Ever since humans began to cultivate \Lplant\ls as crops, they have been troubled with plant diseases. Early civilizations regarded plant diseases as a manifestation of godly displeasure. Not until the beginning of the 19th century was the nature of plant disease established scientifically. Even this discovery, however, did not avert some disastrous outbreaks of disease. In the mid-1840s famine struck Ireland when the potato crops were destroyed by a fungus. From 1845 to 1860, 1 million people died from this famine, and 1.5 million emigrated. Nearly a century later (1942-1943), another fungus, brown spot disease, Helminhosporium oryzae, ravaged the rice crop in Bengal; some 2 million people died of starvation. Even in those countries with economic and social structures that preclude widespread famine, the losses caused by plant disease are considerable. PATHOGENS The living agents, such as bacteria, that cause plant disease are called pathogens. No generally accepted term has been found to describe nonliving, disease-causing agents, which include mineral excess or deficiency, atmospheric pollutants (such as sulfur dioxide), pesticide overdosage, or faulty herbicides. These are variously called nonparasitic agents, abiotic factors, or pathogens. Most plant pathologists, however, restrict the use of the term pathogen to living agents. The pathogens may be divided into seven groups: \Tbacteria\t; \Tfungi\t; \Lvirus\les; \LMycoplasma\ls and other related microorganisms; \Lnematode\ls; some other animals, such as insects and mites; and a few flowering plants, such as \Tdodder\t, Cuscuta; \Tbroomrape\t, Orobanche; and \Twitchweed\t, Striga. The plants that support pathogen activity are called hosts, and the sequence of events in disease development, beginning with the initial contact between a pathogen and its host, is called pathogenesis. Not all pathogens, however, live exclusively on their hosts. Some can use dead organic material (substrates) for food as well; that is, they live as saprophytes. The colonization of these substrates is called saprogenesis. SYMPTOMS Like many biological phenomena, plant disease is difficult to define, although certain features are recognized: (1) abnormality--plant development is altered in some way from that expected in the particular environment; and (2) impairment--plant physiology is affected and progressively so, resulting in injury or death. Disease results from the interaction of a pathogen with its host, although the intensity and extent of this interaction is affected markedly by environmental factors such as temperature, rain, humidity, light, soil fertility, and pH. In any diseased plant, symptoms indicate the nature and extent of the pathogen-host interaction. The main types of symptoms are: (1) death of the tissues, or necrosis, especially on leaves, where the localized areas of diseased tissue (lesions) generally assume characteristic shapes; (2) an abnormal increase in the size or number of the host's cells, which leads to an abnormal abundance of shoots (witches'-broom), swollen roots (clubroot), abnormal protuberances (galls), or localized callus formation around dead areas on trees (\Lcanker\ls), fruits, or long-lived organs such as tubers (scab); (3) a failure to attain normal size or development; (4) a change in color, such as the leaves turning yellow (chlorosis) or developing red pigments (anthocyanescence); (5) wilting, which usually indicates an invasive interference with the normal movement of water within the plant; (6) disintegration of the tissues, by bacteria or fungi, often accompanied by a release of fluids from the plant cells (wet rot) or sometimes by a drying out of the cells to produce a powdery mass (dry rot); and (7) excessive gum formation (gummosis), occurring especially in some tree diseases. Collectively, the symptoms for a disease are called a syndrome, and the syndrome is often so characteristic that it identifies the disease and its pathogen. In many fungal diseases, the appearance of the spore-bearing organs (fructifications) of the pathogens are a certain guide to the nature of the disease. These visible growths are often called the signs of the disease to distinguish them from the symptoms. PATHOGENESIS Pathogens show great diversity in the ways they perennate (survive from season to season), in the types of inoculum (infective particle) they produce, in the way these inocula are dispersed, and in the range of plants they infect. Systemic Infection A typical route of pathogenesis is that of late blight of potatoes. It was this disease, formerly known as potato murrain, that caused the disastrous potato famine in Ireland. The late blight pathogen is the fungus