in Vegetable Tissues," Journal of the Linnean Society, 1882, Vol. XIX., p. 1; and Shattock "On the Fall of Branchlets in the Aspen," Journal of Botany, 1883, Vol. XXI., p. 306. Also Richards, "The Respiration of Wounded Plants," Annals of Botany, Vol. X., 1896, p. 531; and "The Evolution of Heat by Wounded Plants," Ann. of Bot., Vol. XI., 1897, p. 29.
For details and figures respecting callus, see Sorauer, Physiol. of Plants, p. 175.
In respect to the irritable movements referred to see Darwin, The Power of Movements in Plants, 1880, chapter III. The recent work of Nawaschin, Beobachtungen ueber den feineren Bau u. Umwandlungen von Plasmodiophora, Flora, Vol. LXXXVI., 1899, p. 404, should be read for details and literature concerning "Finger and Toe."
CHAPTER XIV.
NATURE OF DISEASE (Continued)
Actions of poisons in small doses—Results of killing a few cells—Malformation—Enzymes—Secretions and excretions—Acids, poisons, etc.—Chemotactic phenomena—Parasitism—Epiphytes and endophytes—Symbiosis—Galls.
Physiological research has shown that the respiratory activity of cells may be increased by small doses of poisons, and even that growth may be accelerated by them—e.g. chloroform, ether—and, still more remarkable, that fermentative activity may be enhanced by minute doses of such powerful mineral poisons as mercuric chloride, iodine salts, etc., and that the cells may be gradually accustomed to larger doses without injury. Unfertilised eggs of insects have been started into growth by treatment with acids and those of frogs with mercury salts, and the germination of beans quickened by various poisonous alkaloids. In other words, graduated doses of poison may alter the physiological activity of living cells, inducing pathological phenomena, while larger doses kill them.
Now we know at least one parasitic fungus which poisons the cells of its host, and kills them, with similar symptoms to those resulting from excessive doses of the above-named toxic agents. Botrytis hyphæ, living in the cell-walls of plants, but not entering the cells, excretes a poison which kills the protoplasm, and the fungus then feeds on the debris. Numerous other fungi form powerful poisons, but we do not know whether or how they employ them—e.g. Ergot.
It is obvious that if all the young cells of a root-tip or of the apex of a shoot, or those of a young leaf, are growing and dividing regularly, the killing of one or a few cells at one point on the side of the organ must result in irregularities—in malformation—of the adult organ. This has been proved experimentally by destroying a few cells with a needle. It can also be done by planting a minute mycelium of Botrytis laterally on a young organ—e.g. a very young lily-bud. The fungus adheres to the surface, kills a few epidermis cells, and forms a foxy-red spot, which becomes concave as the dead cells lose water and dry. Since the rest of the bud goes on growing, however, while this dead point remains stationary, the latter gradually becomes the centre of a concavity, the growing tissues having grown round it: the bud is deformed. Numerous cases of malformed organs are explained in this way; a minute insect has bitten or pierced the young tissue, or a fungus has killed a minute area, or a drop of acid condensed from fumes in the air is the lethal agent, and so forth. And even on a much larger scale we see the same kinds of agents at work. Wherever a patch of cells is killed whilst those around go on growing, there must result some deformation of the resulting organ, since had the injury been withheld the number and sizes of the cells now fixed in death would have increased and covered a larger area: they now serve to pull over to their side the still living and growing cells. The same results follow on any lateral wound: the killed spot of tissue serves as a point round which the continued growth of other parts of the organ turns. Hence the malformation is in these cases a secondary effect, and not, as in simple hypertrophy, a direct effect of the action of the cells involved in the injury.
There is another class of bodies secreted by fungi, however, which act directly on cells, viz. enzymes—that is, soluble bodies which are able to dissolve cellulose (cytases), starch (diastases), proteids (proteolytic enzymes), and other substances, by peculiar alterations in their constitution. It is by means of its cytase that Botrytis hyphae pierce the cellulose walls of plants, and no doubt in all cases where fungi pierce cell-walls it is by the solvent action of such a cytase, and similarly when haustoria penetrate into the cells. It is also by means of these starch-dissolving enzymes (diastases) and proteolytic enzymes, etc., that the hyphae inside the cells are enabled to make use of the starch, proteids, etc., they find there.
