grape_diseases.9-15

grape_diseases.9-15 - Part |. Diseases Caused by Biotic...

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Unformatted text preview: Part |. Diseases Caused by Biotic Factors Fruit and Foliar Diseases Caused by Fungi Powdery Mildew The powdery mildew fungus (also called oidium) was first described in North America by Schweinitz in [834. The disease caused minor damage on native American grapes and did not gain notoriety until 1845, when it was first observed in England (see Introductionfil-listorical Significance of Diseases in Grape Production). Today this disease can be found in most grape- growing areas ofthe world, including the tropics. Uncontrolled, powdery mildew reduces vine growth and yield and affects quality and winterhardiness. Only members of the Vitaceae are susceptible to the causal fungus. Symptoms The powdery mildew fungus can infect all green tissues ofthe grapevine. The fungus penetrates only the epidermal cells, sending haustoria into them to absorb nutrients. Although haustoria are found only in epidermal cells, neighboring noninvaded cells may become necrotic. The presence of mycelia with conidiophores and conidia on the surface ofthe host tissue gives it a whitish gray, dusty or powdery appearance (Plate 1). Both surfaces of leaves of any age are susceptible to infection. Occasionally, the upper surface of infected leaves exhibits chlorotic or shiny spots that resemble the “oil spot” symptoms of downy mildew. Young, expanding leaves that are infected become distorted and stunted (Plate 2). Petioles and cluster stems are susceptible to infection throughout the growing season; once infected, they become brittle and may break as the season progresses. When green shoots are infected, the affected tissues appear dark brown to black in feathery patches (Plate 3), which later appear reddish brown on the surface of dormant canes. Only remnants of collapsed hyphal fragments can be found at this stage of development. Cluster infection before or shortly after bloom may result in poor fruit set and considerable crop loss. Berries are susceptible to infection until their sugar content reaches about 8%, although established infections continue to produce spores until the berries contain [5% sugar. lf berries are infected before they attain full size, the epidermal cells are killed, and growth of the epidermis is thus prevented. As the pulp continues to expand, the berry splits from internal pressure. Split berries either dry up or rot, frequently becoming infected by Botrytis ('inerea. Berries of nonwhite cultivars that are infected as they begin to ripen fail to color properly and have a blotchy appearance at harvest (Plate 4). A netlike pattern ofscar tissue (Plate 5) may be observed on the surface of infected berries. Such fruit is unmarketable as fresh fruit, and wines made from it may have off-flavors. In most viticultural regions, the fungus produces its sexual structures, black spherical bodies called cleistothecia (Plate 6), on the surface ofinfected leaves, shoots, and clusters during the latter part of the growing season. Causal Organism Uncinula necator (Schw.) Burr. (syns. Erysiphe necator Schw., E. tuckeri Berk., U. americana Howe, U. spiralis Berk. & Curt., U. subfusaz Berk. & Curt.; anamorph Oidium tuckeri Berk), the fungus that causes powdery mildew, is an obligate parasite on the Vitaceae genera Ampelopsis, Cissus, Parthenocissus, and Vitis. The superficial but semipersistent, septate, hyaline hyphae (4-5 pm in diameter) develop characteristic multilobed appressoria from which penetration pegs are formed. After penetration ofthe cuticle and cell wall, a globose haustorium is formed within the epidermal cell. Multiseptate conidiophores (10-400 ,um long) form perpendicularly on the prostrate hyphae at frequent intervals. Conidia are hyaline and cylindro—ovoid, measure 27*47 >< 14—21 ,um, and accumulate in chains (Plate 7). The oldest eonidium is at the distal end ofthe chain. Under field conditions the chains are rather short, with three to five conidia. Cleistothecia, formed after fusion of hyphae of opposite mating types, are globose(84-105 pm in diameter) and may be found on the surface of all infected parts of the host. Cleistothecia have long, flexuous, multiseptate appendages that have a characteristic crook at the apex when mature. Cleisto— thecia change from white to yellow to dark brown as they mature (Plate 6). They contain four to six asci (rarely more) that are ovate to subglobose and measure 50-60 >< 25—40 ,um. Asci contain four to seven (most commonly four at maturity) ovate to ellipsoid, hyaline ascospores measuring 15—25 X 10-14 pm (Fig. 9). Similar to conidia, viable ascospores germinate with one or more short germ tubes, each quickly forming a multi— lobed appressorium. Disease Cycle and Epidemiology U. necator may overwinter as