/

VIRUS DISEASES

AND NONINFECTIOUS

DISORDERS

OF STONE FRUITS

IN NORTH AMERICA

Agriculture Handbook No. 437

Agricultural Research Service

UNITED STATES DEPARTMENT OF AGRICULTURE
VIRUS DISEASES

AND NONINFECTIOUS

DISORDERS

OF STONE FRUITS

IN NORTH AMERICA

Agriculture Handbook No. 437

This handbook supersedes Agriculture Handbook 10, Virus Diseases and Other

Disorders with Viruslike Symptoms of Stone Fruits in North America.

Agricultural Research Service

UNITED STATES DEPARTMENT OF AGRICULTURE

Washington, D.C. ISSUED JANUARY 1976

For sale by the Superintendent of Documents, U.S. Government Printing Office

Washington, D.C 20402 — Price $7.10 (Paper Cover)

Stock Number 0100-02691
FOREWORD

The study of fruit tree virus diseases is a tedious process because of the

time needed to produce experimental woody plants and, often, the long interval

from inoculation until the development of diagnostic symptoms. The need for

cooperation and interchange of information among investigators of these diseases

has been apparent for a long time. As early as 1941, a conference was called

by Director V. R. Gardner at Michigan State University to discuss the problem.

One result of this early conference was the selection of a committee (E. M.

Hildebrand, G. H. Berkeley, and D. Cation) to collect and classify both

published and unpublished data on the nomenclature, symptoms, host range,

geographical distribution, and other pertinent information on stone fruit virus

diseases. This information was used to prepare a "Handbook of Stone Fruit

Virus Diseases in North America," which was published in 1942 as a miscellaneous publication of the Michigan Agricultural Experiment Station.

At a second conference of stone fruit virus disease workers held in Cleveland,

Ohio, in 1944 under the chairmanship of Director Gardner, a Publication

Committee (D. Cation, G. H. Berkeley, L. C. Cochran, F. P. CuUinan, and

R. J. Haskell was appointed to revise the text of the first handbook. This

revision resulted in the publication in 1951 of Agriculture Handbook 10,

"Virus Diseases and Other Disorders with Viruslike Symptoms of Stone

Fruits in North America." The work of this committee was helped greatly by

the passage of the Research and Marketing Act of 1946 and the subsequent

establishment and funding of regional research projects to investigate stone

fruit virus diseases. Research and Marketing Act funds were used to publish

Handbook 10.

State workers in the several regions cooperated through an informal Interregional Research Committee that functioned actively, and helped to establish

the formal IR-2 Committee and project. The regional projects, with the active

cooperation of the United States Department of Agriculture and the Canadian

Department of Agriculture, have reduced duplication of research efforts and

improved dissemination of information to the public. The formation of the

European Committee for Cooperation in Fruit Tree Virus Research has aided

the cooperative effort in North America through exchanges of information

and personnel and has helped to establish international standards for the

detection and control of fruit tree virus diseases.

Since the publication of Handbook 10, several pathologists, who were prominent authors in that book, have retired from active teaching or research. Because

so much of our present knowledge about stone fruit virus diseases was obtained

from their pioneering efforts, we wish to acknowledge their influence on this

discipline and acknowledge our debt to the guidance they provided in the

original edition from which we have drawn freely in this new handbook. We

particularly want to thank G. H. Berkeley (deceased), E. M. Hildebrand, Lee

III
M. Hutchins, G. W. Keitt (deceased), T. B. Lott, John A. Milbrath, D. H.

Palmiter (deceased), T. E. Rawlins (deceased), E. L. Reeves, B. L. Richards,

and R. S. Willison.

Illustrations in this book were taken from Agriculture Handbook 10, "Virus

Diseases and Other Disorders With Viruslike Symptoms of Stone Fruits in

North America," or were submitted by the authors of the various sections. Credit

is gratefully extended to the following contributors of illustrations for sections

of which they are not authors: American Potash Institute, figure 152; Neis R.

Benson, figures 145, 146, and 147; and A. E. Hitchcock, figures 142, 143, and

144.

This handbook is the result of the cooperative effort of the authors, who

represent all the fruit-growing regions of North America. The Editorial and

Publication Committee is deeply indebted to them for their willingness to participate in the preparation of this revision. Special credit is due L. C. Cochran,

retired, former chief. Fruit and Nut Crops Research Branch, Plant Science

Research Division, ARS, for his help in initiating the production of this book.

We want to recognize J. R. McGrew, plant pathologist, USDA, for his technical

advice and review of the manuscript and his efforts in collecting of the illustrations.

R. M. Gilmer

J. Duain Moore

George Nyland

M. F. Welsh

T. S. Pine, chairman,

Editorial and Publication Committee

[Thomas Sheffield Pine, who served as chairman of the Editorial and Publication Committee for this book, died April 2, 1970, after an illness of several

months. The other members of the Editorial and Publication Committee wish to

give special recognition to his dedication, organizational ability, and hard work

in assembling the manuscripts, unifying and verifying literature citations, and

mounting the illustrations. He completed the work on schedule under extremely

difficult conditions and failing health.}

IV
CONTENTS

Page

Introduction VIII

Techniques of Investigating Stone Fruit Viruses 1

Control of Stone Fruit Virus Diseases 10

IR-2, The Interregional Deciduous Tree Fruit Repository 16

Quarantine and the Detection of Stone Fruit Viruses in Plant

Importations 23

Virus Diseases of Almond and Apricot 33

Almond virus bud failure 33

Apricot pucker leaf 43

Apricot ring pox 45

Virus Diseases of Peach 50

Asteroid spot 50

Peach blotch 56

Peach calico 58

Peach mosaic 61

Peach mottle 71

Peach rosette 73

Peach stem pitting 77

Peach wart 88

Peach yellows 91

Phony 96

Prunus ring spot group 104

Red suture 133

Rosette mosaic 135

Stubby twig 139

Weak peach 144

X-disease 145

Yellow bud mosaic 156

Virus Diseases of Plum and Prune 166

Plum line pattern 166

Prune diamond canker 176

Prune dwarf 179

Virus Diseases of Sour Cherry 191

Bark splitting in Montmorency cherry 191

Green ring mottle 193

Pink fruit 200

Virus gummosis of Montmorency 202

V
Page

Virus Diseases of Sweet Cherry 204

Albino 204

Apple chlorotic leaf spot and other filamentous virus

infections in Prunus 206

Black canker 209

Blossom anomaly of cherry 211

Cherry boron rosette 213

Cherry mottle leaf 216

Cherry rasp leaf 219

Cherry twisted leaf 222

Freckle fruit 226

Fruit pitting of sweet cherry 227

Little cherry 231

Cucumber mosaic virus infection in Prunus 238

Rough bark of sweet cherry 240

Rusty mottle group 242

Short stem 250

Spur cherry 252

Sweet cherry rough fruit 254

Tobacco mosaic virus infection m Prunus 256

Xylem aberration 257

Nontransmissible Disorders That Resemble Virus Diseases 259

Almond corky spot 259

Apricot gumboil 261

Chlorotic fleck of myrobalan plum 265

Constriction disease of Stanley prune 268

High temperature mottle of Montmorency cherry 272

Italian Prune leaf spot 274

Italian Prune sparse leaf 277

Noninfectious bud failure in almond 278

Noninfectious plum crinkle leaf 283

Noninfectious plum shot hole 285

Peach false wart 288

Peach variegation 290

Peach yellow spot 292

Plum rusty blotch 294

Prune crinkle leaf 297

VI
Page

Prune leaf casting mottle 299

Pustular canker of Tragedy prune 302

Standard prune constricting mosaic 304

Sweet cherry crinkle leaf, deep suture, and variegation 306

Diagnosis of Stone Fruit Virus Diseases and Certain Disorders

That Resemble Virus Diseases 314

Nutritional Disorders That Resemble Virus Diseases 316

Herbicide Injuries That Resemble Virus Diseases 347

Air Pollution Injuries That Resemble Virus Diseases 355

Literature Cited 365

Appendix 405

Common and Scientific Names of Plants mentioned

in the Text 405

Contributors 408

References to Stone Fruit Virus Diseases Published After

Closing Date for Receipt of Manuscripts 411

Host-Disease Index 424

Trade names are used in this publication solely for the purpose of

providing specific information. Mention of a trade name does not constitute a guarantee or warranty of the product by the U.S. Department

of Agriculture or an endorsement by the Department over other products

not mentioned.

In citing this handbook, the Editorial and Publication Committee would be

pleased if authors would refer directly to particular authors and sections, for

example—

NYLAND, GEORGE.

1974. ALMOND VIRUS BUD FAILURE. In Virus Diseascs and Noninfectious

Disorders of Stone Fruits in North America. U.S. Dept. Agr., Agr.

Handbook 437.

VII
INTRODUCTION

Much new information has been obtained about stone fruit viruses and the

diseases they incite since the publication of Agriculture Handbook 10 in 1951.

The purpose of this new publication is to provide professional investigators

and students with an updated reference work and agricultural technicians and

orchardists with an illustrated handbook to help in diagnosing virus diseases in

the field. Therefore, this book contains sections on the basic and applied

approaches to research on stone fruit virus diseases as well as extensive descriptive material on the symptoms, distribution, control, and economic factors

pertaining to these diseases.

Progress in our knowledge of fruit tree virus diseases has not simplified the

role of the scientist in explaining them or the field adviser in diagnosing them.

Only five virus diseases of stone fruit trees were recognized in 1930; 48 were

known in 1951. This publication describes 95 virus diseases. Although this may

appear to indicate a phenomenal rise in the number of virus diseases in North

American orchards, the figures are somewhat misleading. Many diseases occur

in very limited areas and are not economically important. They are described

briefly in this book.

It is now known that several diseases, previously described under different

names or from different areas of the continent, are caused by viruses so

similar to each other that they justify being grouped as strains. Thus, some

diseases mentioned individually in Agriculture Handbook 10 will be found

under different headings in this book. Diseases thought to be virus-induced, but

for which no virus has yet been isolated and purified, have been retained as

virus diseases ; however, this does not preclude the possibility that future research

will show they are caused by mycoplasms or still unidentified pathogenic agents.

Plant virology is a dynamic discipline, and réévaluation of present knowledge

should be expected.

The diagnosis of virus diseases in orchard trees often is confused by the

presence of many nontransmissible disorders with symptoms resembling those

caused by viruses. These disorders include genetic abnormalities, nutritional

deficiencies or excesses, injuries caused by the improper use of pesticides and

herbicides, and injuries caused by air pollutants. Because these disorders must be

considered when attempting to diagnose virus disease problems in the field,

chapters on these subjects are included in this handbook.

