Apple Scab
lesions. Conidia remain attached to the conidiophores in dry weather, but upon wetting during a rain they are easily detached, and may b e w a s h ed down or blown away to other leaves or fruit on which they germinate and cause infection in the same way ascospores do. Addi-tional infections by conidia continue throughout the growing season following a rain of sufficient duration. Infections, however, are more abundant in the cool, wet periods of spring and early summer and again in the fall. T h e y are more infrequent, if not entirely absent, in the dry, hot summer weather.
After infected leaves fall to the ground the mycelium penetrates into the interior of the leaf, the hyphae branch b e t w e en the cells, and if they come in contact with hyphae of the compatible mating type from adjacent infections, they form perithecia which carry the fungus through the winter; otherwise, the hyphae degenerate and play no part in the overwintering of the fungus.
Control
Although some apple varieties are more resistant to apple scab than others, neither varietal resistance nor s o me occasionally advocated cultural practices are important in the control of apple scab. Apple scab can b e thoroughly controlled today, even on the most susceptible varieties, by timely sprays with the proper fungicides.
For an effective apple scab control program, apple trees must b e dil-igently sprayed or dusted before, during, or immediately after a rain from the time of b ud break until all the.ascospores are discharged from the perithecia. If these primary infections from ascospores are checked, there will b e little n e e d to spray for scab the remainder of the season. If primary infections do develop, spraying may have to b e continued throughout the season. Sprays b e g in in the spring when a wetting period (rain) is sufficiently long at the existing temperature to produce an infection, and are repeated every 5 -7 days, or according to rainfall, until petal fall. O ne must make sure that the ne w tissues on rapidly expanding young leaves and fruit are always covered with fungicide during an infection period. After petal fall, ahd d e p e n d i ng on the success of the control program to that point, sprays are usually repeated every 10-14 days for several more times.
Several fungicides that give excellent control of apple scab are available. All of them are protectant, since they can protect a plant from b e c o m i ng infected, but they cannot cure an infection, although some of them have so-called " k i c k b a c k" action, i.e., ability to stop infections which may have started, and s o me have an eradicant action,
271
i.e., they can "burn-out" young scab spots early in the season. D o d i ne (= Cyprex) gives excellent scab control and is one of the fungicides exhibiting local systemic action. It reduces spore formation on scab spots and inhibits germination of spores produced on such spots. Ex-cellent scab control is also obtained with captan, ferbam, Glyodin, Glyodex (a mixture of dodine and Glyodin), dichlone ( = Phygon), thi-ram, sulfur, etc. T h e se fungicides may be u s ed alone or in combina-tions since they differ in their ability to control scab or other diseases, in duration of " k i c k b a c k" action, and in phytotoxicity.
Selected References
Albert, J. J., and A. B. Groves. 1965. T h e efficacy of glyodin plus d o d i ne on the conidia of Venturia inaequalis. Phytopathology 55: 503 (abstr.).
Bratley, C. O. 1937. I n c i d e n ce and d e v e l o p m e nt of a p p le s c ab on fruit during the late s u m m er a nd w h i le in storage. U.S. Dept. Agr. Tech. Bull. 563: 4 5 pp.
Keitt, G. W., a nd L. K. J o n e s. 1926. S t u d i es of the e p i d e m i o l o gy a nd control of a p p le scab. Wisconsin Agr. Expt. Sta. Res. Bull. 73: 104 p p.
Keitt, G. W., D. M. B o o n e, a nd J. R. Shay. 1959. G e n e t ic a nd nutritional controls of host-parasite interactions in a p p le scab. In " P l a nt Pathology —Problems and Progress 1 9 0 8 - 1 9 5 8 " (C. S. Holton et al, e d s ), pp. 157-167. Univ. of Wisconsin Press, Madi-son, Wisconsin.
Mitchell, J. E., a nd J. D. Moore. 1962. Relation of d o d i ne r e s i d ue levels a nd s c ab devel-o p m e nt devel-on a p p le fruit a nd leaves. Phytdevel-opathdevel-oldevel-ogy 52: 5 7 2 - 5 8 0 .
