The Symposium dealt successively with known and potential dangers to world forestry from root rots, cankers, stem rusts, heartrots, mistetoes, viruses and virus-like disorders, vascular wilts, foliage diseases and seed and seedling diseases, with well-documented and illustrated evidence being presented for each category of disease.
Root rots cause damage directly through cull and mortality and indirectly by modifying the structure and spatial arrangement of trees in stands. The latter is important because damage from root rot should be calculated finally in terms of crop trees. The hazards from both direct and indirect damage are heightened by monoculture silviculture and by any one or more of a variety of factors that combine to predispose trees to root rot. Investigations of root rot should not, therefore, be mainly mycological; they should rather be ecologically oriented.
Environmental stresses probably rank first among predisposing factors, and in the long run these are most apt to be frequent and critical in sites that are suboptimal for the growth and survival of a desired tree species. It cannot be assumed that species that are not known to be affected by given root pathogens are in fact nonsusceptible. Rather, all that can be assumed, even after negative inoculation trials, is that the pathogens and suscepts have not been brought together under the proper circumstances. Accordingly, all diseases of foreign origin potentially threaten indigenous hosts. Foresters should not be totally preoccupied, however, with the threat from foreign diseases, but should concentrate as well on the threat from indigenous pathogens, for example, Fomes annosus, Armillaria mellea, Polyporus tomentosus, which, if given the requisite conditions, could cause severe damage such as Rhizina undulata.
Root rot is difficult to control, and measures to limit the; possibilities for introductions into new areas should be unrelenting. Most important should be prohibition of the movement of living plant material from one country or region to another. When control action is necessary, the remedial measures contemplated should be carefully appraised beforehand for possible side effects, for example, aggravation of another disease situation in the treated area.
Infectious cankers are worldwide on forest and shade trees of all ages and, depending upon the nature of the infectious agent and the host, they either kill trees or cause damage ranging from stem deformation and breakage, wood discoloration and deterioration, to increased susceptibility to attack from other infectious agents. Most canker diseases are caused by fungi; relatively few by bacteria. The economic importance of cankers can be roughly correlated with one or other of four distinct canker types that are themselves distinguishable according to symptomatology, viz., open perennial cankers (Type 1), covered perennial cankers (Type 2), covered ephemeral cankers (Type 3), generalized bark necrosis (Type 4).
Type 1 cankers have permanent callus at the edges of bark lesions and a large part of the affected wood is exposed to external influences. The lesions usually progress slowly, and damage is mainly from stem deformations in older trees, for example, Trichosyphella willkommii, Strumella coryneoidea, Nectria galligena, Pseudomonas quercus. Type 2 cankers are usually covered with dead bark which may be sunken and fissured. Slight swellings sometimes occur at the canker site. The lesions often cause mortality (Hypoxylon pruinatum, in aspen), top-killing (Coryneum cardinale in Cupressus macrocarpa), stem deformation and wood discoloration (Atropellis piniphila in lodgepole pine). Type 3 cankers involve limited areas of bark within which the pathogen is operative for only one year. The necrotic area is covered rapidly and, unless secondary pathogens become operative, the damage is generally minor. A notable exception is the "brown spot disease," a relatively newly recognized disease, which is very destructive to Euroamerican poplars in Europe. Type 4 cankers exhibit rapid bark necrosis, sometimes slight swelling at the canker site, and do not have callus. The fungi involved frequently intensify and spread as epiphytotics and result in mass killings, for example Endothia parasitica, Septoria musiva, Nectria coccinea var. faginata, Chondroplea poplea.
Canker diseases should be investigated along ecological lines because of the many predisposing factors involved. Drought is a major conditioning factor of canker diseases as it lowers bark moistures to levels that facilitate fungal invasion. The pathogen-host relationships vary considerably, but pure, dense, even-aged stands are conducive to epiphytotics. The present high losses in European poplar plantations are probably due to the use of low-resistant cultivars, dense plantings, and monoculture. Intercontinental spread of canker pathogens is assured so long as living plant materials are transported on anything but a restricted basis. Phytosanitary measures against canker pathogens should be rigidly enforced.