All living cells form materials, resulting from the activity of the protoplasm, which we may compare with the refuse or by-products formed in any great manufacturing industry: these by-products have to be got rid of if they are injurious or noisome (excretions), and if not—i.e. if they are capable of further use (secretions)—they have to be stored away till required. Some of the most prominent of these bodies excreted by fungi are, as we have seen, poisonous acids, such as oxalic acid, enzymes, and organic poisons, such as those in ergot. But similar enzymes, acids, poisons, etc., to those found in fungi are also found in the cells of other plants and animals; for only by means of their solvent actions can processes like digestion and assimilation of the starchy and other materials into the body-substance be accomplished, and we have seen that it is a general property of living cells to form acids, and other excretions and secretions.
Now we know very little about what may happen when an organism—say a fungus—secreting especially one kind of enzyme or poison or other active substance, comes into intimate contact with another—say a leaf-cell—which secretes predominantly others, but what we do know points to the certainty that various complications will occur.
For instance, if certain bacteria which prefer an alkaline medium, and yeasts which prefer an acid environment are mixed in a saccharine solution, it depends on the reaction of the liquid which organism gains the upper hand: if the liquid is acid the yeast may dominate the bacteria; if alkaline it may be suppressed by them.
That a parasite may be prevented from successfully attacking a particular plant is shown by the failure of Cuscuta to establish its haustoria in poisonous plants such as Euphorbia, Aloe, etc., and it has been pointed out that poisonous secretions in the cells of the plant protect them against the penetration of fungi. This cannot be taken as meaning that any poison protects against any parasite, however, for Euphorbia is itself subject to attacks of Uredineae, and Pangium edule, which contains prussic acid and is extremely poisonous to most animals, is eaten with avidity by several insects, while nematode worms can live in its tissues. This is no more remarkable, however, than the fact that Fontaria, a myriapod, secretes prussic acid in its own tissues, or than that certain glands of the stomach secrete free hydrochloric acid, and Dolium forms sulphuric acid in its glands.
There is yet a further point to notice here. It has been proved that certain substances formed in plant-cells, not necessarily nutritive, attract the hyphae of parasitic fungi or repel them, according to the kind and degree of concentration. So clear has this proof been made that it was possible in experiments conducted apart from a host plant, to make the hyphae on one side of an artificial membrane—e.g. collodion—penetrate it by placing one of these attractive (chemotropic) substances in suitable proportions on the other side. The hyphae dissolved holes in the membrane by means of enzymes and plunged into the attractive substance on the other side.
The foregoing sketch gives us a glimpse into the causes at work in parasitism.
Suppose a fungus on the outside of the epidermis of a young organ—say a leaf. It may be unable to penetrate into the plant, and finding no suitable food outside it dies: or it may be satisfied with the traces of organic matter on the epidermis and then lives the life of a saprophyte. Or it may be able to establish a hold-fast on the tender epidermal surface, but without entering the cells, and irritate the developing organ by contact stimulation, inducing slight abnormalities; if in its further, purely superficial growth such an epiphyte covers large areas of the leaf, and especially if the hyphae are dark coloured—e.g. Dematium and other "Sooty Moulds"—injury may be done to the leaf owing to the shading action which deprives the chlorophyll below of its full supply of solar energy. Some epiphytes, however, are able to fix their hyphae to the epidermis by sending minute peg-like projections into the cuticle—Trichosphaeria, Herpotrichia—while others send haustoria right through the outer epidermal walls—e.g. Erysiphe—and thus supplement mere contact-irritation and shading by actual absorption from the external cells. Here the fungus is a parasitic epiphyte.
A stage further is attained in those fungi which enter the stomata and live in the intercellular spaces—e.g. many Uredineae and Phytophthora—and many such intercellular endophytes increase their attack on the cells by piercing their walls with minute (Cystopus) or large and branched (Peronospora) haustoria, or even eventually pierce the cells and traverse them bodily (Pythium). In all these cases it is clear that conflicts must occur between poison and antidote, acid and alkali, attractive and repellent substances, enzyme and enzyme, etc., as was hinted at above; and the same must take place when the parasite is endophytic and intracellular from the first, as in Chytridiaceae, etc., the zoospores of which pierce the outer cell-walls and forthwith grow into the cells. There are also fungi which, while able to pierce the outer cell-walls, and grow forward in the thickness of the wall itself, cannot enter the living cells themselves—e.g. Botrytis. In the example mentioned, the fungus excretes a poison, oxalic acid, which soaks into and kills the cells next its point of attack: into these dead cells it then extends, and, invigorated by feeding on them, extends into other cell-walls and excretes more poison, and so on.