N u s b a u m, C. J., a nd G. W. Keitt. 1938. A cytological study of host-parasite relations of Venturia inaequalis on a p p le l e a v e s . /. Agr. Res. 56: 5 9 5 - 6 1 8 .
Roosie, G. S. 1963. R e s e a r ch on a p p le a nd pear scab in the Netherlands from 1938 until 1961. Neth.J. Plant Pathol. 69: 132-137.
Dutch E lm D i s e a se
Occurrence and Importance
Dutch elm d i s e a se owes its name to the fact that it was first de-scribed on elm in Holland in 1921. Since then the disease has spread throughout E u r o p e, parts of Asia, and most of North America. In the United States the disease was first found in Ohio and some states in the east coast in the early 1930's; it has since spread westward as far as Idaho, and it is expected to continue to spread.
Dutch Elm Disease 273
Dutch elm d i s e a se is the most destructive s h a de tree d i s e a se in the United States today. It affects all e lm s p e c i e s, although s o me of them are more seriously affected than others. T h e American elm, which is the most valuable native elm shade tree, is one of the most severely affected. T h e d i s e a se may kill branches and entire trees within a few weeks or a few years from the time of infection. T h o u s a n ds of elm trees in towns across the country die from Dutch e lm d i s e a se every year. In Massachusetts alone 150,000 e lm trees were killed by the dis-e a sdis-e in thdis-e past two d dis-e c a d dis-e s. T h dis-e cost of cutting down d dis-e ad dis-e lm trdis-edis-es amounts to many millions of dollars per year. And, of course, no one can estimate the value of the natural beauty of streets and towns de-stroyed by the disease.
Symptoms
T h e first symptoms of the d i s e a se appear as s u d d en or prolonged wilting of the leaves of individual branches or of the entire tree (Fig.
36). Wilted leaves frequently curl, first turn yellow, then brown, and finally fall off the tree earlier than normal. Most affected branches die immediately after defoliation. T h e d i s e a se usually appears first on one or several branches and then spreads to other portions of the tree.
Thus, many d e ad branches may appear on a tree or a portion of a tree.
Such trees may die gradually, branch by branch, over a period of sev-eral years or they may recover. Sometimes, however, entire trees sud-denly d e v e l op d i s e a se symptoms and usually die within a few weeks.
Usually trees that b e c o me infected in the spring or early s u m m er die quickly, while those infected in late s u m m er are much less seriously affected and may even recover, unless they b e c o me reinfected.
Whe n the bark of infected twigs or branches is p e e l ed back, brown streaking or mottling appears on the outer layer of wood. In cross sec-tion of the branch, the browning appears as a broken or continuous ring in the outer rings of the w o od (Fig. 37A).
The Pathogen: Ceratocystis ulmi
T h e fungus causing Dutch elm d i s e a se is an ascomycete. T h e myce-lium is creamy white (Fig. 37B) and lives in the xylem vessels of in-fected elm trees and in the w o od and bark of trees killed by the dis-ease. T h e mycelium may also b e carried to and grow in the bark of elm trees or cut logs killed from causes other than this disease.
While in the vessels, the mycelium produces short hyphal branches
F i g. 36. An American e lm tree infected with D u t ch e lm d i s e a s e. Inset: Infected y o u ng twigs s h o w i ng wilted, rolled l e a v e s, a nd the characteristic hook of the terminals.
(Photo by courtesy of S h a de T r e e Laboratory, University of Massachusetts.)
on which clusters of Cephalosporium type conidia are formed (Fig.
38). In dying or d e ad trees the mycelium produces s o me Cephalospor-ium, but mostly Graphium type spores on coremia d e v e l o p i ng on bark which is somewhat loose from the w o od and in tunnels m a de in the bark by insects. T h e coremia consist of hyphae g r o u p ed into an erect, dark, solid stalk, and a colorless, flaring h e ad to which the spores ad-here , forming a sticky glistening, whitish at first, and later slightly yel-lowish, droplet.