The ultimate objective of all research on stone fruit virus diseases is the

control of these diseases in the orchard. Three sections of this handbook deal

directly with problems of control, ranging from fundamental orchard housekeeping to Federal quarantines against the chance importation of foreign

viruses. Today it is possible for orchardists to plant fruit trees that are free from

all known viruses, but preventing virus infection in the orchard is still a major

problem. The insect or mite vectors of only a few fruit tree viruses have been

VIII
identified. At least two viruses are transmitted from diseased to healthy trees in

pollen. Nematodes are known vectors of viruses but have been implicated in the

spread of very few stone fruit diseases. Native herbaceous and woody plants that

may act as reservoirs of virus for spread to fruit trees have been identified for

relatively few diseases. For many tree fruit virus diseases the only known means

of spread is in infected propagating materials. Therefore, despite progress in

our ability to identify viruses and to produce virus-free trees, much work

remains to be done on disease control in the orchard.

Virus diseases of stone fruit trees are generally referred to by their common

names. Terminology used in the study of these diseases varies widely, but the

text adheres as closely as possible to the terms suggested by Welsh (7.74).^

^Italic numbers in parentheses refer to Literature Cited, p. 365.

IX
TECHNIQUES OF INVESTIGATING STONE

FRUIT VIRUSES

ROBERT W. FULTON

The association of a causal agent with a disease is fundamental in pathology.

The mere study of symptoms in a diseased plant is inadequate to demonstrate the

cause of the disease or its relationship to other diseases. The requirements

outlined in the classical Koch's postulates are just as necessary for virus diseases

as for those caused by fungi and bacteria.

Progress in research on viruses infecting woody plants has lagged behind

the general development of plant virology. Stone fruits, like other rosaceous

plants, are difficult to inoculate and are poor inoculum sources. Most stone

fruit viruses are unstable. Usually they are present in low concentration.

The difficulties of inoculating and transmitting some stone fruit viruses have

been overcome, and their properties, morphology, and serology have been

investigated. This has provided the opportunity to associate causal agents with

diseases by a sequence similar to that outlined in Koch's postulates.

In this section we will concern ourselves only with mechanical transmission

of stone fruit viruses, not their transmission by insect or nematode vectors,

dodder, or pollen. Information pertaining to viruses not occurring in North

America will usually not be included. Many potentially useful techniques have

been applied to viruses similar to those in stone fruits, but a discussion of

these is beyond the scope of this section.

Mechanical Transmission

Source of inoculum. — Transmission of necrotic ring spot virus from cherry

to cucumber {473) was first accomplished by grinding in buffer young expanding leaves showing shock symptoms and applying the homogenate to carborundum-dusted cucumber cotyledons. Immature leaves are usually a good source of

inoculum even when the virus is latent. Older leaves, or any leaves after terminal

growth has ceased, usually make weakly infective inoculum, and often virus

cannot be transmitted from them.

Although young leaves with recently developed symptoms usually provide

choice inoculum, other tissues are sometimes effective. Petals may provide

infective inoculum of some viruses difficult to transmit from leaves {251, 432,

446, 668). Viruses also have been transmitted by mechanical inoculation from

pollen, inner bark, buds, fruit, seeds, and roots {16, 172, 196, 725, 758).

The species of Prunus host may have a marked effect on the infectivity of

extracts prepared from it. P. tomentosa is difficult to transmit virus from by

mechanical inoculation {252)\ P. pensylvanica, P. mahaleb, and P. pérsica are

1
2 VIRUS DISEASES OF STONE FRUIT

much better sources of most viruses. Plum line pattern virus, for example, was

much more readily transmitted from P. mahaleb than from P. domestica {312).

Transmission of virus by grafting from an unsatisfactory host to a host amenable

to mechanical transmission is a relatively unexplored field. Viruses may sometimes be transmitted by approach grafting between woody and herbaceous hosts

{172, 234, 494).

Preparation of inoculum. — Inoculum is usually prepared by grinding infected

tissue in phosphate buffer. An optimum of about pH 8 was found for infectivity

of a number of stone fruit viruses {226). The optimum concentration of buffer

for infectivity, however, is around 0.03 M, which is not likely to maintain the

pH unless the proportion of tissue to buffer is small. Many viruses infecting

stone fruit are inactivated rapidly by oxidized materials in plant sap. Thus,

the inclusion in extracts of an antioxidant helps prevent rapid loss of infectivity.

The most useful antioxidant is probably 2-mercaptoethanol (2-ME) at about

0.02M {232, 512). Sodium diethyldithiocarbamate (DIECA) inhibits polyphenol oxidase and thereby stabilizes some viruses {271). Unfortunately, it is

itself an inactivator of certain viruses {22) and should not be used in inoculum

indiscriminately.

Various compounds adsorbing or reacting with tannins or other virusinactivating substances have been used to increase infection. Alkaloids form

insoluble complexes with tannins; nicotine base (2.5 percent) was included in

inoculum of plum line pattern virus {372) in transmitting it from plum to

herbaceous plants. Similarly, caffeine has been beneficial in the transmission of

necrotic ring spot virus {190). Alumina also adsorbs tannins and has been

used as an aid in mechanical transmission {102). Although these additives may

increase infectivity, none has been essential; some transmission can usually be

obtained without them.

Application of inoculum. — Inoculum may be efficiently applied to abrasivedusted leaves with a gauze pad, forefinger, glass spatula, or brush. Washing

inoculated leaves with water is usually detrimental to infection {226), although

plant extracts left on the abraded leaf surface may be toxic. Wiping inoculum

from the leaves immediately with the pad used to inoculate, or fresh gauze, so

that the inoculated surface dries quickly, results in good infection with a

minimum of injury {753).

Application of inoculum with an artist's spray gun has been described as

more efficient than wiping {402). An air pressure of 60 pounds, with the

nozzle held 1 cm. from the surface being inoculated, was recommended. An

inoculum delivery rate of 10 ml. per minute was optimal. Carborundum

(1 percent, w/v) was incorporated in the inoculum.

Inoculations also may be made rapidly by rubbing the freshly cut surface of a

stack of disks, or a roll, of infected tissue over the surface of carborundumdusted, buffer-sprayed leaves {754). This method is used to overcome difficulties

arising from oxidation in extracts.
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 3

Characterizing and Identifying Stone Fruit Viruses

Once a stone fruit virus has been transmitted to an herbaceous host, it can be

characterized by methods conventional for mechanically transmitted viruses.

Determining the host range is a useful first step. The host range can be compared with host ranges, including diagnostic and differential hosts, that have

been described for other viruses. Another purpose in investigating host ranges

is to find hosts suitable for producing virus for purification and to find a host

suitable for infectivity assays.

When the host range and symptoms of an unknown isolate match those of a

known isolate, the identity of the two usually can be presumed. Unfortunately,

strains of a virus often vary in host range as well as in symptoms caused, so

that host range differences need not indicate that the viruses are unrelated. For

prunus ring spot and prune dwarf viruses, some hosts consistently differentiate

a wide range of strains of each virus, whereas other hosts do not (JO6).

The use of differential hosts to identify stone fruit viruses is subject to the

same difficulties as the use of host ranges; strains may vary in the symptoms

they produce. On some hosts, however, symptoms are relatively consistent for

many isolates. Prunus ring spot and prune dwarf virus strains, for example,

produce typical reactions on Sesbama exaltata, Momordica halsamina, Cyamopsis

tetragonaloha, and Cucúrbita maxima cv. Buttercup {106^.

Host ranges and symptom type are also useful in separating mixtures of

viruses. Inoculation of a mixture to a host which is insusceptible to or which

localizes one of the viruses makes possible the isolation of the other virus.

This can be done with Prunus inoculum provided it is sufficiently infective.

Some differential hosts are not particularly easy to infect, however, and may

be infected by inoculum from cucumber more readily than by inoculum from

Prunus. Table 1 lists some hosts reported as being diagnostic or differential for

stone fruit viruses.

Properties. — As with other mechanically transmitted viruses, the thermal

inactivation point, resistance to aging in vitro, and dilution end point vary

among the stone fruit viruses (table 2). The dilution end point of most of

the stone fruit viruses is highly variable and depends to a great extent on the

choice of host supplying the extract and the length of the incubation period.

Cucumber cotyledons, for example, provide more infective extracts 4 or 5 days

after inoculation with necrotic ring spot virus or prune dwarf virus than after

7 or 8 days (228). The dilution end point, therefore, is not particularly useful

in the differentiation of stone fruit viruses.

Several stone fruit viruses lose infectivity very rapidly in crude sap; a loss

of 95 percent of the infectivity within 2 minutes is common (226). This

lability will differentiate prune dwarf, Prunus ring spot, plum line pattern, and

apple chlorotic leaf spot viruses from the somewhat more stable peach yellow

bud mosaic, tomato bushy stunt, and cucumber mosaic viruses. Aging in vitro,
VIRUS DISEASES OF STONE FRUIT

TABLE 1.—Reactions of some diagnostic herbaceous hosts to

certain viruses found in Prunus ^

Virus

Host PRSV ' PDV PLV YBMV CMV CLSV

Chenopodium amaranticolor

Cucúrbita maxima

Cyamopsis tetragonaloba . .

Gomphrena globosa . Momordica balsamina

Phaseolus vulgaris

Ricinus communis

Sesbania exaltata

Tithonia speciosa

Physalis floridana

S-CP

NorCl

S-N

S-NSp

NLl

- orSM

± or —

+ H

S-C

-or LI

- or LNSp

SM

SM

NLl

- or SC

+ orCLL

LNl

NLl

S-CM

LI

S-Sp

Ll-SM

NLl

S-M

S-M

LI

SM

LSC

LI

^ Adapted from 225, S7Uy 512, 706,

- PRSV, Prunus ring spot virus; PDV, prune dwarf virus ; PLV, plum line

pattern virus; YBMV, yellow bud mosaic virus; CMV, cucumber mosaic virus;

CLSV, apple chlorotic leaf spot virus.

^ S, systemic; C, chlorotic; L, local; 1, lesion; H, no symptoms; N, necrotic;

M, mottling; Sp, spotting; -f, infection; —, no infection.

however, does not provide a criterion for differentiation among the very

labile viruses.

As conventionally determined, aging tests determine the last bit of infectivity

remaining in an extract. The rate of infectivity loss provides more useful information and can be expressed conveniently by determining the half-life of the

virus (739). This determination requires reasonably accurate quantitative assays

of infectivity. In determining the infectivity loss of very unstable viruses, the

extrinsic factors are probably more important than the intrinsic factors. Therefore, unless tests are carefully controlled, differences between viruses may

reflect differences in the type of extract.