On the basis of the foregoing it seems possible to sketch a general view of the nature of parasitism. In order that a fungus may enter the cells it must be able to overcome not only the resistance of the cell-walls, but that of the living protoplasm also: if it cannot do the latter it must remain outside, as a mere epiphyte, or at most an intercellular endophyte. If it can do neither it must either content itself with a saprophytic existence or fail, so far as that particular host-plant is concerned. Its inability to enter may be due to there being no chemotropic attraction, or to its incapacity to dissolve the cell-walls, or to the existence in the cell of some antagonistic substance which neutralises its acid secretions, destroys its enzymes or poisons, or is even directly poisonous to it.
Moreover when once inside it does not follow that it can kill the cell. The protoplasm of the latter may have been unable to prevent the fungus enemy from breaking through its first line of defence—the cell-wall, but it may be quite capable of maintaining the fight at close quarters, and we see signs of the progress of the struggle in hypertrophy, accumulation of stores, and other changes in the invaded cells and their contents.
Finally, the invested or invaded cell may so adapt itself to the demands of the invader that a sort of arrangement is arrived at by which life in common—Symbiosis—is established, each organism doing something for the other and each taking something from the other. In this latter case, which is often realised—e.g. lichens, leguminous plants and the organisms in their root-nodules, mycorrhiza, etc.—we leave the domain of disease, which supervenes indeed if the other symbiont is lacking.
Some interesting facts bearing on the matters here under discussion, have been obtained from the study of Galls, the curious outgrowths found on many plants and due to the action of insects.
A typical gall exhibits three distinct and characteristic layers of tissue surrounding the hollow chamber in which the larva of the insect lies, viz., an outer layer of soft cells forming a parenchyma covered with an epidermis, and frequently also with a layer of cork; an inner stratum consisting of very thin-walled delicate cells filled with protoplasmic and reserve food-materials on which the larva feeds; and between the two a more or less definite layer of thick-walled sclerenchyma cells which serve as a protection against accidents to the larva as the outer layer shrivels or rots, or if it is exposed to the attack of marauders. This layer may be absent from galls which have a short life only. Vascular bundles run into the outer layer from the leaf-veins or the stele of the shoot, etc. Such galls abound in tannin, and are frequently of use in the arts on this account: they also contain starch, and proteid substances and crystals of calcium oxalate. When the larva has consumed the stores of food material and reached the adult stage it eats its way out and escapes.
The growth of such a gall is preceded by the laying of an egg on or in the embryonic tissue of a leaf, stem, or other young part, and it is interesting to note that only organs in the meristematic stage can form galls, and that it is by no means necessary that the tissues should be wounded. Moreover, the egg as such is incapable of stimulating the plant tissues, but when it hatches, the resulting larva, beginning to feed on the cells, irritates the tissues and rapid growth and cell-division occur, as in the case of other wounds or of fungus attacks. The actual wound made by the ovipositor heals up at once. It is evident from numerous recent researches that these true galls are not due to any poisonous or irritating liquid injected by the parent, but that the stimulus to the tissue formation is similar to that exerted by a wound. The young gall is in fact a callus enclosing the living larva, and it is the continued irritation of the latter which keeps up the stimulation. The final shape and constitution of the gall depend on mutual reactions—not as yet explained in detail—between the species of plant and the species of gall-insect concerned, as may readily be seen from the extraordinary variations in size, shape, colouring, hairiness and other structural peculiarities of the galls on one species of, for instance, the common oak. From what we have learnt about fungus parasites, however, there can be little doubt that reactions between the cells and the larva of the insect occur, resembling those which take place between the cells and the hyphae of the fungus, and this is borne out by the study of other hypertrophies due to animals; e.g. Nematode worms in roots, and the remarkable galls—the simplest known—on Vaucheria, caused by the entrance into this alga of a species of Notommata, which induces a different gall on each of the various species of its host plants.