Phytophthora infestans, which grows in the leaves and stems. It progressively kills the tissues and reduces the effective photosynthetic area of the plant. Consequently, little synthesized material passes to the tubers (potatoes). These stop growing, and yield is reduced. Under moist conditions, the fungus grows out from the infected tissues and can be seen, especially on the lower leaf surface, as a white bloom at the edge of the lesion. The spores are dispersed by rain and initiate new infections on leaves and stems; or, when they are washed into the soil, they infect the developing tubers. Tubers also may be infected at harvesting if they contact diseased foliage that bears spores. Some infected tubers rot in storage because other microorganisms, especially bacteria, invade them through the blight lesion. Others do not rot, and if these are used to establish a new crop, a few may give rise to an infected shoot bearing a lesion with sporulating P. infestans. Infected tubers discarded at harvest or from storage may also be a similar source of spores that initiate infections on adjacent young potato crops. Thus two distinct phases occur during the disease cycle of P. infestans: an active colonization (infection) of the growing plant, that involves some agency (in this instance, rain) to distribute its infective particle, or spores; and a less active period between crops (perennation), spent in infected tubers. Although similar phases can be distinguished in other diseases, pathogens show great diversity in the ways they perennate, in the types of inoculum (infective particle) they produce, in the way these inocula are dispersed, and in the range of plants they infect. Many pathogens of annual crops survive in association with their hosts because they infect the planting material or seed. Pathogens on woody perennials often survive in localized areas of diseased tissue, such as cankers, witches'-brooms, or galls. An example is Erwinia amylovora, the causal bacterium of fire blight in apples and pears. This bacterium enters through the flowers and young shoots, causing them to blacken and to appear scorched, as if by fire. Its downward movement in the plant becomes progressively restricted by various host reactions, such as cork formation, and cankers often develop at the base of the infected spur or twig. The bacterium remains dormant in some of these cankers ("hold-over" cankers). In the spring it exudes in sticky masses that are dispersed by splashing rain or by insects. Other pathogens survive in the buds of their hosts. The powdery \Tmildew\t fungus, Podosphaera leucotricha, which during the spring and summer covers the young leaves of apple trees with its white growth, becomes established in some buds. It remains there, protected by the bud scales, until the following year. When these buds open, they give rise to severely mildewed shoots, and the spores formed on these initiate a new disease cycle. A similar pattern is observed with downy mildew, caused by a number of lower fungi. Perennation in association with the host is the general means by which plant pathogenic viruses survive. All viruses require living host cells to multiply; few survive in crop debris. An exception is tobacco mosaic virus, which, as its name implies, causes a mosaic pattern of light and dark patches on infected tobacco leaves. (Such mottling of leaves typifies all mosaic viral infections.) This was the first virus to be studied and purified and thus occupies a unique place in virology. Similarly, few plant pathogenic bacteria can live apart from their hosts. Some exceptions are the crown-gall organism, Agrobacterium tumefaciens, which survives in soil, and the bacterium causing cotton blight, Xanthomonas malvacearum, which survives in dry crop debris. In contrast, many fungi form thick-walled spores or fruiting bodies that enable them to survive adverse conditions, or they live saprophytically on crop debris or on organic matter in soil. Many of the fungi that cause damping-off of seedlings and root rots belong to the latter category. Fungi such as rusts and smuts are examples of pathogens whose spores are dispersed by rain and wind. Pathogen Dispersal Fungi such as rust and smuts are examples of pathogens whose spores are dispersed by rain and wind. Diversity of inocula is seen at its extreme in the rust fungi, especially Puccinia graminis, which causes stem rust of cereals, a serious problem involving wheat in the United States and Canada. On wheat, P. graminis first produces orange-brown masses of single-celled spores (uredospores) that are dispersed by wind and infect other wheat plants. Later in the season, and often in the same pustule, it forms