Bunch Disease of Black Walnut

[Paper expanded from a talk given at the 41st annual meeting of NNGA in 1950.]

John W. McKay, horticulturist, and Harley L. Crane, principal horticulturist, United States Department of Agriculture, Agricultural Research Administration, Bureau of Plant Industry, Soils, and Agricultural Engineering, Division of Fruit & Vegetable Crops and Diseases, Plant Industry Station, Beltsville, Maryland

Introduction

For the past several years observations have been made on the development and spread of the bunch (brooming)[13] disease on Juglans nigra and on other species of walnut growing in the orchards at Plant Industry Station at Beltsville, Maryland. Because of the widespread interest in growing walnuts a brief survey of these observations will be given in this paper together with a summary of the history of the disease and a discussion of its possible effect on walnut production.

History of the Disease

The bunch disease of walnut has been known for years. Waite[14] in 1932 said, "It turned up in Delaware several years ago, where quite a variety of walnuts, including the Persian, the Japanese Group, and the American Black Walnut, were found to be affected. At Arlington Farm, Virginia, during the past 15 years it has boldly riddled the collection of nut trees assembled in the grounds for study and ornamental purposes." Photographs made in 1914 of Japanese walnut trees growing in Georgia and thought to be affected by rosette (now known to be caused by zinc deficiency) have been found in the files of the U. S. Department of Agriculture. Now that the symptoms of the two different disorders are known, it seems clear that the bunch disease was present in those two states at that early date.

Becker,[15] of Climax, Michigan in 1940 reported on his observation of this disease in that area. He reports that he observed several cases of it on Persian walnut, Japanese walnut, and butternut, in addition to many diseased eastern black walnuts. He says, "My conclusions are that in witches'-broom (bunch disease) we have a very bad disease that threatens the black walnut trees everywhere".

In 1939, the late Howard E. Parsons, pathologist of the U. S. Department of Agriculture, made an inspection trip to Climax and other areas in Michigan where he studied and photographed diseased trees. Parsons at that time was working on a similar disease of pecan and

water hickory and was of the opinion that the disease found on the various species of walnuts in Michigan was similar to the one he was studying.

For the past 20 years the bunch disease of walnuts has been under observation by the writers and it seems clear that its incidence has increased greatly during that time. In 1935 scions and buds were taken from diseased eastern black walnut and butternut trees growing at Arlington Farm and grafted or budded on eastern black walnut stock growing in the original nut tree nursery at the Plant Industry Station at Beltsville, Maryland. This was done in an attempt to determine whether the disease was caused by a mineral deficiency or by a virus. All buds and scions died, but the following year two of the seedling rootstocks showed characteristic symptoms of the bunch disease. Since this disease was already present on the station farm it was not definitely known that it was transmitted to the stocks by budding or grafting the diseased material on them.

In December of 1946 Hutchins and Wester[16] presented a paper before the American Phytopathology Society giving the results of their studies on the bunch disease. In this paper they reported that the disease was transmitted by patch bark grafts performed in 1944 and 1945 and that the incubation period varied from several months to two years. It was concluded that since the disease was transmitted by grafting, and in the absence of a visible pathogen, a virus causal agent was indicated.

Symptoms

The characteristic symptoms of the bunch disease are mainly the production of brooms or sucker shoot growth on the tree trunk and main branches and the tufting of terminals, profusion of small branches from axillary buds, the dwarfing and narrowing of the leaflets, and the dying back of the trees resulting sometimes in the death of the trees. The principal symptom is the production during summer of bushy, wiry growth caused by the breaking into growth of lateral buds that normally would remain dormant over the winter. These buds produce shoots that again branch from lateral buds and the process may be repeated for three or four times, resulting in a tightly packed mass or bunch of small, wiry twigs and undersized leaves. Another characteristic symptom is that this growth proliferation continues unabated until the first frost, and, since the wood of these shoots is thus not properly matured, killing back of the diseased portions of the tree usually occurs with the first hard freezes of winter.