hyphae inside dormant buds of the grapevine, as cleistothecia on the surface ofthe vine, or both (Fig. 10). In greenhouses and in tropical climates, mycelia and conidia may survive from one season to the next on green tissue remaining on the vine. Developing buds are infected during the growing season. The fungus grows into the bud, where it remains in a dormant state on the inner bud scales until the following season. Shortly after budbreak, the fungus is reactivated and covers the emergent 9 shoot with white mycelium (Plate 8). Conidia are produced abundantly ontheseinfected shoots (called flag shoots)and are readily disseminated by wind to neighboring vines. In viticultural regions where cleistothecia are an important source of primary inoculum, the first infections may be observed as individual colonies on the surface ofleaves growing in close proximity to bark. Shoots growing near bark are frequently infected first, presumably because they are close to cleistothecia that were trapped in bark crevices after being washed there from leaves, canes, and cluster stems during autumn rains. In spring, the cleistothecia split when wetted by rain, and the ascospores are forcibly discharged. Ascospores germinate and infect green tissue, resulting in colonies that produce conidia for secondary spread. The effects of environmental factors such as temperature, moisture, and light on the survival and germination of conidia and on colony development have been studied extensively, Fig. 9. Cleistothecium ot Uncinu/a necator with asci containing ascospores. (Courtesy R. C. Pearson) . / fungus overwmters Q: a [7 /. / //// infected developing buds become infected cleistothecia are produced on leaves, shoots and berries in late summer Fig. 10. Disease cycle of powdery mildew. (Drawing by R. Sticht) 10 OSCUS 25ft , containing ascospores grape cluster shoots and berries \ / fungus on leaves, produces conidia that are spread by wind \__/ Temperature appears to be the major limiting environmental parameter for the development ofthe fungus. Temperatures of 20-27°C are optimal for infection and disease development, although fungal growth can occur from 6 to 32°C. Tempera~ tures above 35°C inhibit germination of conidia, and above 40°C they are killed. At 25° C, conidia germinate in approxi- mately 5 hr. The time from inoculation to sporulation at 23—30°C can be as short as five to six days, whereas at 7°C, more than 32 days are required. Mildew colonies are reported to be killed after exposure to 36°C for 10 hr or 39°C for 6 hr. Temperature and moisture requirements of ascospores are unknown. Free water often results in poor and abnormal germination of conidia as well as bursting of conidia, presumably because of excessive turgor pressure. Rainfall can be detrimental to disease development by removing conidia and disrupting mycelium. Atmospheric moisture in the range of 40-lOO% relative humidity is sufficient for germination of conidia and infection, although germination has also been reported at less than 20% relative humidity. Humidity appears to have a greater effect on sporulation than on germination. For example, two, three, and four to five conidia have been reported to form during a 24-hr period at 3&40, 60-70, and 90—100% relative humidity. respectively. Low, diffuse light favors disease development. In fact, bright sunlight is reported to inhibit germination of conidia; in one study, germination of conidia was 47% in diffuse light but only l6% in sunlight. Control Control of powdery mildew in commercial vineyards is generally based on the use of fungicides. Sulfur was the first effective fungicide used to control this disease and, because of its efficacy (both preventive and curative) and low cost, it is still the most widely used fungicide for this purpose. Sulfur is commonly applied as a dust or as a wettable powder. In dry climates sulfur dust is preferred, whereas in regions where rainfall is plentiful during the growing season, wettable powder in dormant buds infected buds give rise to young shoots completely covered by fungus ascospores are fungus released in O sporulates on surface of green shoots and leaves conidia and ascospores infect green tissue fiiiflflflflflfltlfl till or flowable formulations are preferred for their retentive qualities. Much ofthe fungicidal activity of sulfur is associated with its vapor phase. The production of vapors and their effectiveness depend on the type ofsulfur as well as on environmental factors, primarily temperature. The optimal temperature range for sulfur activity is 25-300C, and the fungicide may not be effective below 18° C. Above 30°C the risk of phytotoxicity increases greatly, and applications at 35°C or higher are not recommended. Sulfur is less active in humid air than in dry air. Copper formulations and several organic fungicides. such as dinocap. benomyl. and