Thermal inactivation trials involve exposure of infectious extracts to controlled temperatures for 10 minutes. With undiluted or concentrated plant sap,

this period is sufficient for most of the infectivity to disappear even at room

temperature. Determination of thermal stability, therefore, requires diluted

extracts in which infectivity has been stabilized by chemical additives. For

practical purposes, the diluent is usually phosphate buffer containing DIECA,

2-ME, or other antioxidants known to stabilize infectivity. Such preparations

contain more infective virus than nonstabilized crude extracts, and higher thermal

inactivation points result. Thermal inactivation points for Prunus ring spot virus

of 52° to 54° C. and for prune dwarf virus of AA° were reported for dilute
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 5

extracts without stabilizing chemicals (226). Tests with a wide range of isolates

similarly diluted, but stabilized with antioxidants, gave end points of 55° to 62°

for necrotic ring spot virus and 45° to 54° for prune dwarf virus {706),

Although dilution lowers the virus concentration, data obtained from such

extracts do show differences among stone fruit viruses and are probably comparable with conventional data on more stable viruses in undiluted sap.

Preservation of Virus Isolates

The maintenance of stock cultures of stone fruit viruses requires attention

because an assured supply of inoculum is necessary during an investigation,

and later, when comparisons with new isolates become important. Maintaining

a virus in living plants is the method of choice when inoculum is needed frequently. However, this has disadvantages; plants may grow sufficiently rapidly

to require frequent transfer of the virus. If they grow slowly, transmission of

TABLE 2.—Properties of viruses isolated from Prunus

[Italic numbers in parentheses refer to Literature Cited, p. 365]

Thermal

inactivation

point

Virus (°C.) Stability Size and shape

Prunus ring spot .... 55° to 62° (706) Very unstable 23 mfjL sphere (228)

Prune dwarf 45° to 54° (706) ... do 22 m/jL sphere (228)

Plum line pattern . . . 66° (512) ... do 30 m/jL sphere

Apple chlorotic 49° to 52° (A05) ... do 12 by 500 to 700 m/i

leaf spot flexuous rod (4Ö5)

Peach yellow bud 60° (107) Several days 25 to 28 nv* sphere

mosaic (107)

Cucumber mosaic 65° to 70° ... do 28 to 30 m/i sphere

(736)

Tomato bushy stunt 80° ... do 30 mfjL sphere

(16)

Tobacco mosaic (251) 94° Very stable 18 by 300 m/x

rigid rod

Cherry rasp leaf (Í7Í) 55° to 60° 15 to 21 days 30 mfjL sphere (281 )

(Arabis mosaic

virus).

Cherry rasp leaf (Í7Í) 65° to 70° ... do Do.

(Raspberry ring

spot).

Cherry leaf roll (170) 55° to 60° 5 to 10 days Do.

Sarka (350) 45° to 47° Very unstable 20 by 764 m/x rods

(350)

Peach shoot stunting 58° 7 days 30m/>tspher€ (281)

(^71) (tomato black

ring).
6 VIRUS DISEASES OF STONE FRUIT

the virus may be difficult from old or dormant tissue. Infectious inoculum is

not always available from woody hosts that undergo a cycle of growth and

dormancy. Furthermore, cultures in living plants are subject to contamination

with unwanted viruses. Some of these difficulties may be avoided by keeping

several cultures of each virus. We keep cultures in Frunus hosts (P. mahaleb

or P. pérsica whenever possible), and also, when possible, in Vinca rosea,

which can be cut back severely from time to time. The young leaves of V. rosea

usually provide infectious inoculum.

A better method of maintaining cultures is in the form of vacuum-dried

tissue {371). In this form, the virus is not subject to contamination or change

and is readily available. The tissue selected for preservation should contain a

high concentration of infectious virus. Some isolates are more readily maintained in this way than others. Without previous experience with an isolate,

preserved material should be tested periodically to detect decreases in infectivity

that might foreshadow loss of the culture.

Transmission to the Original Host

Transmission of virus to plants of the original host species is of primary

importance in identifying stone fruit viruses. No amount of correlation between

symptoms and type of virus isolated will equal the direct demonstration that

a characterized virus isolate will cause a specific disease when introduced into

known hosts.

The susceptibility of Vrtinus to mechanical inoculation is low, unfortunately,

and trees must usually be infected by budding or grafting techniques. However,

young six- to eight-leaf seedings of a number of species, particularly P. pensylvanica, P. mahaleb, and P. pérsica, are susceptible to mechanical inoculation

{227, 757). After infected seedlings reach sufficient size, virus may be

transmitted by budding from them to older Prunus trees.

Young Prunus trees also may be infected by implanting infected herbaceous

stem tissue beneath a bark flap. The tissue is trimmed so that cut surfaces contact those of the woody host {175, 473). This is not, however, an efficient

method of transmission. A somewhat similar technique, involving approach

grafts between woody and infectious herbaceous hosts, seems to be more

effective with Malus than Prunus {172, 234).

Grafts made at bud break often induce symptoms within a few weeks. Symptoms result sooner from grafts made close to growing points than lower on the

stem. After terminal growth has ceased, grafts usually do not induce symptoms

until dormancy is broken.

Virus Purification

As with other viruses, purification of stone fruit viruses involves solving a

number of problems in logical order as discussed in the following sections.

Selection of host. — The concentration of stone fruit viruses is relatively

low in the tissues of many herbaceous plants, which are hardly better than

Prunus tissues as a source of virus for purification. It is necessary not only to
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 7

select a host in which the virus reaches the highest concentration, but also to

harvest infected tissue at the optimum time.

For Vrunus ring spot and related viruses, the inoculated cotyledons of

cucumber provide highly infective extracts if harvested 4 to 5 days after being

heavily inoculated {22^~). Inoculation to cucumber cotyledons is tedious and

slow, however. Because inoculation is slow, inoculum is best prepared in successive small batches that do not lose significant infectivity before the last

batch is used. The inoculum must be highly infectious so that the chlorotic

primary lesions are confluent on the inoculated cotyledons. Before a high degree

of infection is obtained, two or more transmissions to stock plants with inoculum

consisting of only chlorotic lesion tissue may be required. Heavily infected

cucumber cotyledons tend to become necrotic with some virus isolates. Necrosis

can be prevented or retarded by exposing inoculated plants to day lengths of 18

hours or more.

The conditions under which cucumbers are grown affect their susceptibility

and the yield of virus from them. Short days are detrimental, as are long days

with low light intensity. Very dark-green cotyledons with very short hypocotyls,

resulting from high intensities of artificial light, are relatively insusceptible.

A number of viruses reach a higher concentration in inoculated leaf tissue

than in systemically invaded tissue (A. Q. Paulson and R. W. Fulton, unpublished data). Prune dwarf virus, however, reaches a high concentration in

systemically infected leaves of Cucúrbita maxima cv. Buttercup.

Stabilization of infectivity during purification. — If the properties of a virus

indicate that infectivity wall decrease in extracts within an hour or two, then

seme method of stabilizing infectivity must be devised. These methods have

usually involved antioxidants such as ascorbic acid, sodium thioglycollate, sodium

sulphite, cysteine-HCl, or 2-mercaptoethanol, either alone or with an enzyme

inhibitor such as sodium cyanide or DIECA. Of these, w.e have found 2-ME

and DIECA the most effective. DIECA, however, inactivates certain viruses,

and some lots of the chemical are more detrimental than others. Its use should

follow controlled testing.

Because stone fruit viruses may be more stable in diluted than in undiluted

extracts, tissue for purification is usually ground in buffer in which are dissolved stabilizers of infectivity. A high-speed mechanical homogenizer seems

to be the most efficient way of preparing extracts. Hand grinders are too slow

and are not adapted to rapid mixing of homogenized tissue and buffer.

Clarification. — Methods of removing the bulk of the particulate, nonvirus

material from extracts must necessarily be mild. Low-speed centrifugation is

not sufficient. Much of the particulate cellular matter is adsorbed by hydrated

calcium phosphate, which is prepared by mixing 0.1 M solutions of Na2HP04

and CaCl2 and washing the precipitate thoroughly to remove all but traces of

soluble salts {228). The hydrated calcium phosphate and host material sediment

readily on low-speed centrifugation. Adsorption is a function of the ionic
8 VIRUS DISEASES OF STONE FRUIT

concentration; for example, host material, but neither prune dwarf virus nor

Primus ring spot virus, is adsorbed from 0.03 M phosphate buffer. Higher

concentrations of phosphate result in less host material being adsorbed; lower

concentrations result in some virus being adsorbed also. Certain viruses are

adsorbed by calcium phosphate from 0.03 M buffer so this method of clarification

cannot be used indiscriminately.

Acidification to pH 4.8 to 5.0 with citric acid {505 and A. Q. Paulson and R.

W. Fulton, unpublished data) is an effective clarification method. As is true

with other treatments, some viruses are lost with acidification, so the method

should be used only after testing.

Precipitation of host protein by adding n-butanol to a concentration of 7 to

9 percent is an effective clarification method for some viruses. The n-butanol

technique has been used to clarify grape yellow vein virus (=: peach yellow bud

mosaic virus) {266), but is too drastic for cherry necrotic ring spot virus (R.

W. Fulton, unpublished data). Clarification by emulsification with three

volumes of cold chloroform has been described for necrotic ring spot virus {14).

Emulsification of one volume of extract with two volumes of a 1:1 mixture of

chloroform and n-butanol has been used to clarify peach yellow bud mosaic

virus {711). Gel-filtration has also been used in purification {270).

Almost all purification methods for stone fruit viruses involve high-speed

centrifugation of clarified extracts to concentrate the virus and eliminate low

molecular weight contaminants. The times and speeds used have varied somewhat, but are typical of what is theoretically required to sediment small,

spherical viruses. Once pelleted, the virus may be resuspended in buffer by

gentle shaking or by simply allowing the buffer to cover the pellet overnight at

low temperature. The degree of contamination of the virus pellet may be

reflected in the rapidity with which it resuspends; badly contaminated virus

resuspends more slowly than pure virus. After a high-speed run, there is

usually some insoluble, denatured material that does not resuspend; it can be

removed by a short run at low speed.

Additional steps to remove host material are usually desirable after centrifugation. Any of the following should remove practically all nonvirus antigenic

material from the preparation: density gradient centrifugation {14, 266), zone

electrophoresis {570), acidification {303), and precipitation of host protein

with the gamma globulin portion of antihost serum (A. Q. Paulson and R. W.