The many rust fungi that invade the bark of coniferous trees, causing cankers and hypertrophies and eventual mortality, belong mainly to the genera Chrysomyxa, Cronartium, Melampsora, Gymnosporangium, and the form genus Peridermium. Most are heteroecious, with alternate stages on the foliage of deciduous plants including broadleaved forest trees, for example, poplars and willows, but some are autoecious. Cronartium spp. are particularly damaging, but with few exceptions are confined to North America. Gymnosporangium spp. are more widely distributed.
Rust fungi on the whole are most damaging to seedlings and young trees, with some notable exceptions. Although rusts characteristically have a wide range of primary hosts, the hosts for individual rust fungi form closely-related groups, such as hard or soft pines. Rust control is variously facilitated and confounded by multispored life cycles and by an extensive range of alternate hosts. Eradication of alternate hosts is recommendable from the biological viewpoint, but can be a continuing and costly process. Selection and breeding of resistant propagative material offer more permanent solutions, albeit long-range, and substantial progress has already been made against Cronartium ribicola on Pinus monticola and P. strobus and against C. fusiforma on slash and loblolly pines. The indicated resistance of individual trees and species of pines to Peridermium pini and Melampsora pinitorqua offers further promise for the assembly of rust-resistant propagative material. In the absence of such material, however, the use of rust-free planting stock and the prevention of rust invasions into young plantations is recommendable. Sanitary measures to reduce the inoculum supply and to prevent the spread of mycelium from branches to stems are legitimate control measures within economic limits. Chemical control in nurseries and the use of antibiotics in natural stands require considerably more evaluation to establish their efficacy in rust control. Similarly, microclimatic studies of rust fungi could possibly lead to refinements in already established control measures.
However effective the control measures that are finally evolved against stem rusts may be, it is abundantly clear that known and potentially susceptible trees and other plants should not be introduced into rust-free areas. The rust-free blue pine of India, for example, should not be threatened by the introduction of known rust-susceptible pines from other parts of the world. The host affinities of rust-susceptible trees and secondary hosts should serve to focus attention on the special danger of intercontinental spread of rust fungi.
Heartrot destroys the usefulness of wood and often renders adjacent sound wood useless for anything but fuelwood. Accordingly, heartrot losses are greater than the volume of rot indicates. It is a major loss factor in all forested regions of the world, and while a considerable amount is known about it, greater application of control measures is needed.
The disease results almost exclusively from fungal action in heartwood and dead sapwood, most of the fungi gaining entry into these tissues via breaks in the normally protective sheath of functional bark and sapwood. Most infection courts are created by wounds, dead branches, and branch stubs, but some infections occur in uninjured roots. Reliable indicators of heartrot vary greatly between trees and species of trees, the only completely reliable ones being sporophores, punk knots and swollen knots. Less reliable indicators are wounds, swellings, dead tops and cankers. In estimating the incidence and amount of heartrot, the reliability of indicators needs to be verified for given species of trees in a variety of site and age conditions. This can be done only by carefully executed volumetric surveys.
Heartrot is initiated and intensified by predisposing factors among which are fire, frost, breakage and some other diseases, for example, cankers produced by rusts and dwarf mistletoe. Suboptimal sites generally favor a high incidence of heartrot because of early and proportionately abundant heartwood and late natural branch suppression. Root rot can be important in more or less direct ratio with the amount of inoculum present in the roots and stumps of the former stand. Stem rot is important mainly in older stands, particularly in the older trees of uneven-aged stands but less noticeably in the older trees of even-aged stands.
Control of heartrot is a matter of restricting its incidence and volume through silvicultural and management practices that are aimed at reducing the impact of predisposing factors. Chemical and biological control is effective in some instances, for example, Fomes annosus. The most likely means of intercontinental and interregional spread are from shipments of logs and unseasoned wood containing incipient decay and from shipments of plants that are parasitized by certain heartrotting fungi, for example, Poria weirii, Armillaria mellea, Fomes annosus.
Some 1,300 species of mistletoes in 36 genera of Loranthaceae parasitize forest trees and cause major losses in the form of deformations, retardation of growth, reduction in seed, cankers, top-killing, and mortality. Losses of growth of more than 50 percent are common. Dwarf mistletoes (Arceuthobium spp.) have small branches, degenerate leaves, an extensive endophytic system, but no phloem. Leafy mistletoes (mainly Loranthus spp., Phorodendron spp., Viscum spp.) are larger plants with more typical leaves. Host specificity varies from relatively specific for dwarf mistletoes to generally less specific for leafy mistletoes. Dwarf mistletoes are confined to softwoods, leafy mistletoes parasitize either only hardwood (Loranthus spp.) or both hardwoods and softwoods. The fact that introduced tree species may be attacked by indigenous mistletoes mitigates against promiscuous introductions of foreign trees.