compounds belonging to the sterol biosynthesis inhibitor group (e.g., triadimefon), are also used commercially to control powdery mildew, although not as extensively as sulfur. The organic fungicides maintain activity over a wider temperature range than sulfur and, with the exception of dinocap, exhibit less phytotoxicity. Cultural practices may reduce the severity of disease and can increase the effectiveness of chemical control. Planting in sites with good air circulation and sun exposure and orienting rows to take advantage of these factors are helpful. The use of training systems that allow good air movement through the canopy and prevent excess shading is also beneficial. An open canopy not only maintains a microclimate less favorable for disease development but also allows better penetration of fungicide. Vitis species differ greatly in susceptibility to powdery mildew. V. vinz'fera and Asiatic species such as V. betulifolia, V. pubescens, V. davidii, V. pagnucii, and V. piasezkii are highly susceptible. By comparison, American species such as V. aestivalis, V. berlandierz', V. cinerea, V. labrusca, V. riparia, and V. rupestris are much less susceptible. Grape breeders have crossed V. vinifera with various combinations of American species to produce hybrids with varying levels of resistance. To date. biological control has not been applied to U. necator. The most commonly reported mycoparasites are Ampelomyc'es quisqualis Ces. (syn. Cicinnobolus cesatii De Bary) and Tilletiopsis sp. Although use of these fungi may have application in the controlled environment ofa greenhouse, they have not been used to control grape powdery mildew commercially under field conditions. Selected References Boubals, D. 1961. Etude des causes de la r’esistance des Vitacées a l'o‘i'dium de la VigneiUncinula necalor (Schw.) Burr.‘et de leur mode de transmission hereditaire. Ann. Amelior. Plant. ll:40l-500. Bulit. J., and Lafon. R. 1978. Powdery mildew of the vine. Pages 525—548 in: The Powdery Mildews. D. M. Spencer, ed. Academic Press, New York. 565 pp. Delp. C. .l. 1954. Effect of temperature and humidity on the grape powdery mildew fungus. Phytopathology 44:615-626. Kapoor. J. N. 1967. Uncinula Iterator. Descriptions of Pathogenic Fungi and Bacteria, No. l60. Commonwealth Mycological Institute. Kew, Surrey, England. Lafon. R. 1982. Faire face a l’oidium. Vititechnique 57:10—14. Pearson. R. C.. and Gadoury. D. M. 1987. Cleistothecia. the source of primary inoculum for grape powdery mildew in New York. Phytopathology 77:]509—l514. ‘ Pearson, R. C.. and Game]. W. 1985. Occurrence ofhyphae of Uncinu/a necalor in buds of grapevine. Plant Dis. 69:149451. Pool. R. M.. Pearson, R. C.. Welser, M. J.. Lakso. A. N., and Seem. R. C. 1984. Influence of powdery mildew on yield and growth of Rosette grapevines. Plant Dis. 68:590-593. Sall. M. A. 1980. Epidemiology of grape powdery mildew: A model. Phytopathology 70:338—342. (Prepared by R. C. Pearson) Downy Mildew Grape downy mildew occurs in regions where it is warm and wet during the vegetative growth of the vine (e.g., Europe. South Africa, Argentina. Brazil. eastern North America. eastern Australia. New Zealand. China, and Japan). The absence of rainfall in spring and summer limits the spread ofthe disease in certain areas (e.g., Afghanistan. California. and Chile). as does insufficient warmth during the spring in northern vineyards. Cultivars within V. vinifera are highly susceptible to downy mildew. V. aestivalis and V. labrusca are less susceptible. and V. cordifolia, V. rupestris. and V. rotundifolia are relatively resistant. Symptoms The causal fungus attacks all green parts of the vine, particularly the leaves. Depending on incubation period and leaf age, lesions are yellowish and oily (Plate 9) or angular. yellow to reddish brown, and limited by the veins (Plate 10). Sporulation of the fungusia delicate. dense. white. cottony growth—characteristically occurs on the lower leaf surface (Plate ll). Leaf infection is most important as a source of inoculum for berry infection and as overwintering inoculum. Severely infected leaves generally drop. Such defoliation reduces sugar accumulation in fruit and decreases hardiness of overwintering buds. Infected shoot tips thicken, curl (“shepherd’s crook”), and become white with Sporulation (Plate l2); they eventually turn brown and die. Similar symptoms are seen on petioles, tendrils, and young inflorescences. which, if attacked early enough, ultimately turn brown. dry up. and drop. The young berries are highly susceptible. appearing grayish when infected (gray rot) and covered with a downy felt of fungus Sporulation (Plates 13 and 14). Although berries become less susceptible as they mature. infection of the rachis can spread into older berries (Plate 15) (brown rot, without Sporulation). Infected older berries of white cultivars