the overwintering two-celled black spores (teliospores), which are not able to infect wheat. In the spring, teliospores germinate to form small, colorless, thin-walled spores (basidiospores), which can infect only barberry, Berberis, or some Mahonia species. On these hosts two further distinct spore types are produced, but neither can infect the host on which it is formed. One type, spermatia, is involved only in fertilization; the other, produced in cuplike structures (aeciospores), infects wheat and so completes the disease cycle. Other pathogens, such as the anthracnose fungi, are distributed primarily through insect activity. The fungus Ceratocystis ulmi, which causes \TDutch elm disease\t, is carried from tree to tree by certain species of bark-boring beetles. These beetles become contaminated with spores because the fungus grows well in the galleries these insects make in elm bark. When the beetles emerge and feed on young twigs of healthy elms, they introduce the fungus, which then multiplies in the vascular system, causing leaf yellowing, defoliation, and rapid death of the tree. Many viruses are also spread by insects, especially aphids, leafhoppers, and whiteflies. The insects acquire the viruses when feeding on an infected plant and transmit them when feeding on a healthy plant. Pathogens can take advantage of the physical damage that is caused by scale insects and other insect pests as well. Humans also help spread pathogens by handling infected and healthy plants in succession, by distributing infected planting material, and by transferring contaminated soil from one site to another on agricultural machinery. Pathogen Specificity Some pathogens, such as Ceratocystis ulmi, which is restricted to elm species, can colonize only a few hosts. Others, such as the fungi Pythium ultimum and Rhizoctonia solani, which cause damping-off, successfully colonize the seedlings of many diverse plant species. The horticultural development of particular varieties (cultivars) of a plant species to satisfy commercial requirements, such as high yield, has led to the appearance of different races of a single pathogen, which are specialized in their ability to attack the different cultivars. The extensive cultivation of one type of cultivar (monoculture) provides a uniform host population within which these races can develop. Many races now exist of Puccinia graminis, which attacks wheat, and of Phytophthora infestans, which attacks potatoes. CONTROL The amount of disease in a crop at any one time depends on the amount of the pathogen initially present (initial inoculum), the rate at which it infects plants (infection rate), and the time available for infection. The aim of most control methods is to counter these elements by excluding any initial inoculum, by reducing the amount of inoculum, or by reducing the infection rate. Exclusion Phytophthora infestans probably came to Ireland on potatoes from the New World. Today most countries not only have regulations to prevent the introduction of foreign pathogens, but they also have special quarantine sites where imported planting material can be grown and inspected. Disease control by legislation is often extended to restrict the movement of infected material within a given political territory. The same principle of exclusion is applied to the growing of crops by planting only pathogen-free stock. Various methods are used to obtain such stock. In some instances seed crops can be grown in areas unfavorable for particular pathogens. Dwarf beans (Phaseolus vulgaris), for example, grown in dry climates are unlikely to yield seed infected with the halo-blight bacterium, Pseudomonas phaseolicola. Potatoes for planting are grown in areas where aphid populations are low, to minimize virus spread. Portions of selected tubers are then planted in insect-proof greenhouses, and the young plants tested for viruses to assess the purity of the stock, a process known as "tuber-indexing." Seeds of many crops are treated with chemicals before planting to eliminate fungal pathogens. Reducing Inocula Sometimes pathogens are introduced into an area despite all attempts to exclude them. The fire blight bacterium, Erwinia amylovora, well-known for more than a century as a serious pathogen of apples and pears in the United States, suddenly appeared in the Kent orchards of southeast England in the late 1950s. The coffee leaf rust fungus, Hemileia vastatrix, known in the Old World since the 1860s, appeared in Brazil in 1970. The problem in these instances was how to reduce the inocula quickly. The obvious solution was to destroy infected plants. This was attempted in England for fire blight control. It has not been entirely