Fulton, unpublished data).

Serology

One of the important purposes for purifying any virus is to provide antigen

suitable for antiserum production. Few published data indicate that one route

of animal injection is superior to another. For a number of stone fruit viruses,

intramuscular injection of virus emulsified in Freund's complete or incomplete

adjuvant at rather frequent intervals (3 to 4 days) has been effective {232, 312).

The amounts of virus injected have usually been, by necessity, relatively small,
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 9

probably less than 1 mg. of virus per injection. Such doses usually result in

antiserum titers of 1:320 to 1:1280 after 8 to 12 injections. Injections at less

frequent intervals than every 3 to 4 days may result in a decrease in antiserum

titer between injections (R. W. Fulton, unpublished data).

The various types of serological tests used for other plant viruses are

applicable to the stone fruit viruses. The microprecipitin test requires purified

virus or well-clarified extracts; clarification by hydrated calcium phosphate has

been convenient for this purpose (706).

The serological test most generally convenient is probably the double diffusion

test in agar gel. Clarified extracts are not necessary, and a relatively large number

of tests may be set up in a short time in one or two petri dishes. Washed lonagar

No. 2 at 0.6 to 0.7 percent, made up with water and with 0.02 percent NaNo

is added just before solidification to inhibit microbial growth. Wells 6 mm. in

diameter, spaced 4 mm. apart are convenient. Templates can be made which

will punch a circle of six wells equidistant from a center well. Tests involving

diffusion of antigen in agar cannot be applied to long filamentous viruses such

as apple chlorotic leaf spot unless the virus is disrupted into small pieces that

will diffuse readily.

A problem commonly encountered in serological tests with stone fruit viruses is

that test antigen concentrations are not sufficiently high to give a visible reaction.

There are a number of ways of coping with this problem. Wells can be spaced

more closely in agar gel tests. Antiserum should be appropriately diluted when

this is done to avoid reactions at the edge of the antigen well that might be

overlooked. Virus can be transferred from a host in which it is present in low

concentration to one in which it will reach a much higher concentration within

a few days. Virus may be concentrated by high-speed centrifugation from dilute

extracts, resuspended in a small volume of liquid and serological tests run with

this concentrate, including impurities in agar gel tests.

Serology has not been widely used on virus-containing Prunus material. Virus

concentrations are low, except during the shock phases of some diseases, or except

in young leaves early in the season. The mucilaginous character of ground

Prunus leaves and the rapidity with which the extract turns brown are also

probably detrimental to serology. However, virus is detectable in Prunus material {169, 371, 393, 669). Young leaves forced from Prunus branches held

at 20° to 25° C. have been reported to be a more reliable source of virus for

serological tests than leaves produced naturally out of doors (393).

Relationships among viruses infecting Prunus have been established by means

of serology. Thus, peach yellow bud mosaic virus is the same as tomato ring

spot and grape yellow vein viruses (107, 266). Viruses isolated from hops and

rose (759) have been identified as Prunus ring spot (75). A number of viruses

causing line pattern symptoms in plum have been differentiated on the basis of

serological unrelatedness (A. Q. Paulson and R. W. Fulton, unpublished data).
CONTROL OF STONE FRUIT VIRUS

DISEASES

MAURICE F. WELSH

All control practices must be preventive, because there are no cures for virus

diseases that can be applied on a commercial scale. Although preventive

measures for long-lived woody plants are characteristically laborious and costly,

such measures have been remarkably effective against many of the virus diseases

of stone fruits.

The traditional recommendations for prevention of stone fruit virus diseases

include: (1) propagating cultivars and stocks from sources that are free from

detectable viruses; (2) isolating uninfected plantings from sources of infection;

(3) replacing susceptible cultivars with resistant or tolerant cultivars; and (4)

minimizing natural spread by suppression of vectors and other agents of spread.

In addition, control by heat therapy has limited uses. Recently there has been

increased hope that chemotherapeutic methods can be developed. Indexing

techniques contribute to many virus control procedures.

Virus-Free Propagating Materials

The most broadly applicable recommendation for reducing virus incidence

in stone fruit crops is the propagation of healthy trees. Its effectiveness is

governed only by the extent to which such plantings are subsequently exposed

to or protected from natural infection, and inevitably by the availability of

suitably indexed propagating materials. Most nurserymen and growers now have

access to these materials.

In fruit-growing States and Provinces of the United States and Canada, and

in many other countries, certification schemes have been established to provide

tree fruit seeds, clonal stocks, and cultivars that are free from all detectable

viruses. Such certification programs require the participation of pomologists

to verify trueness to type and of plant pathologists to determine that the clones

are free from recognized viruses. The administrative details of the schemes

vary greatly, but the basic procedures for ensuring adequate virus screening

are common to all of them. The customary first step is the indexing of numerous

trees of a variety in a search for one that can be certified as free from known

viruses. The term usually used is 'Virus-indexed," which indicates that by the

indexing techniques currently in use, no virus infection can be detected. If the

cultivar proves to be characteristically virus-infected, the healthiest available

material is given heat therapy to eliminate virus infection.

The availability of fully indexed materials of most stone fruit cultivars

from the IR—2 Interregional Tree Fruit Repository has obviated the need

to derive such materials independently for regional certification schemes, each

10
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE H

of which can use IR-2 materials for estabhshment of its own nuclear plantings.

Such 'mother orchards" are protected from reinfection by all practical means

and reindexed at regular intervals. In some established schemes, the nurseryman or grower is provided with his full requirements of budwood and seed

directly from these plantings. In other schemes, he is required to establish his

own bud- and seed-source trees, using propagating materials from the nuclear

planting and maintaining these trees under conditions prescribed by the certifying authority. The nursery plantings are inspected at least once during the

growing season and usually again at the time of digging. Most administering

agencies provide tags or other evidence of certification to nurserymen who

satisfy the requirements of the program.

The procedures for indexing stone fruit clones and for heat therapy are outlined in subsequent sections.

Isolation From Sources of Virus Infection

Healthy trees may be protected from infection in several ways. These include

roguing diseased trees, eliminating other plants that serve as hosts of the virus,

and establishing new plantings remote from existing diseased orchards or other

sources of infection. Quarantine measures can also be classified as a means of

isolating plantings from sources of infection.

Removal of diseased trees is especially effective against viruses that have low

or moderate rates of natural spread and that display characteristic symptoms

after short incubation periods. Individual tree roguing has been adequate for

such diseases as red suture, peach yellows, and peach rosette. Enforced eradication programs applied to extensive acreages have been necessary to reduce

incidence of more rapidly spreading diseases such as phony peach and peach

mosaic.

Reservoir hosts of viruses can complicate control by tree removal. The host

range of a virus must be determined before tree removal can be recommended.

The opportunities for implementing eradication programs are especially prejudiced if some cultivars or kinds of cultivated fruits are symptomless carriers

of the virus.

The viruses that cause many of the diseases of cultivated stone fruits are

harbored in native plants, most commonly. Prunus spp. Eradication of these wild

hosts within suitable distances of orchards has been an effective measure for

X-disease, peach rosette, and phony peach. Eradication of wild hosts must

accompany programs of orchard tree removal. Indeed, for X-disease in fruit

districts of eastern North America, eradication of wild chokecherry is more

effective than the roguing of diseased orchard trees, apparently because of the

patterns of movement of the principal vector.

Isolation of new plantings from older infected ones is especially important

for materials used in breeding programs, or for materials serving as sources for

nursery propagation. In commercial orchards, there is usually less opportunity

to achieve such isolation. However, interplanting of healthy trees with estab-
12 VIRUS DISEASES OF STONE FRUIT

lished infected ones should be avoided where possible, because it provides

maximum exposure to infection for the young trees.

Natw}?al and regional quarantines and other regulatory measures that are

imposed to prevent entry of viruses and their vectors to new countries, regions,

or districts, constitute a type of isolation procedure. The administration of

national quarantines is described in the section "Quarantine and the Detection

of Stone Fruit Viruses in Plant Importation." Many States and Provinces

restrict entry of fruit trees from regions of the continent from which new

diseases can be introduced. The restriction may be a total prohibition of the

movement of certain plant species, or it may involve combinations of inspection,

fumigation, indexing procedures, and periods of postentry growth in isolation.

Sometimes even more limited quarantine areas may be established, usually for

restriction of spread of a specific virus. Such local restrictions have been directed,

with considerable success, against phony peach virus in southeastern United

States, and against little cherry virus between the two major cherry-growing

districts in British Columbia.

Resistant Cultivars

In tree fruit crops, few cultivars have been found that possesss total resistance

or "immunity" to virus infection. Identification of cultivars with ability to

escape natural infection has also been rare but has been demonstrated for Napa

Long Stem Bing growing on mazzard rootstocks in California orchards invaded

by Buckskin (X-disease virus). Tolerance to infection is much more common.

The use of tolerant cultivars, or their development in breeding programs, has

been recommended for little cherry, cherry mottle leaf, and peach mosaic.

However, tolerance is seldom complete and consistent. Moreover, tolerant

cultivars can serve as a reservoir of virus, and, thus as a source of inoculum for

neighboring trees of sensitive cultivars.

Suppression of Agents of Natural Spread

Agents that have been shown responsible for transmission of viruses in stone

fruits are insects, mites, nematodes, and pollen. Usually there need be concern

for only one means of transmission for each virus. Moreover, the insect or mite

vectors of a given virus are usually comprehended within one family ; frequently

within one genus.

Eradication or suppression of insect or mite vectors is an obvious and attractive measure but rarely effective. However, a spray program has been devised to

reduce populations of the eriophyid mite vector of peach mosaic virus, and thus

reduce the rate of spread of the disease. For control of peach yellows and little

peach, spraying to reduce plum leafhopper populations is suggested as a

precaution to supplement tree roguing.

The possibility of effectively depressing populations of nematode vectors by

use of soil fumigants has been demonstrated for peach yellow bud mosaic.

Precautions should be taken against movement of nematode-infested trees from

diseased plantings to other orchards or districts.
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 13

Pollen transmission of prune dwarf and necrotic ring spot viruses can be

prevented in valuable experimental, repository, or mother orchard plantings by

deblossoming annually, but can be minimized in commercial orchards only by

adequately separating healthy and diseased plantings.

Heat Therapy

Two types of heat therapy have been used successfully to eliminate viruses

from stone fruits—exposing scion sticks to high temperatures for short periods

or maintaining potted trees at lower temperatures for much longer periods

(344, 491).