may turn dull gray-green, while those of black cultivars turn pinkish red. Infected berries remain firm compared to healthy berries, which soften as they ripen. These infected berries drop easily, leaving a dry stem scar. Portions of the rachis or the entire cluster also may drop. Causal Organism Plasmopara viticola (Berk. & Curt.) Berl. & de Toni, the cause of downy mildew, is an obligate parasite. It develops intercellularly within the parasitized tissues of the vine in the form of tubular. coenocytic hyphae 8—10 ,um in diameter. bearing globular haustoria that are 4—10 ,um in diameter. The haustoria enter the host cell by invaginating the cellular membrane in which they are ensheathed. Asexual reproduction occurs by the formation of Sporangia, which are ellipsoid and hyaline and measure 14 X ll um. Sporangia are borne on treelike sporangiophores (140*250 ,um long) (Fig. ll). Each sporangium gives rise to one to 10 biflagellate zoospores measuring 6—8 X 4-5 pm. The zoospores escape from the side of the sporangium opposite its point of attachment. either through an opening in a papilla or by directly perforating the wall. Zoospores are mainly uninucleate. Protoplasmic fusions between hyphae originating from different zoospores may occur inside parasitized tissues and give rise to heterokaryotic mycelium. Sexual reproduction begins early in the summer and occurs by the fusion ofan antheridium and an oogonium derived from the terminal expansion of hyphae. An oospore (20-l20 ,um in diameter) forms and is enveloped by two membranes and covered by the wrinkled wall of the oogonium. Oospores form in leaves or possibly throughout the parasitized organ. The following spring, oospores germinate in free water, giving rise to one or occasionally two slender germ tubes, 2-3 ,um in diameter and of variable length. The germ tubes terminate in a pyriform sporangium (28 X 36 ,um). which produces 30-56 zoospores. 11 SANDOZ Fig. 11. Sporangia of Plasmopara wtico/a on treelike sporangiophores emerge through stomata on the underside of a leaf. (Micrograph by R. Guggenheim; reprinted, by permission, from “The new orazolidinone class of systemic fungicides” by R. Sandmeier, Produits Sandoz, RueiI-Malmaison Cedex, France) Zoospore « Encysted zoospore ’\ /’ / ‘\_'\\t“‘ \ Germinating / T \ sporongium/W \ ~ __ \ _ _ _ \a )4 _ \Sporongiophore 1 3 \\ Mycelium in dormant twig Germinating oospore Oospore on ‘ the gr0und Oospore inside infected leaves Oospore ~-———~>Q‘E} \Berry infection Twig infection » .w, ’.) \ ‘* \\ , A? if Spomngium _ Germinating sporungium Sporongium Disease Cycle and Epidemiology P. viricola overwinters mainly as oospores in fallen leaves, although it can survive as mycelium in buds and in persistent leaves, the latter in regions with mild winters (Fig. l2). Oospores survive best in the surface layers of moist soil; survival is little affected by temperature. Oospores germinate in water in spring as soon as temperatures reach 11°C to produce a sporangium from which primary dispersal of zoospores occurs by rain-splash. Sporangiophores and sporangia are produced only through the stomata ofinfected organs, a process that requires 95— l00% relative humidity and at least 4 hr of darkness. The optimal temperature for Sporulation is l8—22° C. The sporangia are detached from sporangiophores by the dissolution of a cross- wall of callose. moisture again being required. The sporangia are dispersed by wind to leaves, where they germinate in free water (optimal temperature 22-250 C) to release zoospores. Zoospores swim to and encyst near stomata. which are entered by germ tubes from germinating cysts. Because the fungus penetrates the host exclusively via the stomata, only those plant Structures with functional stomata are susceptible to infection. Under optimal conditions. the time from germination to penetration is less than 90 min. Because sporangia are usually formed at night and are inactivated by several hours” exposure to sunlight. infection generally occurs in the morning. The time from infection to the Leafy/g infection 3.. lntercellulor myceiium with ‘3 ghoustorio infected grape infected auger waded twrg I Fig. 12. Disease cycle of downy mildew. (Reprinted, by permission, from G. N. Agrios, Plant Pathology, 2nd ed., 1978, Academic Press, New York) 12 first appearance of symptoms is approximately four days. depending on leaf age. cultivar. temperature, and humidity. Downy mildew is favored by all factors that increase the moisture content of soil. air. and host plant. Therefore, rain is the principal factor promoting epidemics. Temperature plays a less important role by retarding or accelerating the develop— ment of the disease. The optimal temperature for development of the fungus is about 25°C. the extremes ranging from 10 to 300C. The most serious epidemics of downy mildew occur when a wet winter is