successful for two reasons: it has proved impossible to monitor individual apple and pear trees in home gardens, and the presence of alternate hosts--the bacterium can also infect Crataegus species, which are widely planted as ornamentals. The mobility, reproductive patterns, and behavior of insect vectors, or carriers, of the pathogen also work against the success of an eradication scheme, as has been apparent in the unsuccessful attempts to eradicate Dutch elm disease. The long-distance spread of spores is another major obstacle. In the United States, the local eradication of barberry, the alternate host of Puccinia graminis, has not eliminated stem rust of wheat because the uredospores can be carried many kilometers by wind. Nevertheless, eradication schemes have often proved useful in slowing the rate of disease spread, and small-scale eradication, such as the steaming or fumigation of seedbeds to kill perennating inocula, remains the standard method for controlling root pathogens. Two other ways of reducing inoculum are used that are more appropriate for controlling established pathogens. Some wheat cultivars are resistant to certain races of Puccinia graminis but are susceptible to others. This resistance is of an "all-or-nothing" type and is called race-specific resistance. Planting such a cultivar reduces the effective number of inocula, because if 99 percent of the uredospores entering the field are of races to which the cultivar is resistant, then the rust disease must develop from the remaining 1 percent. It is relatively easy for plant breeders to test seedlings in the greenhouses for this type of resistance. The genes for resistance are often derived from wild Triticum species (relatives of wheat). The aim is to incorporate several genes into a commercially acceptable cultivar, which is then crossed with other cultivars to confer resistance to all existing races. There is one major disadvantage in this approach. If a new race of the pathogen P. graminis develops by mutation and is able to infect a cultivar, that cultivar succumbs completely. Several disastrous outbreaks of stem rust in the United States have been associated with the appearance of new races of P. graminis and the so-called breakdown of resistance of established wheat cultivars. Fungicides are now used that are absorbed by and become distributed within the plant. A plant treated with such a systemic fungicide resembles one with race-specific resistance. In both types, the fungus is killed upon entry, and effective inoculum is thus reduced. In race-specific resistance, this is caused by a gene-controlled defense mechanism; in systemic treatment, this is caused by a chemical disruption of some part of the pathogen's metabolism. Just as new fungoid races can arise to overcome the resistance of specific genes, however, new races can develop that can grow on plants treated with systemic fungicides. This does not mean that such materials are useless. On the contrary, systemics are another way to combat plant disease. Reducing Infection Two control methods are used to reduce infection rate. One is the classical approach of applying chemicals to foliage. These chemicals inhibit the growth of infective materials that land on the foliage. Unlike systemic fungicides, these \Tpesticides\t are not absorbed and so become progressively diluted by plant growth and the abrasive action of rain and wind. As such they seldom give 100 percent control, but they do delay the epidemic. Most fungicides--for example, the different compounds of copper--act in this way. The second method used is relatively new. Some wheat cultivars are susceptible to all races of P. graminis, but rust develops rather slowly on them. Thus a level of resistance exists not specifically associated with a particular race. This is called race nonspecific resistance. Cultivars with race nonspecific resistance react similarly to any new race of the pathogen that arises. While sustaining a certain amount of disease, they do not succumb disastrously as do cultivars with race-specific resistance. Many factors are involved: the fungus grows more slowly in the tissues; it thus takes longer to sporulate; and when it does sporulate, it does so less effectively. Because it is much more difficult to test progeny for this resistance in breeding lines, the method has not been fully exploited. B. E. J. \TWheeler\t Bibliography: Agrios, George N., Plant Pathology, 3rd ed. (1988); Asada, Y., et al., eds., Plant Infection (1982); Chet, Ilan, Innovative Approaches to Plant Disease Control (1987); Harris, Kerry, and Maramorosch, Karl, Pathogens, Vectors and Plant Diseases (1982); Milne, R.G., ed., The Plant Viruses (1988).