The higher temperature, short-period exposure is commonly achieved by

immersing scion sticks in large volumes of actively circulating water at temperatures between 50° and 52° C. for 10 to 15 minutes. The scion sticks must be

cooled quickly, and the buds transferred to clean rootstocks.

Much more success has been attained with lower temperature, long-exposure

treatment. Plants are grown in containers, and when well established are placed

in a chamber which supplies continuously circulating air at temperatures between

37° and 38° C. Effective periods vary from 2 weeks to the limit of tree tolerance. If growth is maintained in the chamber, tip buds attached to short wedges

of shoot can be grafted to clean rootstocks. The wedges are inserted in incisions

on the stems of the rootstocks, wrapped with surgical gauze, and protected for

several days in plastic envelopes.

An alternative is to remove lateral buds from the heated trees and apply them

to clean rootstocks by shield budding or T-budding. This second method

depends on heat-induced inactivation of the virus, whereas the propagation of

tip buds exploits the reduced ability of viruses to invade tissues laid down

during the high-temperature exposure. Trees survive better if given pretreatment of 1 or more weeks at 33° to 35° C. and if humidity in the chamber

is maintained below 60 percent.

Another modification of the lower temperature, long-exposure procedure is

the insertion of diseased buds singly into container-grown rootstocks that are

known to be uninfected. For 3 to 7 days after budding the trees are placed in

the heat chamber for the desired period. After removal, the dormant buds are

forced by suitable pruning of the rootstocks, either immediately or after a period

of dormancy.

Heat treatment survivals that appear to be freed of virus infection in the first

indexing should be reindexed after 2 years to detect previously undetected

infection.

Chemotherapy

Relatively few new methods for control of virus diseases of stone fruits have

been introduced in the last 30 years. As this handbook is being prepared, there

is promise that new types of treatment may be developed. Dimethylsulfoxide

(DMSO) has been shown to move quickly and systemically through plant tissues

and to suppress the symptoms of several plant virus diseases, including those
14 VIRUS DISEASES OF STONE FRUIT

of peach mosaic in peach {322). Such materials, acting as antiviral agents themselves, or as carriers for other antiviral agents, may allow the development of

curative procedures for some stone fruit virus diseases. Recent demonstrations

of the association of mycoplasmalike structures with the occurrence of several

yellows type plant virus diseases, and the reported effectiveness of antibiotic

applications against such diseases, offer additional hope that cures for such

diseases may soon be available.

Indexing

Indexing is used in the search for stone fruit clones that are free from known

virus infection, and in periodic checking of virus-indexed clones to ensure that

they have not become infected.

The indicator list devised for the IR-2 Repository (p. 22) serves as a basis

for all stone fruit indexing programs in North America. All materials submitted to mother plantings should have been indexed on the full indicator range.

For indexing of imported materials, the IR-2 list is supplemented by selections

from host ranges devised by plant pathologists on other continents; notably by

the European Committee for Cooperation in Fruit Tree Virus Research.

For routine reindexing of mother trees in certification programs, modifications

in the IR-2 indicator range, or at least of the indexing schedule, are often

possible. In most schemes, annual indexing is practiced for ring spot and

prune dwarf viruses, either on both woody and herbaceous hosts each year, or

alternating between them. Indexing for slow-spreading viruses may be spaced

at longer intervals in a rotation schedule.

Specific Recommendations for Control of Viruses in Nurseries

1. Use only virus-indexed budwood, if possible by participation in a regional

certification scheme.

2. Minimize risk of seed transmission by obtaining seeds from indexed trees

or seedlings certified as having been grown from such seeds.

3. Avoid rebudding of rootstocks on which buds have failed. This doubles

the chance of introducing viruses. Moreover, bud failure is often an indication

of virus infection.

4. Adjust spacing between different varieties or clones to minimize the

possibility of natural root grafting.

5. Segregate tree fruit nursery stock as far as possible from ornamental Prunus

species that may serve as reservoir hosts of dangerous viruses. Ornamental

Prunus are seldom as adequately indexed as commercial fruit-producing clones.

6. Rogue abnormal trees in nursery rows as soon as they are observed.

Specific Recommendations for Control of Viruses in Orchards

1. Buy trees from nurseries that participate in certification schemes or that

take equivalent precautions in their own independent programs. The orchardist

who grows his own nursery stock should observe all precautions recommended

above for nurserymen.

2. Avoid as far as possible the interplanting of indexed nursery stock with
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 15

established trees that are virus-infected. This is especially important for sour

cherries.

3. Be familiar with the symptoms of virus diseases; be prompt in removal of

diseased trees, especially if the disease has an appreciable rate of spread; report

occurrence of serious diseases to local advisory or regulatory officials; cooperate

with them in eradication programs, when they deem them necessary.

4. Know host ranges of serious viruses, and remove wild hosts growing

near enough to orchard plantings to be hazardous.

In Breeding and Other Research Programs

1. Use virus-indexed materials for all types of trials to obtain best tree

performance and results that can be duplicated.

2. Establish breeding programs with virus-indexed materials to minimize the

risk of creating new varieties that are infected. Varieties originated as seedlings

can be infected because of seed or pollen transmission. When genetic changes

are sought by irradiation or chemical treatment, the selection of clean clones is

especially critical.

3. Multiply new cultivars by own-rooting whenever possible; topwork them

on certified rootstocks if they cannot be own-rooted. The traditional practice

of topworking on unindexed bearing trees to stimulate early fruiting is especially

dangerous.

4. Add virus resistance screening to the usual performance tests for new

cultivars and rootstocks.

5. Index new cultivars, mutants, and rootstock clones on all appropriate

indicators immediately before their release to verify virus freedom.

6. When assembling cultivars and clones from widely separated regions,

adhere rigidly to quarantine precautions to avoid introducing new viruses to

your country or region.
IR-2, THE INTERREGIONAL DECIDUOUS

TREE FRUIT REPOSITORY

PAUL R. FRIDLUND

Between 1935 and 1945, when rapid advances were being made in the

identiñcation of virus diseases of deciduous tree fruits, most plant pathologists

in this research field recognized the need for assembling and maintaining clones

of virus-free deciduous tree fruits which could be used as sources of test materials

for research programs. The need for more general use of such materials to

improve and standardize all types of tree fruit research and testing programs,

and to improve the performance and quality of commercial nursery stock also

became increasingly apparent.

Assembling and maintaining numerous virus-free clones by many individuals

appeared both unnecessarily duplicative and economically impractical. Furthermore, the prime requisite of adequate isolation from other diseased trees, either

by screen or distance, often was unavailable. In other instances, unfavorable

local climate might have prevented the survival of some important clonal lines.

Additionally, the adequate facilities, experience, labor, and funding necessary

for the intensive indexing and maintenance of many clonal lines were usually

lacking.

The logical solution appeared to be repositories. Plans for several regional

repositories were tentatively devised by scientists within the various regions.

However, some of the problems which would be encountered by individuals

also remained for regional repositories. After further consideration, a single

national respository was deemed advisable, and the plans were formulated by

cooperative effort of many scientists from all regions. These plans were enthusiastically supported by the Deciduous Fruit and Nut Tree Research and Marketing

Advisory Committee, an advisory committee to the Federal Government,

composed of members of the industry.

Organization

The Interregional Research Project IR-2 was initiated on July 1, 1955, and

is supported by regional research funds appropriated by the Federal Government

under provisions of the Hatch Experiment Station Act of 1887. The headquarters, screenhouses, field plots, and other facilities are located at the Irrigated

Agriculture Research and Extension Center, Prosser, Wash., a branch of the

Washington Agricultural Experiment Stations system (fig. 1). Supervision is

provided by a resident plant pathologist in charge. An isolated repository is

maintained in the desert near Moxee, Wash. The latter is adjacent to a facility

operated by the Washington State Department of Agriculture with whom

irrigation water, labor, and machinery are shared (fig. 2).

The project has four objectives: to assemble virus-free clones of desirable

16
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE I7

v,^ä,?S'!&%^5'

FIGURE l.—IR-2 facilities at Prosser, Wash., include a greenhouse and several screenhouses, two of which are shown on the left.

deciduous fruit trees, to verify their virus-freedom by intensive indexing procedures, to maintain the clones in isolated repositories, and to distribute propagating materials to cooperators as foundation clones for research or for release to

industry. The objectives also include provision for conducting research on

methods of eliminating viruses from infected clones and on indexing techniques

and related problems. The term "virus-free" as used herein, means that the

plant material is considered to be free from viruses that are detectable by indexing. Cooperators may be defined as all State and Federal research and regulatory

scientists.

IR-2 originally limited clonal accumulation and indexing to Prunus because

only in this genus were the infecting viruses and their indicators understood

sufficiently to establish an effective virus-free repository. However, many contemporary studies were being made, including those by an interregional subproject of IR-2, which elucidated some of the missing information relating to

the viruses of Malus and their indicators. The results have recently allowed

IR-2 to assemble and effectively index cultivars of Malus. These research

results also may have additional value because it now appears that some deciduous

tree fruit viruses have a multiple generic host range including Prunus, Malus, and

possibly the Rosaceae in general.

Procedures

Acccumulation of clones.—Potentially valuable. Prunus candidate clones are

either proposed for the repository by cooperating scientists or solicited from

them by the technical committee. Virus-freedom, as determined by previous

limited indexing, is desirable before submission.

An approved candidate clone is received as budwood from which three

trees are propagated on virus-free seedlings in a screenhouse. The remainder
18 VIRUS DISEASES OF STONE FRUIT

nw,'iwwj.4auûw

FIGURE 2.—The isolated IR-2 repository site near Moxee, Wash., before tree planting.

The buildings in the distance ate a part of a facility operated by the cooperating

Washington State Department of Agriculture.

of the budwood is used for preliminary indexing of the candidate clone on

one or more of the standard index hosts. The hosts selected for this preliminary

screening vary because experience with Prunus introductions has shown that

some varieties and species, particularly from certain areas, are more prone

than others to contain specific virus contaminant. The clone is discarded if

the initial indexing detects an infecting virus. Meanwhile an attempt is made

to find a noninfected source of the clone.

Methods of indexing.—The propagated trees are grown under screen in

5-gallon containers until they are large enough to provide adequate budwood

for indexing. One of the three trees of each clone is indexed by budding three

inoculum buds into three trees each of 10 Prunus indicators (p. 22). Additionally, the propagated trees are indexed by sap inoculation of Chenopodium

quinoa. The indicator list is not static; it is changed by addition or deletion

in response to the results of research and experience (fig. 3).