followed by a wet spring and a warm summer with intermittent rainstorms every 8-15 days. These conditions ensure the survival ofoospores and their abundant germination in spring as well as permit the development ofthe disease and its spread within the vineyard. Successive periods of rain stimulate the production of young. susceptible shoots with functional stomata (preparatory rains) and ensure their infection (infection rains). Control Preventive management practices for downy mildew consist of draining soils. reducing the sources of overwintering inoculum. and pruning out the ends of infected shoots. However. because none of these measures is practical or sufficient in vineyards susceptible to downy mildew. chemical control must inevitably be used. Fungicides are the most important control measure on suscep— tible cultivars grown in regions with high disease pressure. Nonsystemic surface chemicals (cupric salts. dithiocarbamates. and phthalimides) are efficacious only as preventive treatments. They are fungitoxic at several cellular sites in fungi. and P. viricola has not become resistant to them. Only the treated organs are protected. generally for seven to 10 days. Cymoxanil is a nonsystemic penetrating fungicide specific to mildew. 1t penetrates the treated organs and synergistically increases the efficacy of nonsystemic surface fungicides combined with it. However. the principal advantage of cymoxanil is its capacity to act curatively during the two or three days following an infection period. Two classes of systemic fungicides are active against the downy mildew fungus. fosetyl aluminum and the phenylamides (or anti—oomycete anilides). These products penetrate the plant and have three principal advantages: the active substance is not removed by rainfall, treatment is curative. and vegetation formed after treatment is protected. The interval between applications can be 14 days. The phenylamides (benalaxyl. metalaxyl. ofurace. oxadixyl) are very effective but are specific to P. viticola, and resistant strains have developed since 1981 in France. South Africa. Switzerland, and Uruguay. Resistant strains are less competi- tive than sensitive strains. so the use of phenylamides in combination with at least one nonsystemic fungicide and limited to only two or three applications per year is recommended. Selected References Blaeser. M.. and Weltzien. H. C. 1977. Untersuchungen fiber die lnfektion von Weinreben mit Plasmopara viticola in Abhangigkeit von der Blattn'assedauer. Meded. Fac. Landbouwwet. Rijksuniv. Gent 42:967i976. Blaeser. M.. and Weltzien. H. C. 1978. Die Bedeutung von Sporangienbildung. -ausbreitung und-keimung fiir die Epidemiebil- dung von Plasma/Jam vilit'ola. Z. Pflanzenkr. Pflanzenschutz 85:155-161. Lafon. R. 1985. Les fongicides viticoles. Pages 191-198 in: Fungicides for Crop Protection. Vol. I. l. M. Smith. ed. Monogr. 31. British Crop Protection Council. Croydon. England. 504 pp. Lafon. R.. and Bulit. J. 1981. Downy mildew ofthe vine. Pages 601-614 in: The Downy Mildews. Academic Press. New York. D. M. Spencer. ed. 636 pp. Langcake. 1).. and Lovell. A. 1980. Light and electron microscopical studies of the infection of Vilix spp. by P/asmopara \WffO/a, the downy mildew pathogen. Vitis 19:321i337. Leroux, P.. and Clerjeau. M. 1985. Resistance of Botrytis ('inerva l’ers. and Plasma/mm \vitit'ula (Berk. & Curt.) Berl. and dc Toni to fungicides in the French vineyards. Crop 1’rot.4:137*|60. (Prepared by R. Lafon and M. Clerjeau) Botrytis Bunch Rot and Blight Botrytis bunch rot or gray mold exists in all vineyards in the world. It was considered a secondary disease for a long time but became increasingly important in Europe after the phylloxera epidemic and the reconstitution of vineyards by grafting. Temperate or cold. damp climates favor this disease. Botrytis bunch rot seriously reduces quality and quantity of the crop. The reduction in yield may be associated with the premature drop of bunches from stalk rot or with the loss of juice and the desiccation of berries. In table grape production. loss of fruit quality in the field. in storage. or during transit can be substantial. In wine production. the most serious damage is qualitative. from the modified chemical composition of diseased berries. The fungus converts simple sugars (glucose and fructose) to glycerol and gluconic acid and produces enzymes that catalyze the oxidation of phenolic compounds. It also secretes polysaccharides such as B-glucan. which hinder the clarification of wine. Wines produced from rotten grapes have off—flavors and are fragile and sensitive to oxidation and bacterial contamination. making them unsuitable for aging. However. in certain cultivars and especially under certain climatic conditions in the fall. Botrytis infection of grape clusters takes on a particular form known as “noble rot.” This rot is