T h e fungus is heterothallic and requires contact of two sexually compatible strains for sexual reproduction. Since, frequently, only
Dutch Elm Disease
one of the mating types is found in large areas in nature, sexual repro-duction is extremely rare. In the United States, for example, the fun-gus rarely reproduces sexually, but it does so rather frequently in E u r o p e. Whe n the two mating types do c o me in contact, however, fer-tilization takes place and perithecia develop. T h e perithecia are
F i g. 37. (A) D i a g o n al a nd cross sections of e lm twig a nd branch affected with D u t ch e lm d i s e a s e. T h e twig s h o ws a ring of b r o wn discoloration near its surface, w h i le the discoloration in the branch is d e e p e r in the w o o d. (B) Y o u n g culture of Ceratocystis ulmi g r o wn from a section of d i s c o l o r ed w o od p l a c ed on a nutrient m e -dium. (Photos by courtesy of S h a de T r e e Laboratory, University of Massachusetts.)
275
spherical and black, about 120 μ in diameter, and have a long (about 300-400 μ) neck terminating at an ostiole with a fringe of colorless hyphae. A few hyphal strands also d e v e l op from the outer layer of the perithecial coat. Perithecia form singly or in groups and in the s a me areas in the bark as the coremia.
Inside the perithecium many asci develop, each containing eight colorless, slightly curved ascospores. As the asci mature, they disinte-grate leaving the ascospores free in the perithecial cavity. T h e asco-spores are discharged through the nec k canal and accumulate in a sticky droplet which is supported by the fringe of hyphae surrounding the ostiole.
Development of Disease
Dutch elm d i s e a se is the result of an unusual partnership b e t w e en a fungus and an insect (Fig. 38). Although the fungus alone is responsi-ble for the disease, the insect is the indispensaresponsi-ble vector of the fun-gus, carrying the fungus spores from infected e lm w o od to healthy e lm trees. T h e insects responsible for the spread of the d i s e a se are the E u r o p e an elm bark beetle (Scolytus multistriatus) and the native elm bark bettle (Hylurgopinus rufipes) (Fig. 39A).
T h e fungus overwinters in the bark of dying or d e ad elm trees and logs as mycelium and as spore-bearing coremia. E lm bark beetles pre-fer to lay their eggs in the intersurface b e t w e en bark and w o od of trees w e a k e n ed or dying by drought, d i s e a s e, etc. T h e adult female b e e t le tunnels through the bark and opens a gallery parallel with the grain of the w o od with Scolytus, and at a 45-degree angle with Hylurgopinus.
T h e female lays eggs along the sides of the gallery, the eggs soon hatch, and the larvae open tunnels at right angles to the maternal gal-lery. If the tree was already infected with the fungus, the latter pro-duces mycelium and sticky, Graphium type spores in the b e e t le tun-nels. Whe n the adult beetles e m e r g e they carry thousands of fungus spores on and in their bodies. Scolytus beetles fee d in the crotches of living, vigorous elm twigs. Hylurgopinus beetles fee d on stems 2-12 cm in diameter (Fig. 39B). T h e se beetles burrow into the bark and wood, the spores are deposited in the w o u n d ed tissues of the tree, germinate, and grow rapidly into the injured bark and the wood.
Whe n the fungus reaches the large xylem vessels of the spring wood, it produces Cephalosporium type spores which are carried up by the sap stream. T h e se spores reproduce by yeastlike b u d d i n g, germinate, and start ne w infections. T h e extent of symptoms in the crown is cor-related with the extent of vascular invasion. In early stages of
infec-Fig. 38. Disease cycle of Dutch elm disease caused by Ceratocystis ulmi.
Tunnels of female beetle and larvae in elm bark Fungus spreads through naturalroot graft
Diseased *,
Beetles breed ^ in elm logs and diseased trees
il Ascospores p^vreleased from f \\perithecium •W Perithecium Perfect stage seldom found in nature Fungus grows in elm bark and tunnels
CoremiaQ
Coremium
m Graphium-type conidia Emerging adult / beetle carrying / fungus spores ,] Beetle carries^! ή spores to 1 / healthy elm trees J Beetle carrying |I fungus spores Leaves above ut infection \ point wilt *
Mycelium and Cephalosporium-type spores in xylem vessels of elm
Discolored ring of xylem in infected stem Mycelium and spores in vessels
F i g. 39. (A) B e e t le carriers of the D u t ch e lm d i s e a s e. S i de a nd top v i e ws of the E u r o-p e an (a) a nd the native (b) e lm bark b e e t l e s, (c) L a r va of the E u r o o-p e an e lm bark b e e t l e. (B) Galleries b e n e a th the bark of d e ad e lm trees m a de by the female a nd the larvae of the E u r o p e an (upper left) a nd the native (lower right) e lm bark b e e -tles. At u p p er right and lower left can b e s e en the bark punctures or w o u n ds on healthy e lm m a de by the adult E u r o p e an a nd native e lm bark beetles, respectively.