The period of observation varies with the indicator and the viruses to be

detected. Some indicators require only one growing season of observation,

whereas others must be retained long enough to inspect them for fruit symptoms.

Virus-infected clones.—If the first clonal propagant is found to be infected,

a second tree of the clone is similarly indexed (fig. 4). If the second tree is

infected, the clone is rejected, and a search is made for a different healthy

source. If no healthy source is found, the rejected clone may be treated with

thermotherapy in an attempt to eliminate the infecting virus. However, this

procedure is not always successful. Thus, some important clones are not
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE I9

represented in the repository because no healthy individuals could be found

or produced.

Maintenance of virus-free clones.—If the tree under test is found to be

virus-free, it is moved to a second screenhouse where it is maintained indefinitely

as the nucleus mother tree of that clone. The remaining propagants of the

clone are discarded. Some of these nucleus mother trees have been maintained

for as long as 11 years in a 5-gallon container without having survival problems.

Usually two subpropagations are made from each nucleus mother tree for

orchard-style planting in the isolated repository. Whenever possible the subpropagations are made by rooting softwood cuttings under mist. This prevents

chance viral contamination of the clone from infected rootstocks. All trees of

peach, mahaleb, and the miscellaneous species, planted in the repository, are

on their own roots, as are most trees of apricot, plum, and sour cherry. All

trees of sweet cherry, almond, and other varieties impossible to root from

cuttings are bud propagated on seedlings grown from virus-free seed produced

in the repository.

Reindexing of virus-free clones.—^Maintenance indexing of a repository tree

begins as soon as it is accepted as a nucleus mother tree or planted as a subpropagation in the repository. All trees are reindexed annually on Shiro-fugen

ornamental cherry. This indicator is superior for detecting the latent viruses

which presumably would spread most readily to healthy trees. The nucleus

mother trees have been reindexed biennially on the 10 prescribed index hosts.

The trees planted in the field at Moxee are indexed at less frequent intervals.

To date, no virus spread has been detected either into the screenhouses or the

isolated field plantings. This information has helped demonstrate the practicality of maintaining virus-free trees in screenhouses and isolated repositories.

• , -'- - - .1 • ji,"-. ja'-'

FIGURE 3.—A field of 1-year-oId, sweet cherry, virus indicator trees at Prosser, Wash.
20 VIRUS DISEASES OF STONE FRUIT

FIGURE 4.—Trees from the rows shown in figure 3. Virus infected trees are on the left;

healthy, on the right.

Cultivar identification. — Meanwhile, a program of cultivar identification

verifies that the clones are true-to-name. The final identifications are made by

competent pomologists. Although budwood of introductions to IR-2 usually

originates from bearing trees, several inadvertent errors have been discovered.

The best method for verification of a cultivar is to fruit the tree in the field

as is done in the repository. Identification in screenhouses is extremely difficult.

Consequently, scions from greenhouse-grown trees are top-worked to trees in

the field and forced to fruit for identification.

Release of virus-free materials. — The elapsed time from receipt of candidate

clones until release to cooperators is at least 5 years. Lists of available clones

are distributed periodically. The IR-2 repository began distributing virus-free

budwood in 1965. Propagation material has been requested primarily by

cooperating plant pathologists, pomologists, and entomologists representing

State and Federal research agencies and State regulatory agencies. Considerable

interest also has been shown by foreign research scientists, primarily Europeans.

The exact uses made of repository releases are difficult to ascertain. However,

it is known that some releases have been used for research in several disciplines

to establish virus-free blocks for evaluation or breeding, and as support for

nursery improvement programs administered by State regulatory agencies. In the

latter case, several States and Canadian Provinces have based the major portions

of their programs on IR-2 clones, whereas other States have used these clones
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 21

to supplement their own. Interest in most foreign countries has centered on

obtaining starts of the virus indicators used by IR-2. This service is provided

in cooperation with Agricultural Research Service, USDA, and is helping to

standardize research indicators.

Other Results and Observations

IR-2 procedures for virus detection currently are based solely on biologic

responses of indicators, primarily because other techniques are not yet sufficiently

refined to provide an adequate substitute. Sole dependence upon biologic

indexing under the field conditions of one area is not without risks because the

local environment may not be suitable for symptom expression of some viruses in

some hosts.

About 16 percent of the clones submitted to IR-2 were found to be virusinfected even though most had a previous record of some indexing. Frunus

ring spot and prune dwarf viruses predominated among the contaminants

detected, with green ring mottle viruses next in frequency. The latter virus was

never detected in sour cherry accessions, but rather it was found primarily in

sweet cherries bred in the West and in peaches bred in one area of the Midwest.

The little cherry virus was found in almost all of Japanese flowering cherry

cultivars, and the remaining viruses detected were a random assortment in

diverse hosts.

Suggestion has been made that all candidate clones should be given routine

thermotherapeutic exposure upon receipt. This procedure may have some merit,

but it is not without considerable hazard when working with unsuspected diseased clones. Although thermotherapy can now eliminate most of the viruses

which infect Prunus, all propagative units obtained from treated plants may not

be virus-free. Careful indexing using approved methods is required as it is for

untreated plants.

Insecticides and miticides have never been used in the isolated respository

during the 10 years that trees have been in the field. Although small numbers

of virus vectors (e.g., aphids, leafhoppers, and mites) are usually present,

particularly in the spring, populations never become dense nor is a particular

species observed throughout the growing season. Cursory observations suggest

that populations of these arthropods are reduced to insignificance by undisturbed

biological control. The seasonal presence of dense populations of the parasitic

Ichneumonidae, Braconidae, and Asilidae lends circumstantial support for this

hypothesis.

CURRENT MINIMUM RANGE OF IR-2 INDICATOR

VARIETIES

The following Prunus cultivars were selected as the principle indicators for

detection of the viruses listed within the environment of Prosser, Wash. Most

viruses may also cause symptoms in one or more of the other indicators. All
22 VIRUS DISEASES OF STONE FRUIT

indicators are inoculated in the field except Prunus tomeyitosa and Chenopodium

quinoa, which are inoculated in the greenhouse at approximately 22° C. Different principle indicators for some viruses may be preferable or necessary in

other environments. The reader is referred to the host range of a virus in

question if a substitution appears advisable.

P. serrulata cv. Shiro-fugen : prune dwarf, Prunus ring spot.

P. serrulata cv. Kwanzan: Green ring mottle.

P. avium cv. Bing: Albino, black canker, freckle fruit, mottle leaf, rasp leaf, rusty

mottle, short stem, spur Bing, sweet cherry rough fruit, twisted leaf, Utah Dixie rusty

mottle, xylem aberration.

P. avium cv. Sam: Little cherry, necrotic rusty mottle.

P. armeniaca cv. Tilton: Apricot pucker leaf, apricot ring pox.

P. pérsica cv. Elberta: Peach asteroid spot, peach blotch, peach calico, peach mosaic,

peach mottle, peach rosette, peach yellows, peach wart, phony, red suture, rosette

mosaic, stubby twig, weak peach, X-disease, yellow bud mosaic.

P. cerasus cv. Montmorency: Pink fruit.

Prunus hybrid cv. Shiro plum: Plum line pattern, plum white spot.

P. domestica cv. Italian Prune: Prune mottle; prune dwarf.

P. tomentosa seedlings : Bark splitting of Montmorency.

Chenopodium quinoa: Apple chlorotic leaf spot, cucumber mosaic, tobacco mosaic.
QUARANTINE AND THE DETECTION OF

STONE FRUIT VIRUSES IN PLANT

IMPORTATIONS

ROBERT P. KAHN

Quarantines are regulations promulgated by governments to prevent or delay

man from inadvertently upsetting the balance of nature to the detriment of the

agriculture of a region or country, Man's previous experience in disrupting this

system of checks and balances has resulted in devastating losses to plant and

animal life such as the introduction of rabbits into Australia, measles into Africa,

Klamath weed into Canada, the United States, and Australia, and both giant

snails and hoof-and-mouth virus into many countries.

Viruses that are known to infect Prunus throughout the world include some

of particular quarantine significance to the United States and Canada. Methods

and indicators used to detect these viruses are discussed in this chapter. Literature citations are presented as sources of more detailed information about

specific points or viruses rather than as surveys of the literature.

Quarantine

Legal basis. — The legal basis for quarantine may be found in (1) international plant protection conventions such as the Food and Agriculture Organization's International Plant Protection Convention (404), (2) intergovernmental agreements such as the European and Mediterranean Plant Protection

Organization (199, 200), (3) Federal regulations issued by ministries or

departments of agriculture such as USDA's Plant Quarantine Act of 1912

(677), and (4) State or provincial regulations.

The government regulations issued by ministries or departments of agriculture

have been reviewed and abstracted for most countries (676). In general, these

regulations (1) specify requirements of import permits, (2) require phytosanitary certificates, (3) require certificates of origin, (4) stipulate inspection

upon arrival, (5) prescribe treatment upon arrival to eliminate a risk, and (6)

prescribe quarantine or postentry quarantine, depending on the nature of the risk.

Quarantine status of plant importations. — Quarantine regulations of various

countries utilize one or more of four classifications for plant importation with

reference to their quarantine status: (1) absolute prohibition, (2) quarantine,

(3) postentry quarantine, and (4) restricted entry.

Absolute prohibition is used when the risk of introducing pests or pathogens

is so great that importation should be denied even to government services.

Absolute quarantines are invoked when safeguards are inadequate and isolation

from commercial crop production is not feasible.

Quarantine is used for plants imported from a country where hazardous pests

or pathogens are known to occur. Admission of plants under quarantine is

23
24 VIRUS DISEASES OF STONE FRUIT

usually reserved for government services and is not available to the general

public. Safeguards consist of trained personnel, reliable methods of pest or

pathogen detection, phytosanitation, and quarantine facilities (337).

Postentry quaranthie status is usually assigned to plants for which hazardous

pests or pathogens have been reported from some, but not all, foreign countries,

and the importation originates from a country from which these pests or pathogens have not been reported. Postentry quarantine is usually reserved for

government services, institutions, and qualified individuals whose facilities

meet postentry quarantine requirements. Safeguards consist of inspection upon

arrival and during a specified postentry period, usually for at least two growing

seasons, on the premises of the importer.

Restricted entry status is usually assigned to all other plant introductions.

"Restricted" means that plants are subject to inspection and treatment, if

necessary, upon arrival at a port of entry or inspection station.

Quarantine regulations for Prunus

1. International. — A survey of the abstracts {(^76) of quarantine regulations

of countries where stone fruits are of agricultural importance shows that the

genus Prunus is almost always under quarantine or postentry quarantine.