beneficial and contributes to the production of exceptional sweet white wines. the most prestigious of which are the Tokays of Hungary. the Sauternes of France. and the German wines known as Aus/ese, Beerenauslese, and Trockenbeerenauslese. Symptoms In early spring. buds and young shoots may be infected. turn brown. and dry out. At the end of spring and before bloom. large. irregular. reddish brown. necrotic patches appear on a few leaves of a vine and are often localized on the edge of the lamina (Plate 16). Before capfall (bloom), the fungus may invade inflorescences. which rot or dry out and fall 0ff(P1ate 17). At the end of bloom. Botrytis frequently develops on the withered calyptras. stamens. and aborted berries attached to or trapped in the clusters. From these sites it attacks the pedicel or the rachis. forming small patches that are brown at first and then turn black. Toward the end of summer. these lesions completely surround the pedicel or rachis (compare with stem necrosis). and portions of the cluster below the necrotic area wither and drop off (Plate 18). From véraison (ripening) onward. the grapes are infected directly through the epidermis or through wounds. The mold progressively invades the entire cluster. Rot develops rapidly in compact clusters where maturing berries are compressed together (Plate 19). Infected white grapes turn brown. and black grapes become reddish. During dry weather. infected berries dry out; in wet weather. they tend to burst. and a brownish gray mold forms on the surface. Table grapes in cold storage often develop a wet rot of the rachis. which becomes covered by a mycelial mat (Plate 20). sometimes with sporulation. The infected berries develop circular brown lesions that gradually cover the whole fruit; this condition of the epidermis is known as “slip-skin.” In Europe. poorly hardened canes may become infected late in the season and show a bleaching of the bark. combined with the development of black sclerotia or grayish. sporulating patches of mycelium. Newly grafted grapevine cuttings incubated in callusing 13 boxes at temperatures ofabout 30° C and high humidity may be infected and destroyed by rapid growth of the mycelium of Botrytis. The fungus also develops under the film of paraffin used to seal the graft union ofgrafted vines and thereby inhibits development of the union. Causal Organism The causal fungus is Bolryotinia fuckeliana (de Bary) Whetzel. of which only the conidial form, Botrytis cinerea Pers., is generally observed in vineyards. The mycelium of B. cinerea is composed of brownish olive, septate hyphae, which are cylindrical or slightly swollen at the septa. The hyphae vary in diameter (1 1-23 ,um) according to the conditions ofdevelop- ment. Anastomoses between hyphae are often noted. Conidiophores (1—3 mm long) are stout, dark, slender, and branched. with enlarged apical cells bearing clusters of conidia on short sterigmata (Fig. 13). Conidia (10-12 >< 8—10 pm) are ovoid or globose, smooth, one-celled, slightly ash-colored, and gray in mass. Under adverse conditions the fungus produces sclerotia (2-4 X 1-3 mm), which are dark. discoid, and firmly attached to the substrate. They consist ofa medulla and a dark cortical layer of cells. Sclerotia can germinate at temperatures from 3 to 27° C by conidiophore production. B. ('inerea may also produce microconidia (phialospores). The phialides usually arise freely from single hyphal cells on the old aerial mycelium. The microconidia (2-3 pm in diameter) are hyaline and one—celled, are formed in chains, and are embedded in mucilage. Their sole function is the spermatization of sclerotia, leading to the formation of apothecia. Sclerotia can germinate to form the apothecia of Botryotinia fucke/iana. but apothecia are rarely found in vineyards. Apothecia are cupulate, stalked, and brownish, with a stipe about 4'5 mm long. Ascospores (7 X 5.5 pm) are hyaline. one—celled, ovoid-ellipsoid, and smooth. Disease Cycle and Epidemiology B. cinerea is not specific to grapevines. It attacks many cultivated and wild plants and can live as a saprophyte on necrotic, senescent, or dead tissue. The pathogen overwinters as sclerotia (in Europe), formed in the autumn on the canes (sometimes on mummified grapes), and also as mycelium on the bark and in dormant buds. In spring, the sclerotia and the mycelium produce conidia, which are probably the source ofinoculum for prebloom infection of leaves and young clusters. Conidia are disseminated by rain and wind and are considerably more numerous after véraison. Conidia germinate at temperatures between I and 30°C (18°C is optimal). In water, germination is stimulated by exogenous nutrients from pollen or leaf exudates. In the absence of water, germination occurs if the relative humidity is at least 90%. Infection at the optimal temperatures of 15-20° C Fig. 13. Conidia