The parasite spreads by seeds. Dispersal is aided by an adherent murcilaginous matrix which retards dessication and facilitates germination. Seeds germinate wherever they lodge, presumably without stimulus from the host, and penetration is affected by a primary haustorium emanating from a holdfast. If the host accepts the primary haustorium, the endophytic system ramifies in the host tissue. The parasite supplies few or no photosynthates to the host, rather it depends either heavily or entirely on the host for water and minerals.
Distribution, intensification and development of the parasite is affected by its environment. It thrives best on vigorous hosts and in intense rather than shaded light. Various other environmental factors are pronounced in their effects, although not necessarily consistently. Apparent geographic limitations to individual distributions of mistletoe seem more closely linked to climatic and other ecological factors than to physiographic barriers and immunity of hosts. Natural control agents, although present, require manipulation to be effective. Eradication and subsequent exclusion of the parasite are the most effective means of control, although chemical control of leafy mistletoes with either sprays or injections of 2,4-D is sometimes possible.
Knowledge of virus and viruslike diseases of forest trees lags behind the understanding of comparable disorders in agriculture and horticulture. This is unfortunate because viruses are most damaging to perennial crops, and infected plants remain infected for life. Woody plants, because of their long life span, are the hardest hit. Trees are sometimes killed, but more commonly the most serious effects are retardation of growth and the production of poor quality wood. Plantation-grown trees that are vegetatively propagated are often the most seriously affected because vegetative propagation perpetuates the virus and facilitates widespread distribution. The trend toward monoculture silviculture, with heavy reliance upon vegetative propagation, for example, poplars, enhances the threat of virus diseases in forest plantings, particularly with free intercontinental and interregional shipments of stock.
Intercontinental spread of some viruses is difficult to detect and prevent because of the lack of symptoms for all stages of the disease. Some viruses, for example, cacao swollen shoot, do not produce symptoms on wild host trees. Because of inherent difficulties in recognizing virus-infected material, shipments of trees and propagative material should be restricted to seed and scion material that is known to be virus-free.
Despite their variability, symptoms are the principal means of diagnosing virus diseases. Hence the evolution of terminology to express degrees of chlorosis, nanism, atrophy, hypertrophy and necrosis. This rather inexact method of diagnosis and description has doubtless introduced a number of virus diseases into the literature which are in fact varying expressions of either identical viruses, virus strains, or virus complexes.
Most viruses are naturally transmitted by sucking insects, but many can be transmitted experimentally by some form of graft. Symptom expression can be delayed for more than a year following inoculation. Generally, there are initial acute symptoms that are followed by chronic symptoms. There are instances, however, of progressive development, for example, sandal spike and elm necrosis.
Vascular wilts are few in number and have limited host ranges, but they constitute a rapidly destructive type of forest disease. In consequence, they pose a continuing threat to certain forest and shade trees in many regions of the world, for instance, oak wilt and elm disease. The elm disease is a vivid demonstration of the capacity of a virulent vascular wilt pathogen to establish itself in a new area because of favorable environmental conditions. Efforts to control diseases of this kind lend themselves to co-operative research, that is, research and supporting surveys at all levels of forest and shade tree management.
Vascular wilts are induced by either bacteria or fungi that systematically invade xylary tissue. The pathogen is often distributed generally and rapidly within the host. The invaded vessels become occluded and the twigs and foliage respond with classical wilt symptoms. The disease can also lead to flagging, dieback and mortality. Alternatively, apparently full recovery can occur.
The time, place and conditions of inoculation largely determine disease incidence and eventual symptom expression. Consequently, control measures, which of necessity must be largely preventive to be effective, must be timed to take advantage of weak points in the disease cycle. Once established, vascular wilts can be either inhibited or facilitated in their development by environmental factors, for example, temperature and moisture conditions of the atmosphere and soil. Certain of these factors act alone, others in concert.
The pathogens spread mainly by spores but in different ways, such as in the soil that is adherent to transplant stock, by wind, rain, insects and root grafts. None is known to be transportable on seed or pollen. Accordingly, intercontinental transfer of susceptible plant material can be done safely in this way.