As the disease progresses, the wood in the main branches becomes very brittle and is easily broken by wind or ice. This condition is followed by the dying back of branches and finally the death of the tree. Trees even moderately affected soon become worthless for nut production, as few nuts are set and those that mature are usually poorly filled.

Susceptibility of Species

Extended observations show that of the walnut species now grown in eastern United States, the Japanese walnuts, i.e., the Siebold and the heartnut, are by far the most subject to attack by this disease. These walnuts are so susceptible that in localities where this disease is present the planting of young trees is inadvisable, as they are almost certain to be short lived. Once infected, will endanger other walnut trees in the area.

Observations at Beltsville show that the butternut is almost as susceptible to attack as is the Japanese walnut. Some workers are inclined to believe that the rather serious decrease in numbers of butternut trees in some areas is due to the bunch disease. The Persian (English) walnut is also quite susceptible, although probably not so much so as the butternut or the Japanese walnut. The eastern black walnut seems to be the most resistant of all, although some evidence indicates that at least certain trees of this species may have the disease but not show symptoms of it. Gravatt and Stout[17] report that walnut trees may be affected for a considerable length of time without showing recognizable symptoms. Out of a lot of 300 healthy-appearing trees, 37 per cent showed bunch disease symptoms following pruning. Only four percent of the unpruned check trees developed similar symptoms during the same period of time.

Distribution

At the present time bunch disease is quite widespread in eastern United States, occurring in Maryland, District of Columbia, Delaware, New Jersey, New York, Michigan, Ohio, Indiana, Illinois, Pennsylvania, West Virginia, Virginia, North and South Carolina, Georgia, Tennessee, Alabama, and probably other States. No special surveys have been made for bunch disease, and all distribution information has been obtained from observations of U. S. Department of Agriculture or State workers or from specimens submitted.

Damage Caused

Trees with bunch disease may live for several years in a stag-horned or tufted condition. Affected trees generally set few nuts and the nuts that mature are usually poorly filled and hence low in oil content. It is likely that a part of the unsatisfactory growth and fruiting performance of certain eastern black walnut trees may be due to the disease, even though they do not show the symptoms as they are now known. Severely affected trees are subject to cold injury, and in addition the wood becomes very brittle and is easily broken by storms. Although this disease has been known for several years, it is believed that its seriousness has not been fully appreciated, as it does not cause death as soon as symptoms appear. Several years must elapse before the tree succumbs. In the nut tree plantings made at the Plant Industry Station at Beltsville, Maryland, large numbers of butternut, Japanese walnut, and Persian walnut trees were planted. During the following years, although no records have been kept, several hundred of these trees have become affected and have been removed. Consequently at the present time we do not have any butternut or Japanese walnut trees, and only a few Persian (English) walnut trees left in the plantings. So far, not a single eastern black walnut tree has been removed from the orchards because of the bunch disease. Some trees have shown characteristic symptoms of the disease, but following the removal of the entire diseased limbs the symptoms have not reappeared.

Possible Effects of Bunch Disease on the Walnut Industry

This disease is known to spread to nearby healthy walnut trees, but the means by which it is spread or how infection occurs is not known. No survey has been made to determine whether the disease is present in the various regions in which walnut trees are grown, and hence it is not known how widely it is distributed at present. Its spread is probably associated with an insect vector, and the presence of the vector would determine whether or not local spread would occur. Much more must be learned about this disease before its importance and destructive nature can be fully determined. It seems certain that in localities where the disease is already present there is little use in planting young trees of the most susceptible species unless trees in the vicinity that are already diseased are destroyed. Nurserymen growing trees of the Japanese walnut, butternut, and Persian walnut should be sure that no diseased trees which might infect the nursery trees are close to their nurseries. It is not known how far the inoculum may be carried, but at this time it would seem that in order to be reasonably safe no diseased tree should be allowed to grow within a mile radius of a nursery. Infected nursery trees (or scions) probably constitute the most important means of long-distance spread for a disease of this type.