on conidiophore of Botrytis cinerea. (Courtesy R. Wind) 14 occurs in the presence of free water or at least 90% relative humidity after approximately 15 hr. More time is required at lower temperatures. Hyphae generally penetrate directly through the epidermis of susceptible organs. However, wounds facilitate infection, particularly injuries caused by insects, powdery mildew, hail, or birds. Scanning electron microscopy has shown that conidial germ tubes penetrate berries through numerous microfissures that form around nonfunctional stomata. Under certain conditions, the ovary is infected through the stigma and style at the end of bloom, but the infection remains latent until véraison. Control Cultivars differ in susceptibility to Botrytis bunch rot based on the compactness oftheir clusters, the thickness and anatomy ofthe berry skin, and their chemical composition (anthocyanins and phenolic compounds). It is also known that the vine synthesizes phytoalexins (resveratrol and the viniferins) and that the concentration of these protective substances is related to the relative resistance of cultivars. Susceptible cultivars usually need to be protected against bunch rot by a combination of cultural practices and chemical control. To slow the development of the disease, avoid excessive vegetation through rootstock management and the judicious use of nitrogen fertilization; increase aeration and exposure of clusters to the sun by using appropriate trellising systems and by removing leaves around the fruit; and provide protection against diseases and insect pests capable of injuring the berries, particularly grape berry moths. Chemical control is usually necessary but can be conducted only with preventive treatments. A program of four applica- tions (known as the “standard” method in Europe) has given satisfactory results: first treatment at the end of bloom and the beginning offruit set; second treatmentjust before berry touch; third treatment at the beginning of véraison: and a fourth treatment three weeks before harvest. Chemical treatment may be ineffective if strains of B. cinerea develop resistance to the fungicide, as has happened with the benzimidazoles and dicarboximides. Proper adjustment of spraying equipment to give consistently good penetration and coverage of clusters is essential. Bunch rot in stored table grapes is generally controlled by sulfur dioxide fumigation combined with storage at low temperatures (near 0° C). With a recently developed mathematical model of the epide- miological behavior of B. (‘inerea on the vine, the risk of disease can be predicted at any given moment, and hence the appro- priateness of a chemical treatment can be evaluated. Other research indicates that an antagonistic fungus, Trichoderma harzianum, may be an effective biological means of controlling B. cinerea, A strategy of integrated control using both the antagonist and chemical sprays appears promising. Selected References Bulit, J., and Dubos, B. 1982. Epid'emiologie de la pourriture grise. Bull. OEPPJEPPO Bull, 12:37-48. Bulit, J., and Lafon, R. 1977. Observations sur la contamination des raisins par le Botrytis cinerea Pers. Pages 61-69 in: Travaux Dediés a G. Viennot—Bourgin. Societ'e Francaise de Phytopathologie, Paris. 416 pp. Coley-Smith, J. R., Verhoeff, K., and Jarvis, W. R. 1980, The Biology of Botrytis. Academic Press, New York. 318 pp. Dubos, B.. Jailloux, F., and Bulit. J. 1982. L‘antagonisme microbien dans la lutte contre la pourriture grise de la vigne. Bull. OEPP/ EPPO Bull. 122171475. Hill, G., Stellwaag—Kittler, F., Huth, G., and Schlosser. E. 1981. Resistance of grapes in different developmental stages to Botrytis cinerea. Phytopathol. Z. [02:328i338. Jarvis, W. R. 1977. Botryotinia and Bolrylis Species: Taxonomy, Physiology and Pathogenicity. Monogr. 15. Canada Department of Agriculture, Ottawa, Ontario. 195 pp. McClellan. W. D., and Hewitt. W. B. 1973. Early Botrytis rot ofgrapes: Time ofinfection and latency of Botrytis r-inerea Pers. in Vitis vini/‘era L. Phytopathology 63:1151*1157. Pezet, R., and Pont, V. 1986. Infection florale et latence de Botr_i'tis ('inerea dans les grappes de Vitis vinifem (var. Gamay). Rev. Suisse Vitic. Arboric. Hortic. 