However, the reasons for promulgating these regulations vary among countries.

Most European countries regulate Prunus (or Rosaceae) because of San Jose

scale insects and/or fire blight bacteria. Some of the European countries also

include regulations against virus diseases of fruit trees but such regulations

usually do not name specific virus diseases with the exception of sarka (plum

pox) virus. In some instances. Prunus plants are under regulation if they

originate in soils previously used for grapes or from areas where golden

nematode or the potato wart fungus is known to occur.

2. United States. — Prunus importation into the United States is regulated

by the Nursery Stock, Plant, and Seed Quarantine 37 {677). Prunus species,

including ornamentals, are prohibited because of a "diversity of plant diseases"

from all countries with the following exceptions: (1) The USDA may import

these prohibited species from any country for experimental or scientific purposes.

(2) Vegetatively propagated root stocks may be imported if they originate

from nurseries in foreign countries which are certified by the plant protection

service of the originating country to have been grown from parent plants

that were tested and found free of all diseases of plant quarantine significance including those caused by viruses. (A list of certified nurseries may be

obtained by writing to the Plant Protection and Quarantine Animal and Plant

Health Inspection Service, Federal Center Building, Hyattsville, Md. 20782).

Prunus imported for scientific purposes enter the United States under quarantine at the U.S. Plant Introduction Station, Glenn Dale, Md., to determine

whether the Prunus is infested with pests or infected with pathogens of quaran-
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 25

tine significance. These are defined as hazardous organisms or infectious agents

that (1) are not known to occur in the United States, (2) are not widely

distributed in the United States, or (3) have not been identified.

3. Canada. — Regulations governing importations of Prunus into Canada

from countries other than the United States (2) are similar to the U.S. regulations. However, in addition, Canadian regulations require that Prunus

introductions from the United States to Canada must be accompanied by a

State or Federal certificate stating that the source was inspected during the

growing season and is believed to be free of virus diseases, as may be designated from time-to-time, such as little cherry, peach mosaic, or phony peach.

Also, fumigation may be required (or entry refused) for nursery stock received

as balled-and-burlapped if Xiphinema americanum or other harmful nematodes

are found in the shipment.

Prunus introductions from foreign countries (except the United States) otherwise prohibited, enter Canada for scientific purposes through the quarantine

station at Saanichton, British Columbia.

Quarantine Policy Governing the Release of Virus-infected Plant Introductions. — Federal quarantine regulations, as discussed previously, exclude plants

infested with pests or infected with pathogens of quarantine significance. A

problem arises, however, as to the proper course of action, when an introduction

is infected with a virus that is not of quarantine significance. The problem is

minimized if the importer experiences a conflict of interest between the benefit

of importing new germ plasm and the risk of introducing a pathogen. The

problem takes on added significance when the importer fails to experience a

conflict between benefits and risks — an attitude that fosters a disregard for

phytosanitary aspects of plant introduction. Consequently, the USDA, in

cooperation with State quarantine ofíícials and virus specialists, formulated a

policy governing the release of foreign plants infected with viruses that are

not considered of quarantine significance.

In general, it is the Department's policy to exclude plants infected with

viruses of quarantine significance, and to ask the State quarantine oflicial to

determine the admissibility of plants infected with a virus that already occurs

in his State. Some factors that influence this determination at the State and

Federal level are: (1) Quarantine facilities and phytosanitation awareness of

the importer, (2) the presence of nursery stock certification programs or virusfree clone collections at the location of the importer, (3) the potential

importance of the introduction to the development of the stone fruit industry

in the State, (4) the degree of isolation from commercial production, (5) the

possibility that the foreign source of a virus already in the State might be a

more severe strain, and (6) opinions of virologists. The decision-making

process is essentially a weighing of risks against benefits (337). In practice,

quarantine oflicials consider each case on its individual merits.
26 VIRUS DISEASES OF STONE FRUIT

The situation concerning Prunus is complex. On one hand, some Prunus

breeders expressed more-than-usual concern about the loss of some sources of

germ plasm merely because the plants were virus-infected. On the other hand,

quarantine officials in some States with Prunus nursery stock certification

programs, were equally concerned about jeopardizing virus-free foundation

plantings located at the same institution as the breeder's plots.

Consequently, before formulating a policy for Prunus, the USDA sent

questionnaires in 1963 and 1964 to stone fruit virus specialists and State

quarantine officials. The responses showed that almost all participants concurred

in the Federal quarantine policy, which excluded viruses of quarantine significance. However, 90 percent of the virus specialists and 70 percent of the

quarantine officials in 14 States, that account for 93 percent of the stone fruit

production, also favored the exclusion of foreign sources of viruses already

established in the United States such as Prunus ring spot virus (unless the

Prunus was of exceptional importance to the stone fruit industry).

Consequently, it is the USDA policy to destroy Prunus introductions infected

with virus whether or not the virus is of quarantine significance with the

following exception. If a Prunus introduction is infected with a virus that is

not of quarantine significance and the introduction is judged by the USDA

to be of unusual importance to the improvement of the stone fruit industry, the

introduction may be admitted into a State with the approval of the State

quarantine official. (Frequently, one of the conditions specified is that the

importation be subjected to heat therapy and reindexing). In Canada, important

clones are heat-treated immediately upon receipt (before indexing) if the

source is suspect. Otherwise, these clones are heat-treated if preliminary indexing

is positive.

Viruses Infecting Stone Fruits

Listing of viruses. — Now that we have considered some of the principles

of plant quarantine and the regulations pertaining to Prunus, it would be

convenient to compile a list of Prunus viruses from which those of quarantine

significance might be selected. However, compiling such a list is fraught with

difficulty. The listing of stone fruit viruses and virus diseases is not only

complicated by synonomy and double-virus infections but by the fact that

some naturally occurrmg viruses of stone fruits do not even have a stone fruit

in the virus name. For the sake of discussion, the Review of Applied Mycology

(RAM) (now Review of Plant Pathology) list of plant virus names {439)

can be used as a starting point although the RAM list — and probably any

other list that might be compiled — is not universally accepted by stone fruit

virus workers. The RAM list contains 232 entries for common names of

stone fruit viruses or virus diseases that currently can be associated with 55

viruses, as follows:
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE £7

Number of viruses Number of

with a stone fruit common names

Stone fruit in name of virus in index

Almond 0 4

Apricot 5 13

Cherry 23 107

Nectarine 0 0

Peach 17 56

Plum 6 26

Prune 3 5

Prunus 1 21

55 232

These figures include strains and synonyms but not the Latin nomials although

these are also included in the index.

In addition to the 55 viruses in the RAM list, we should add the viruses

that occur in Prunus but which do not have a stone fruit in the name. Among

these are apple chlorotic leaf spot; tomato bushy stunt; tobacco mosaic; cucumber

mosaic; and the nematode-transmitted, polyhedral (NEPO) viruses such as

arabis mosaic, raspberry ring spot, and tomato black ring viruses. Also,

viruses that have been described since the list was published should be added.

To be complete, the list should also contain the paired names of viruses

which incite a virus disease that is different from the disease incited by either

virus alone, such as (1) arabis mosaic virus -j- prune dwarf virus and

(2) raspberry ring spot virus + prune dwarf virus. These pairs have been

implicated as incitants of cherry Eckelrade, Pfeffinger, and rasp leaf (European)

diseases.

Finally, in considering any listing of viruses one should not be shackled to

the concept of looking only to the genus Prunus as sources of stone fruit viruses ;

for example, apple chlorotic leaf spot virus has been found in Amelanchier,

Sorbus, pear, plum, peach, and raspberry. Prunus ring spot virus has been

found in hops, roses, and apples. Cucumber mosaic, tobacco mosaic, and the

NEPO viruses have wide host ranges in crop and wild species.

Viruses of quarantine significance in the United States and Canada. —

Among the viruses of quarantine significance, and therefore subject to Federal

regulation by the United States and Canada, are: (1) plum pox {1S6, 328, 638),

(2) cherry leaf roll (170), (3) arabis mosaic (103, 104, 280), (4) raspberry

ring spot (104, 280), and (5) tomato black ring (104, 280) viruses; also,

apricot apoplexy (479), which may be incited by a virus. None of these are

known to occur in North America.

Of these viruses, plum pox is of the greatest concern because it spreads

rapidly in commercial stone fruit areas in eastern Europe, it destroys quality

of fruit, and reduces the yield. Arabis mosaic, tomato black ring, and raspberry
28 VIRUS DISEASES OF STONE FRUIT

ring spot viruses are important because they are spread by nematodes and have

broad host ranges in many nonrosaceous crops and wild species.

Among the viruses already present but not widely distributed in the United

States, and either not present or not widely distributed in Canada, and, therefore, subject to State or Federal regulation or both are: (1) peach mosaic,

(2) peach yellows, (3) peach phony, (4) peach rosette, (5) X-disease and

strains, and (6) tomato ring spot, peach yellow bud mosaic strain. In addition,

little cherry (K & S) virus although widely distributed as a latent infection in

flowering cherries is of concern because of its potential severity in sweet cherry

growing regions of the United States and Canada.

Because Federal regulations exclude viruses of quarantine significance and

both State regulations and State or Federal policy exclude almost all other

viruses, the primary objective of the plant introduction and quarantine stations

at Glenn Dale, Md., and Saanichton, British Columbia, is detection. For all

practical purposes, a philosophy of "what's in a name" prevails in routine

testing. Priority is given to detection rather than identification. Identification

does not necessarily come into the picture unless the Prunus introduction is of

extreme importance to the stone fruit industry and a decision must be made

concerning the admission of a virus-infected plant. Of course identification is

a prerequisite to determining whether the virus represents a new strain or

new virus.

Methodology

In quarantine stations, stone fruit viruses are detected in foreign plants by

transmitting an infectious agent that incites virus diseaselike symptoms in one

or more indicator plants. The indicators are woody Prunus species or cultivars or

herbaceous nonrosaceous plants recommended by stone fruit virus specialists.

Transmission to woody plants is effected by some form of grafting and to

herbaceous plants by mechanical transmission.

Mechanical transmission. — Mechanical transmission is accomplished by rubbing carborundum-dusted indicator plants with an inoculum prepared from

leaf, petal, root, or pollen extracts. Prunus-to-Prunus mechanical transmissions

have not proved useful on a routine basis. Transmissions have been inconsistent

presumably because of the exacting requirements of proper age of inoculum

tissue, age of Prunus indicator plants, and the necessity of incorporating additives to the inoculum to suppress inhibitors. However, Pf//;?//j--to-herbaceous

plants (nonrosaceous) have been extensively used for testing a few stone fruit

viruses such as Prunus ring spot {225, 374), prune dwarf (22:5, 374), tomato

bushy stunt (16), tomato black ring (34, 104, 280), and plum pox (343).