Control

The only known method of control of the bunch disease is to prevent healthy trees from becoming infected. This can be done only by destroying completely all diseased trees. In the early stage of the disease, sometimes only one branch on a tree may show symptoms; and complete removal of this branch may result in the tree's not showing additional symptoms for a year or more. Except in the case of black walnut, the disease breaks out again; hence cutting out diseased limbs cannot be considered a satisfactory control measure, except possibly on the eastern black walnut.

Case Histories at Beltsville

As a part of walnut breeding work carried on during the past 14 years, approximately 20 large nigra trees of named horticultural varieties have been topworked to seedlings of natural first-generation hybrids between J. regia and J. nigra for the purpose of forcing the seedling scions into early fruiting. Of these 20 trees, 3 have shown such unusual behavior as to merit a description of each in the form of a case history.

Tree Number 838. This tree was cut back severely in the spring of 1942, and on August 26, 1943 vigorous new shoots were budded to 47.11-P₁₇, a second-generation seedling of the O'Conner natural hybrid. The buds grew vigorously in 1944 and early in the season developed symptoms of the bunch disease. By the end of the growing season of 1944 the scion limbs were heavy with the typical proliferated shoots characteristic of the disease. Also, a few vigorous sucker limbs of the stock tree that grew out from below the point of union of the scions showed typical symptoms of the disease, although these limbs were later outgrown by normal shoots and are not now to be seen. In the early spring of 1945 the diseased limbs were all removed from the tree to prevent the further spread of the disease in the area.

At the same time that the above seedling was budded in the top of this tree, a large lateral limb of the stock tree was budded to seedling number 40.70-P₁. This seedling originated from a nut of the Ohio variety of black walnut that was only about 1/4 the size of nuts typical of the variety. At the time it was thought that this nut resulted from a cross of Ohio with pollen of the Persian walnut, as it was produced under bag and following hand-pollination. Later growth of the seedling indicated, however, that the pistillate flower was probably pollinated by J. nigra before the bagging occurred, since only J. nigra characteristics have shown up in the seedling. In 1950, one bud of the nigra seedling 40.70-P₁ has almost completely regenerated the top of the tree and no symptom of the disease is evident. By contrast in 1944, almost all of the top of the tree was occupied by diseased limbs, five in number, of the O'Conner seedling.

Tree Number 854. This tree has shown behavior almost identical with that of Number 838, but three seedlings were topworked instead of one. All three originated from the Coye hybrid and all were budded on July 27, 1944. Less than one month later all buds had produced a foot or more of growth, and one to two scions of each seedling reached sufficient size and vigor to survive the following winter without damage. None of the scions branched in 1944, and all failed to show symptoms of the disease. Early in 1945 profuse branching occurred on the one surviving scion of seedling number 39.03-P₂, and by midsummer excessive proliferation of the buds of primary shoots had resulted in the formation of a mistletoe-like growth characteristic of the disease. Scions of the two other seedlings, 39.03-P₈ and 39.03-P₁₁, were lost by wind damage in midsummer, but at the time they showed no signs of the disease. Most of the shoots of 39.03-P₂ were killed during the following winter, and in April, 1946, the remaining live portions were removed by the Division of Forest Pathology for use in transmission studies.

On August 18, 1944, four patch buds of the O'Conner natural hybrid were placed on one of the main limbs of this tree. One of these buds grew, and in 1950 has come to occupy more than half the top of the tree. The remainder of the top is made up of the original stock tree. There is no evidence of bunching in the tree at present.

Tree Number 411. This tree was budded to six seedlings of the Fox natural hybrid on April 28, 1943. Only one of these lived, 40.45-P₄, and one scion of this seedling in 1950 comprises the entire crown. No symptom of the disease has appeared in this scion, and the tree is healthy at present.