(Photos by courtesy of S h a de T r e e Laboratory, University of Massachusetts.)
tion, the mycelium invades primarily the vessels, and only occasion-ally tracheids, fibers, and the surrounding parenchyma cells. General invasion of tissue begins at the terminal or extensive dieback phase of the disease, at which time there is also considerable intercellular growth of the fungus b e t w e en the parenchyma cells. T h e mycelium penetrates from cell to cell through pits. Spores, of varying sizes and shape, are p r o d u c ed infrequently and only in v e s s e ls and tracheids.
G u ms and tyloses are produced in the larger vessels and sometimes isolated areas of the sapwood are blocked by a combination of gums, tyloses, and fungal growth. Infection also induces browning of the water-conducting vessels, probably through enzymatic oxidations of substances released by the plant tissues in reaction to toxic fungal
se-Dutch Elm Disease 279
cretions. T h e oxidized, dark-colored substances are then adsorbed on the vessel walls and impart to them the brown coloration.
Infected twigs and branches soon wilt and die. T h e mechanisms by which the Dutch elm d i s e a se fungus induces wilt symptoms are not completely understood. Although p l u g g i ng of the v e s s e ls by my-celium, gums, and tyloses, and thereby blocking of p a s s a ge of water, plays a role in wilt development, the p h e n o m e n on is by no m e a ns general, and is considered by s o me workers to b e i n a d e q u a te to c a u se wilting by itself. T h e secretion of a toxic substance by the fungus has b e e n shown and there are indications of interference with the balance of the auxin system of the plant, but no detailed information on its role in wilt is yet available.
Infections that take place in the spring or early s u m m er result in invasion of the long vessels of the elm springwood through which the spores can b e carried rapidly to all parts of the tree. If vascular inva-sion b e c o m es general, death of the tree may occur within a few weeks.
During later infections, vascular invasion is limited to the outer, shorter vessels of the s u m m e r w o od in which they move only for short distances. As a result, late infections mostly produce only localized infections and seldom cause serious immediate d a m a ge to the tree.
T h e elm bark beetles fee d on living trees for only a few days and then fly back to dying or w e a k e n ed elm w o od in which they construct ne w galleries and lay eggs. T h e r e are usually three generations of beetles per season. In each generation the young adult goes from d e ad or w e a k e n ed elm trees to living, vigorous ones on which it feeds, and then returns to the d e ad or w e a k e n ed trees to lay its eggs. Therefore, once an insect b e c o m es contaminated with fungus spores, it carries them both to healthy and d i s e a s ed wood, in both of which the fungus grows and multiplies and contaminates all the offspring of the insect as well as any other insects that will visit the infected wood.
Control
Great efforts have b e e n m a de and are b e i ng continued to find resist-ant clones within the susceptible American e lm species and in other species. Certain Asiatic species such as the Siberian and the C h i n e se elm are resistant to Dutch elm d i s e a s e, but produce poor shade trees.
Hybrids b e t w e en various species have shown resistance in varying degrees and s o me of them look promising. Several s e e d l i ng selec-tions, such as the Christine B u i s m an elm, have performed well in some areas and are b e i ng planted extensively.
