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NECTRIA CANKER • Nectria canker is one of the most important diseases of apples and pears and of many species of hardwood forest trees in most parts of the world. Losses are greater in young trees because the fungus girdles the trunk or main branches, whereas in older trees only small branches are usually killed directly. Cankers on the main stem of older trees, however, reduce the vigor and value or productivity of the tree, and such trees are subject to wind breakage.
. Nectria cankers usually develop around bud scars, wounds, and twig stubs or in the crotches of limbs. Young carkers are small, circular, brown areas. Later, the central area becomes sunken and black, while the edges are raised above the surrounding healthy bark. In many hosts and under favorable conditions for the host, the fungus grows slowly, the host produces callus tissue around the canker, and the margin of the canker cracks.
Tissues under the black bark in the canker are dead, dry, and spongy, flake off, and fall out, revealing the dead wood and the callus ridge around the cavity. In subsequent years the fungus invades more healthy tissue and new, closely packed, roughly concentric ridges of callus tissue are produced every year, resulting in the typical open, target-shaped Nectria canker.
In some hosts, however, and under conditions that favor the fungus, invasion of the host is more rapid. The bark in the cankered area is roughened and cracked but does not fall off, and the successive callus ridges are some distance apart. Some species of the fungus are associated with certain scale insects and grow profusely in insect-infested tissue.
Through this association, Nectria species have been causing much more serious diseases, such as the "beech" bark disease," than they do in the absence of the insects. In hosts such as apple and pear, fruits are also infected and develop a circular, sunken, brown rot. White or yellowish pustules producing numerous conidia form on rotted areas. Internally, the rotted tissue is soft and has a striated appearance.
The Pathogen • The fungi, Nectria galligena and some related species, attack many different tree hosts. All Nectria species produce two-celled ascospores in brightly colored perithecia on the surface of a cushion-shaped stroma, but different Nectria species produce different anamorphs. Nectria galligena produces single-celled microconidia and, more commonly, two- to four-celled, cylindrical macroconidia of the Cylindrocarpon type on small, white or yellowish orange-pink sporodochia on the surface of the infected bark or on fruit.
Another Nectria species, N. cinnabarina, anamorph Tubercularia vulgaris, causes the Nectria twig blight of trees, especially apple, by infecting and causing cankers on small twigs, which it girdles and kills.
Development of Disease • Conidia are produced more commonly early in the season but also in the summer and early fall. They are spread by wind and by rain and perhaps by insects. Perithecia appear in the cankers in late summer and fall and in the same stroma that earlier produced the conidia, which they eventually replace.
The ascospores are either forcibly discharged and carried by wind or, in moist weather, ooze from the perithecium and are splashed by rain or carried by insects. Ascospores are dispersed more abundantly in late summer and fall but are also released at other times of the year (Fig. 24).
Control • Sanitation i.e., removal and burning of cankered limbs or trees, is often the only control measure possible. Spraying with a fungicide such as captafol or a 8:8:100 Bordeaux mixture immediately after leaf fall helps reduce Nectria infections in fruit trees.
The Pathogen: Venturia Inaequalis • The mycelium in living tissues is located only between the cuticle and the epidermal cells. There, it produces short, erect, brownish conidiophores that give rise to several, one- or two-celled, Spilocaea-type conidia of rather characteristic shape. In dead leaves the mycelium grows through the leaf tissues and produces ascogonia and antheridia; following fertilization, pseudothecia form. The latter are dark brown to black with a slight beak and an opening. Each pseudothecium contains 50 to 100 asci, each with eight ascospores consisting of two cells of unequal size.
Development of Disease • The pathogen overwinters in dead leaves on the ground as immature pseudothecia. Pseudothecia complete their growth in late winter and spring, and ascospores mature as the weather becomes favorable for growth and development of the host. Pseudothecia and asci mature sequentially Some ascospores mature before the apple buds start to open in the spring, but most mature in the period during which the fruit buds open (Fig. 29).
When pseudothecia become thoroughly wet in the spring, the asci forcibly discharge the ascospores into the air; air currents may carry them to susceptible green apple tissues. Ascospore discharge may continue for 3 to 5 weeks after petal fall.
Ascospores germinate and cause infection when kept wet at temperatures ranging from 6 to 26°C. For infection to occur, the spores must be continuously wet for 28 hours at 6°C, for 14 hours at 10°C, for 9 hours at 18-24°C, or for 12 hours at 26°C.
On germination on an apple leaf or fruit, the ascospore germ tube pierces the cuticle and grows between the cuticle and the outer cell wall of the epidermal cells. At first the epidermal cells and later the palisade and the mesophyll cells show a gradual depletion of their contents, eventually collapsing and dying. The fungus, however, continues to remain largely in the subcuticular position. The mycelium soon produces enormous numbers of conidia, which push outward, rupture the cuticle, and, within 8 to 15 days of inoculation, form the olive-green, velvety scab lesions.
During or after a rain, conidia may be washed down or blown away to other leaves or fruit on which they germinate and cause infection in the same way ascospores do. Conidia continue to cause infections during wet weather throughout the growing season. Infections, however, are more abundant during cool, wet periods of spring, early summer, and fall, while they are infrequent or absent in the dry, hot summer weather.