Control of vascular wilts is best accomplished by reducing the inoculum, preventing infection, and limiting further spread. Fungicidal sprays are valueless and chemotherapy is still doubtful. There are no known cures for infected trees other than pruning small infected branches. Elimination or reduction of inoculum can be achieved by phytosanitary measures. Infection can be either eliminated or reduced by insecticidal sprays and systemic insecticides, establishing dead root barriers between infected and healthy trees, prevention of wounds, use of resistant parent material, prohibiting of the movement of diseased plants and plant products, prohibition of the movement of soil from diseased areas to disease-free areas.
Foliar diseases with some notable exceptions are less destructive and alarming than most other forms of forest disease, although the aggregate loss from foliar diseases is admittedly large. In general, trees are killed only under epiphytotic conditions that have persisted for two or more years. In assessing forest damage, undue emphasis upon foliar disease losses can be avoided by distinguishing between diseases whose primary symptoms are expressed on foliage and disease involving foliage only secondarily. The former are regarded as foliar diseases.
There are several kinds of symptoms, for example, anthracnose involving necrosis of foliage and twigs, discrete necrotic spots, rust sori, surface mycelium, powdery conidia and black perithecia, rapid necrosis and casting of foliage, blisters, sooty molds. Perhaps above all other forest diseases foliar diseases are important in direct ratio to the conditioning factors of the environment. Epiphytotics are enhanced with the exposure of either exotic hosts to indigenous pathogens or the introduction of the pathogen and host together into an environment more favorable to the disease. For example, the new environment may increase the reproductive capacity of the pathogen, prolong the viability of inoculum, increase the efficacy of dissemination, decrease the period required for germination and penetration, increase the supply and duration of free moisture, condense the period of the life cycle, provide more and different entry points, and either lower or raise the natural resistance of the host.
Foliar diseases are usually introduced into new areas on either shipments of infected seedlings or on debris accompanying such shipments. With the highest of inspection standards it is still highly probable that diseased material will pass from one region, country or continent to another because of the extended incubation period of some leaf pathogens, for example, Rhabdocline pseudotsugae up to seven years. Thus, isolation and repeated careful inspection of imported living material for several growing seasons prior to general release is essential. Alternatively, surface-sterilized seed should be used.
There is a generally negative attitude toward controlling foliar diseases, apart from various practical control measures having special application in nurseries. Recently, however, systemic fungicides have been developed, and with careful experimentation some of these fungicides could mean the opening of a new era of foliar disease control.
With the exception of heartrot, seedling diseases include all the types of disease that occur in larger trees. There are several kinds of damage resulting from seedling diseases; extensive killing in nurseries, as with damping-off and root rot, mortality and volume loss in plantations from diseases having origin in nursery stock, as with root rots and rusts, and the inadvertent introduction of diseases into new areas on seedlings, as with cankers, rusts and foliar diseases. Intercontinental and interregional spread has been mainly by the movement of infected plants and soil.
The most damaging root and root collar diseases of seedlings are root rot and damping off. Root disease organisms are commonly soil inhabitors, many of which can persist in the absence of suitable hosts. As a rule they do not cause disease unless conditions for their development are favorable. Favorable conditions for disease are frequently coincident with adverse factors affecting the host, for example, nutrient imbalance, high acidity, high alkalinity, drought, excess water. Root disease fungi of nursery plants tend to lack host specificity, rather they affect large numbers of widely different plant species. However, local strains of nonspecific root pathogens can occur which are more or less virulent on individual hosts. Movement of these strains into new areas could presage heavy losses.
The optimum environment for foliar and canker pathogens on seedlings usually includes either high relative humidity or free water at certain stages, for example, sporulation, germination, penetration. Temperature requirements are less critical. Foliar and canker pathogens are generally more host specific than root pathogens, and many are restricted to either a single genus or to a few species within a genus.
Most of the fungi that occur on and within forest tree seeds are saprophytes and cause little or no damage. Some can adversely affect the germinability of seeds that are already low in viability or which have sustained physical damage to the seed coat. Indirect losses of seed can result from diseases of flowers and fruit, such as with rusts, for example, Chrysomyxa pirolata. Seed-borne diseases are similarly uncommon and are mostly limited to trees with large fleshy seeds, like Guignardia robiniae on seeds of Robinia pseudoacacia.