Presently, control of Dutch elm d i s e a se in the United States is at-tempted primarily through sanitation measures and through chemical control of the insect vectors of the fungus. Sanitation involves the removal and destruction of w e a k e n ed or d e ad e lm trees and e lm logs, thus destroying the larvae contained in them or denying the insect and the fungus their overwintering habitat. Pruning out infected twigs and branches will sometimes eliminate the disease. Control of the insect vector by chemicals involves spraying of the healthy elm trees while dormant and in the spring with D DT or methoxychlor. A n e w systemic insecticide, Bidrin, has b e e n u s ed recently against the elm bark beetles, but its effectiveness in controlling the disease is still questionable. U se of Vapam drenche s b e t w e en elm trees kills the roots and prevents root grafts b e t w e en adjacent trees, thus preventing further spread of the disease through root grafts.
Selected References
Banfield, W. M. 1 9 4 1 . Distribution b y the s ap stream of s p o r es of three fungi that i n d u ce vascular wilt d i s e a se of elm. J. Agr. Res. 62: 6 3 7 - 6 8 1 .
Banfield, W. M. 1968. D u t ch e lm d i s e a se recurrenc e a nd recovery in American e l m.
Phytopathol. Z. 62: 2 1 - 6 0 .
Clinton, G. P., a nd F l o r e n ce A. M c C o r m i c k. 1936. D u t ch e lm d i s e a s e. Conn. Agr. Expt.
Sta., New Haven, Bull. 3 8 9 : 7 0 1 - 7 5 2 , with 8 plates.
F e l d m a n, A. W., Í . E . Caroselli, a nd F. L. H o w a r d. 1950. Physiology of toxin produc-tion by Ceratostomella ulmi. Phytopathology 40 : 3 4 1 - 3 5 4 .
H o l m e s, F. W. 1965. Virulence in Ceratocystis ulmi. Neth.J. Plant Pathol. 7 1 : 9 7 - 1 1 2.
Ouellette, G. B. 1962. Morphological characteristics of Ceratocystis ulmi in American e lm trees. Can.]. Botany 40: 1463-1466.
Ouellette, G. B. 1962. S t u d i es on the infection process of Ceratocystis ulmi in American e lm trees. Can. J. Botany 40 : 1 5 6 7 - 1 5 7 5 .
Partridge, A. D. 1968. D u t ch e lm d i s e a se found in Idaho. Plant Disease Reptr. 5 2 : 46.
Whitten, R. R., a nd R. U. S w i n g l e. 1964. T h e D u t ch e lm d i s e a se a nd its control. U.S.
Dept. Agr. Bull. 193: 12 p p.
Wilson, C. L. 1965. Ceratocystis ulmi in e lm wood. Phytopathology 5 5 : 477 .
Brown Rot of Stone Fruits
Occurrence and Importance
Brown rot occurs throughout the world where stone fruits are grown and where there is sufficient rainfall during the ripening period of the
Brown Rot of Stone Fruits
fruit. In the United States it is most serious along the Atlantic sea-board and less so along the western coast, but it also causes d a m a ge in other parts of the country. It affects peaches, cherries, and plums with about equal severity.
L o s s es from brown rot result primarily by rotting of the fruit in the orchard, although serious losses may also appear during transit and marketing of the fruit. Yields may b e r e d u c ed also by destruction of the flowers during the b l o s s om blight stage of the disease. T w ig infec-tions do not always cause losses directly, but may cause indirect losses by furnishing inoculum for fruit infections. In severe infections, and in the a b s e n ce of good control measures, 5 0 - 7 5 % of the fruit may rot in the orchard and the remainder may b e c o me infected before it reaches the market.
Symptoms
T h e first symptoms of the d i s e a se appear on the blossoms, particu-larly the older ones on which the floral parts b e g in to wilt (Fig. 40A).
Brown spots appear on petals, stamens, or pistils and they spread rap-idly, involving the entire flower, and part or all of its stem. In h u m id weather the infected organs are covered with the gray conidia of the fungus and later shrivel and dry up, the rotting mass clinging to the twigs for s o me time. T w i gs bearing infected flowers d e v e l op small, elliptical, sunken, brown cankers around the flower stem which some-times may encircle the stem and cause twig blight. In h u m id weather, g um and also gray tufts of conidia appear on the bark surface.
Fruit symptoms appear w h en the fruit approaches maturity. Small,
Fruit symptoms appear w h en the fruit approaches maturity. Small,