On April 8, 1944, small lateral limbs of the tree were splice-grafted to two Coye seedlings, 39.03-P₈ and 41.26-P₁₀. One scions of each grew vigorously during the summer, and 41.26-P₁₀ first became chlorotic, then diseased. Seedling 39.03-P₈ became chlorotic but at the end of the season had not shown symptoms of the disease. Both were removed from the tree early in 1945 and the living shoots used for scionwood in transmission studies by the Division of Forest Pathology.

An additional case is Tree Number 795. This is a grafted tree of the Graham variety of black walnut that was planted in 1932 within 100 feet of trees of the Bates and Faust varieties of heartnuts. By 1940 the latter trees were heavily infected with bunch disease, but it was not until 1943 or 1944 that symptoms were discovered in the Graham tree. At this time the heartnuts were removed from the orchard. The Graham tree has shown only a few small diseased limbs during the past six or seven years, and in 1950 a fair crop of nuts is in prospect.

Discussion

The following observations should be mentioned briefly before discussing the questions raised by the case histories:

1. Out of more than one hundred seedling scions from 13 hybrids topworked on large nigra trees, three have become diseased the first or second year after the scions began to grow on black walnut stock.

2. The three susceptible seedlings have all been grafted on different nigra stock trees, and the three stock trees have since regenerated only healthy limbs, after removal of the diseased shoots.

3. Seedlings from a total of 13 natural hybrids between J. nigra and J. regia have been used, and only two of these hybrids have yielded susceptible seedlings. However, only a few seedlings were available from certain hybrids.

4. A total of 156 trees of approximately 36 horticultural varieties has been grown at Beltsville, and only one tree of the variety Graham has shown well developed symptoms of the bunch disease. Two other Graham trees have shown slight or questionable symptoms of the disease.

It should be pointed out that a considerable number of heartnut and butternut trees were planted at random in the same orchards with the black walnut trees used in these experiments and at the same time (1932). In many cases black walnut trees grew within 50 or 100 feet of the heartnut trees. The bunch disease first appeared on heartnut trees, the most susceptible walnut species, and spread quickly to butternut, which is also very susceptible. By 1940 most of the diseased heartnuts had been removed from the orchards, but it was not until after the top-working experiments described above were completed that the orchards were cleared of all diseased trees. It is therefore possible that insect vectors or other agencies may have spread the disease to the scions of the topworked seedlings from the infected heartnut and butternut trees.

Number 795 is the only J. nigra tree on the station farm that has consistently shown symptoms of the disease during the past eight years, and in 1950 only a few limbs are affected. On the basis of the admittedly meager information reported here, it can be stated that the black walnut varieties used in these experiments are more resistant to the bunch disease than are varieties and seedlings of heartnut and butternut. That this is generally true is also borne out by the fact that in the vicinity of Beltsville, Maryland, and the District of Columbia, practically all dooryard trees of the Japanese walnut are infected with bunch disease, many of them having already been killed, whereas relatively few black walnut trees in the area show symptoms of the disease.

The suggestion has been made that most varieties and seedlings of black walnut are symptomless carriers of the disease, and only under certain adverse conditions of environment would symptoms appear. This would explain why trees that are cut back severely, as was the case with tree Number 838 described above, show symptoms on the excessively vigorous shoots of the next year's growth.

Little can be said at the present time about the relative resistance of black walnut varieties to the bunch disease because nothing is known about how it is spread from one individual tree to another. The case histories of trees described in the present paper are considered to be worth recording because they show that black walnut trees may support diseased scions and later regenerate apparently healthy tops. In these cases the trees showed a type of resistance to the disease. However, there are many cases known, the majority of which are seedlings, in which black walnut trees became so badly infected with the disease that nut production ceased and the trees later died. Whether the type of resistance described in this paper is widely prevalent in the black walnut as a species will be impossible to determine until more is known about how the disease is spread.

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