18:317-322. Strizyk, S. 1983. Modélisation. La gestion des mod‘eles “EPI.” Phytoma 350:13—19. (Prepared by J. Bulit and B. Dubos) Black Rot Black rot is one of the most economically important diseases ofgrape in the northeastern United States, Canada, and parts of Europe and South America. The disease is indigenous to North America and was probably introduced to other countries via contaminated propagation material. It was introduced into France on phylloxera—resistant stock. Black rot was seen in 1804 in a Kentucky vineyard; however, the first detailed account of the disease was given by Viala and Ravaz in 1886. Crop losses can range from 5 to 80%, depending on the severity of the epidemic, which is governed by inoculum level, weather, and cultivar susceptibility. Symptoms All new growth is susceptible to attack during the growing season. Young leaf laminae, petioles, shoots, tendrils, and peduncles can be infected. The main symptom on leaves is the appearance of small, tan, circular spots on the lamina in spring and early summer. Leaf spots appear one to two weeks after infection. Spots vary from 2 to 10 mm in diameter (Plate 21). Lesions become cream colored, with the color deepening to tan and ultimately to reddish brown on the adaxial surface. Leaf spots are bordered by a narrow band of dark brown tissue. Pycnidia develop in the center of these necrotic spots and appear as small, blackish pimples (Plate 22). Lesions develop on petioles at about the same time leaf lesions appear. Some lesions enlarge, girdle the petiole, and kill the entire leaf. Lesions on peduncles and pedicels are small, darkened depressions, which soon turn black. Elongated black cankers develop on young shoots through— out the season. Lesions vary in length from a few millimeters to 2 cm. Pycnidia are commonly observed on these lesions. Numerous cankers result in blighting 0f the growing tips of shoots. The first indication of infection on berries is the appearance of a small (about 1 mm in diameter) whitish dot. In a matter of hours, this dot is surrounded by a reddish brown ring, which can grow to over 1 cm in diameter within one day. Within a few days, the berry begins to dry, shrivel, and wrinkle until it becomes a hard, blue-black mummy (Plates 23 and 24). The entire cluster may be affected. On berries of muscadine grapes (V. rotundifolia), symptoms appear as small, black, superficial, scabby lesions [-2 mm in diameter (Plate 25). These lesions do not spread or cause decay of maturing berries as on bunch grapes, although infected young berries may drop or mummify. Lesions may coalesce to form a brown to black crust covering a large part of the surface ofa berry. The skin ofthe infected berry often splits at the edge of larger lesions. The surface of the lesion is cracked and roughened with embedded pycnidia. Causal Organism Guignardia bidwellii (Ellis) Viala & Ravaz (anamorph Phyllosticta ampelicida (Engleman) Van der Aa), the cause of black rot, produces ascocarps (pseudothecia) in a stroma on overwintered mummies. Pseudothecia (Fig. 14) are separate, black, and spherical (61-199 pm in diameter), with a flat or papillate ostiole at the apex. The centrum is pseudoparen- ehymatous and without paraphyses. Asci (36-56 X 12-17 pm) are fasciculate, cylindrical to clavate, short-stipitate, and eight—spored (Fig. 14). The ascus wall is thick and composed of two layers. Ascospores (10.6-18.4 >< 4.8—9.0 pm) are hyaline, nonseptate, oval or oblong, straight or inequilateral, rounded at the ends, and biseriate and are often surrounded by a mucilaginous sheath. Black, spherical pycnidia (Fig. 14) 59-196 pm in diameter are produced on the host during the growing season. They are solitary, erumpent, and ostiolate at the apex. On leaf blades they occur in circular, reddish brown, necrotic spots. On stems, tendrils, peduncles, and petioles, they are found in elliptical to elongate, brown to black cankers. On fruits they are present in berry mummies or in brown to black, superficial scabs and cankers. Conidia are hyaline, nonseptate, ovoid to oblong, and rounded at the ends; they measure 7.1—14.6 X 5.3-9.3 ,um. Spermagonia are black, spherical (45-78 pm in diameter), innate, erumpent, and ostiolate at the apex. They are produced toward the end of the growing season on berry mummies and dead leaves in association with ascogonial stromata. Spermatia are hyaline, nonseptate, and bacilliform and measure 2.5 X l,um. A distinct physiologic race of the fungus, differing in pathogenicity from G. bidwellii on American bunch grapes, occurs on muscadine grapes. G. bidwelliz' “f. euvitis Luttrell” is pathogenic to American species of the Vitis section Euvitis and to V. vinifera. G. bidwellz'if. muscadinii Luttrell is pathogenic to V. rotundifolia and V. vinifera. A third race, G. bidwellii “f. parthenocissi Luttrell,” is pathogenic only to Parthenocissus spp. Besides differing in pathogenicity, the race on muscadine grapes also differs in appearance, growth rate of colonies in culture, and size of pseudothecia, ascospores, and conidia. Disease Cycle and Epidemiology The fungus overwinters in mummified berries on the soil or in 25pm Fig. 14. Fruiting bodies and spores of Guignardia bidwe/lii. A,Cross sectionthroughapseudothecium,showing asciwithina locule. B, Ascus and ascospores. C, Cross section through a pycnidium. D, Conidiogenous cells and conidia. (Modified and reprinted, by permission, from Sivanesan and Holliday. 1981) 15 ...
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