After infected leaves fall to the ground, the mycelium invades the interior of the leaf and forms pseudothecia, which carry the fungus through the winter.
Control • Several apple varieties resistant to scab are available, but many popular ones are moderately to highly susceptible. It appears that all apple cultivars are susceptible to some apple scab fungus isolates and resistant to others. A number of fungi are antagonistic to the apple scab fungus, and some of them decrease ascospore production when applied to scab-infected apple leaves on the orchard floor. So far, no effective practical biological control of apple scab has been developed.
Introducing endochiti-nase genes from fungi into apple increased the resistance of apple to scab, but it also reduced vigor of the plant. Shredding of apple leaf litter or treating them with urea in the fall reduced the risk of scab by about 65%. Apple scab, however, can be controlled thoroughly by timely sprays with the proper fungicides.
For an effective apple scab control program, apple trees must be sprayed or dusted diligently before, (luring, or immediately after a rain from the time of budbreak until all the ascospores are discharged from the pseudothecia. If these primary infections from ascospores are prevented, there will be less need to spray for scab during the remainder of the season. If primary infections do develop, spraying will have to be con- tinued throughout the season.
In most areas, the application of fungicides for scab control begins when buds show a slight green tip and a rainy period is sufficiently long at the existing temperature to produce an infection. Sprays are repeated every 5 to 7 days, or according to rainfall, until petal fall. After petal fall, and depending on the success of the control program to that point, sprays are usually repeated every 10 to 14 days for several more times.
Since the early 1990s, considerable progress has been made in developing simple or computerized apple scab I prediction systems of spore release and infection for scheduling fungicide applications for scab control. All the systems are based on the interactions among temperature, amount and duration of rainfall, and duration of leaf wetness, on the one hand, and the period required for the pathogen to initiate infection on the other. The accuracy and dependability of these models vary considerably under different local conditions.
Several fungicides give excellent control of apple scab. Some of them protect a plant from becoming infected, but they cannot cure an infection, whereas some can stop infections that may have started. In some areas, new strains of Venturia inaequalis have now appeared that are resistant to several of the systemic fungicides. These chemicals, therefore, can no longer be relied on to control the disease by themselves; rather, they must be applied in combination with one of the broad-spectrum fungicides.
POSTHARVEST DISEASES OF PLANT PRODUCT CAUSED BY ASCOMYCETES AND DEUTEROMYCETES(MITOSPORIC FUNGI)
Postharvest Disease • Postharvest diseases develop on fruit and other plant products during harvesting, grading, and packing, during transportation to market and to the consumer, and while the product is in the possession of the consumer until the moment of actual consumption or use .
In many cases, such microorganisms also secrete toxic substances that make the remainder of the product unfit for consumption or lower its nutritional and sale value.
All types of plant products are susceptible to postharvest diseases. • Generally, succulent, fleshy fruits and vegetables, cut flowers, bulbs, and corms are often affected by postharvest diseases. • The extent of damage depends on the particular product, on the disease organism or organisms involved, and on the storage conditions.
In addition, postharvest molds and decays of bread, hay, silage, and other feedstuffs are quite common and extensive, and we all frequently have to throw away bread because it has become moldy.
Postharvest diseases destroy 10 to 30% of the total yield of crops, and in some perishable crops, especially in developing countries, they destroy more than 30% of the crop yields. Postharvest diseases usually cause great losses of fresh fruits and vegetables by reducing their quality, quantity, or both.
Mycotoxins • Postharvest diseases of grains and legumes also result in the production by some infecting microorganisms of toxic substances known as mycotoxins. • Mycotoxins are poisonous to humans and animals that consume products made from seeds infected with such microorganisms. • Mycotoxins are also produced by some fungi in infected fresh fruits and vegetables, but in these cases they are generally removed when the rotten fruits or vegetables or their rotten parts are discarded before consumption.
As manufacturers use bulk quantities of fresh fruits and vegetables to make fruit or vegetable juices, purees, cool slaw, baby foods, and so on, quality control of individual fruits and vegetables becomes all but economically impractical; therefore, postharvest infections and mycotoxins in bulk-prepared foods are likely to increase in the future.
Causal organisms • Postharvest diseases are caused primarily by a relatively small number of Ascomycetes and mitosporic fungi and by a few species of Oomycetes, Zygomycetes, Basidiomycetes, and bacteria. • The bacteria are primarily of the genera Erwinia and Pseudomonas • Of the Oomycetes, Pythium and Phytophthora cause only soft rots of fleshy fruits and vegetables that are usually in contact with or very near the soil and they may spread to new, healthy fruit during storage.
Causal organisms • Two Zygomycetes, Rhizopus and Mucor, affect fleshy fruits and vegetables after harvest and also stored grains and legumes, as well as prepared foods such as bread, when moisture conditions are favorable. • Of the Basidiomycetes, Rhizoctonia and Sclerotium cause rotting of fleshy fruits and vegetables, whereas several fungi cause deterioration of wood and wood products.