The most commonly employed Pf/z/^/zi-to-herbaceous plant indexing test is the

Prunus-to-cucurhit test (93, 473) for the detection and identification of Prunus

ring spot and prune dwarf viruses. (See section under "Techniques of Investigating Stone Fruit Viruses.") At Glenn Dale, the following herbaceous varieties

are used as indicators: Improved Long Green Cucumber, White Bush Squash,
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE £9

and Buttercup Squash. High greenhouse temperatures either mask symptoms

or are not conductive to infection. Consequently, because young inoculum tissue

is a requirement for routine indexing and high greenhouse temperatures are

detrimental, the testing is usually confined to the period between February and

May.

Graft transmission. — Grafting is accomplished by budding the foreign

Prunus to woody indicators or by double budding both to an appropriate

seedling rootstock. The buds to be indexed are obtained from a tree that was

derived from a bud cut from an imported scion and budded on a domestic

seedling rootstock. For convenience, the buds subsequently produced on this

tree are referred to as "foreign buds." However, they only stem from a foreign

bud. They were actually produced in a quarantine screenhouse at Glenn Dale.

Two foreign buds are inserted in the usual T-cut on each of two indicator

trees. If the foreign buds do not remain alive at least 3 weeks, the indicator

trees are rebudded. A bud contact period of a few days to 2 weeks has been

reported as necessary for the transmission of several viruses {222, 388). The

ornamental Prunus species, such as P. laurocerasus zabeliana which are incompatible when budded, are either approach-grafted to container-grown indicators

or they are not admitted.

The incubation period, or the period that indicators are observed for

symptoms, varies with the indicator and the viruses to be detected. Some indicators require one growing season whereas others require a period long enough

for fruit development. Foliage is observed for at least 2 years after the year

of budding.

Woody Í7ídicators for stone fruit viruses. — At the Glenn Dale and Saanichton Introduction Stations, a compromise must be reached between the total

number of indicators that have been recommended to detect the viruses that

infect stone fruits throughout the world and the practical limitations imposed

by the availability of facilities, land, personnel, and funds. Perhaps the most

that one can do is to include the indicators described in the previous section

for North American viruses plus those recommended in the foreign literature

for viruses not known to occur in North America — keeping in mind that

stone fruit viruses occur outside of the genus Prunus so that apple and pear

indicators (201) might be included. Certainly the very least that one can do

is to use virus-free seedlings of commercial stone fruit varieties. The former

approach is too conservative to be practical and the latter, too liberal to be safe.

The manner in which this compromise has been reached for the Glenn Dale

and Saanichton Introduction Stations, the IR-2 Repository in Prosser, Wash.,

and stations in Europe has been summarÍ2ed in table 3. The lists vary among

geographic areas depending on the relative importance of the various viruses

and the differences in commercial cultivars. An underlying rule-of-thumb in

selecting cultivars as indicators, where two or more are equally sensitive to a

virus, is to select the one that has the greatest commercial production in the
30 VIRUS DISEASES OF STONE FRUIT

area where indexing occurs. If a new virus should appear on the scene, there

is an advantage in using an important commercial cultivar as an indicator.

The new virus might be latent in the indicator, while causing severe damage

to the commercial cultivar. For example, in eastern Europe, the Pozegaca plum

{Vrimus domesued) is an ideal indicator because it not only detects and difTABLE 3.—Minimum list of stone frtiit virus cultivar indicators

used or recommended in the United States, Canada, and Europe

[-j- = used or recommended; ( + ) = alternative; — = not used]

Prunus indicator

United States

Glenn Dale,

Md/

Prosser,

Wash.'

Canada

Saanichton,

British Columbia "

Europe ^

Cherry :

Bing

Mazzard F12/1

Lambert

Sam

Montmorency . .

Flowering cherry:

Shiro-fugen ...

Kwanzan

Apricot:

Tilton

Wenatchee

Peach :

Seedlings

Elberta

Fairhaven

Almond :

Peerless

Plum and prune :

Shiro

Cambridge

Pozegaca

Italian Prune . .

Prune d'Agen . .

Prunus tomentosa

+

+ ' +

+ +

+ +

+ ' +

+

+

+

+

+

+

+

4-

+

+

+

+

+

+

4-

+

+

+

+

+

( + )

( + )

+

+

+

+

+

+

+

( + )

+

+

+

+

+

+

^ Host Range Committee, Interregional Stone Fruit Virus Research Group.

^ Interregional Project IR-2.

^ Post Entry Quarantine Station, Saanichton.

^ European Committee for Cooperation on Fruit Tree Virus Research.

" Some tests conducted at the Fruit Tree Experiment Station, Wenatchee,

Wash., by E. L. Reeves and P. W. Cheney.

« Effective 1970.
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 3I

ferentiates between plum line pattern and plum pox viruses but also it is of

commercial importance. In North America, Pozegaca is not of commercial

importance. At this writing Pozegaca is grown only in the indexing plots at

Glenn Dale, Prosser, and Saanichton. Shiro plum, which is of commercial

importance, will detect but not differentiate both plum line pattern and plum

pox viruses. Therefore, in the United States, Pozegaca is not expected to replace

Shiro as an indicator but should be useful when virus identification is required.

In an indexing program based on 10 indicators, the testing of 50 Prunus

introductions would require more than 5,000 separate budding operations.

To prepare indicators (unless these are purchased), 2,000 buddings are required

(10 indicators X 2 replications X 2 buds X 50 tests). To prepare one check

per four indicator trees, another 500 buds must be inserted. To index 50

Primus introductions, 2,000 foreign buds must be budded on indicator trees

(10 indicators X 2 replications X 2 buds X 50 tests). Assuming an 80-percent

foreign bud-take, another 500 buddings may be required to insure a 3-week

contact period.

At Glenn Dale, the Pf/z/^^j-to-cucurbit mechanical transmission test is used

to screen introductions prior to indexing on woody plants. Unless the introduction is of unusual horticultural importance, there is no point in entering the

clone into the more expensive woody indexing test if it cannot pass the

Pf//;7/^i-to-cucurbit test.

Some results of virus detection and identification tests have been published for

the Glenn Dale {55S, 339) and Saanichton (713) Introduction Stations.

Identification. — Although the primary objective of indexing tests at a

quarantine station is detection, there are circumstances when additional testing is

warranted in order to identify the virus detected. For example, the identification

of a detected virus would be prerequisite (under State and Federal policies as

discussed previously in this section) to determine whether a tree is infected

with nothing more than a common virus already widely distributed in the U.S.

stone fruit growing areas. Fortunately, many of the symptoms on indicator

plants are sufiîciently diagnostic at least for typical strains to permit identification at the same time as detection on the basis of host range and symptoms.

In addition to host range and symptoms, other tests may be employed to

facilitate identification. Serology has been used to identify some viruses such as

Prunus ring spot and prune dwarf {14, 73, 233, 371, 738), cherry leaf roll

(169), tomato ring spot, peach yellow bud strain (107), and the NEPO viruses

(104, 280). Cross-protection has been used to determine relationships of

Prunus viruses {103, 107, 732). Synergism can also be employed {317).

Comparisons of symptoms incited by "unknowns" and "knowns" on various

hosts are also useful. However, neither cross-protection, synergism, nor comparisons on Prunus hosts in the field are used at Glenn Dale because these tests

require the maintenance of known cultures of stone fruit viruses in living Prunus

hosts — a practice at variance with the policies of phytosanitation at quarantine
32 VIRUS DISEASES OF STONE FRUIT

stations. The electron microscope has been used for characterizations of some

Vrunus viruses {IOS, 281, 345, 312, 757). The determination of properties

such as thermal inactivation point, dilution end point, and longevity in vitro,

although widely employed in virus characterization, is limited in stone fruits

to those viruses that are mechanically transmitted {14, 16, 107, 343, 312).

Finally, viruses may also be characterized by modes of transmission such as

insects and mites {623, 717), seed {219, 233, 238), nematodes {104. 280),

and pollen {261, 708, 723) in addition to sap and grafting.
VIRUS DISEASES OF ALMOND AND

APRICOT

ALMOND VIRUS BUD FAILURE

GEORGE NYLAND

Causal Virus

Almond bud failure virus (ABFV).

Synonyms

Drake almond bud failure (744) ; peach mule's ear (743) ; wild leaf (606).

Peach willow twig (649, 630) has some symptoms similar to almond virus bud

failure in peach and at least some of the trees diagnosed as willow twig were

infected with ABFV (S. M. Alcorn and George Nyland, unpublished data).

Several strains of Frunus ring spot virus (PRSV) also induce bud failure and

Vv^illow twiglike symptoms in peach.

History and Distribution

Almond virus bud failure as a distinct disease of almond was first reported

in 1947 on Drake and Nonpareil almonds (657), In symptomatology, it

resembled a nontransmissible almond bud failure {759, 742) believed to be a

genetic disorder. A peach disorder, possibly related to almond virus bud failure,

was named mule's ear in 1955 (743). Mule's ear resembles a condition in

peach described and named wild leaf in 1932 (606) and probably can be

equated with it. However, there is a wild leaf condition in Carolyn peach that

is nontransmissible, but it is known only from this variety (H. K. Wagnon

and George Nyland, unpublished data). The almond calico strain (AlCs) of

PRSV seems to be associated consistently with almond virus bud failure and

peach mule's ear, where this has been determined, but its causal relationship to

the two diseases has not been clearly established. Whether the peach disease

willow twig should also be considered a synonym of almond virus bud failure

is still open to question because so little is known about the virus or viruses that

are associated with the diseases.

Almond virus bud failure occurs in many older almond orchards and in some

young orchards planted with infected trees in the central valley of California.

Its widespread distribution in almond was not recognized until recent years.

Natural spread of the disease is strongly indicated in at least one orchard of

Nonpareil in Colusa County, Calif., and in several other sites including one in

the Winters district of Yolo County and another in Stanislaus County.

Economic Hosts

The disease occurs naturally in several cultivars of almond and has been

produced by inoculation in Drake, Nonpareil, Peerless, Jordanolo, Mission

(Texas), and Ne Plus Ultra. In peach, the mule's ear disease has been seen in

33
34 VIRUS DISEASES OF STONE FRUIT

nine clingstone cultivars, three freestone cultivars, and in many seedlings of

Lovell peach. At least three nectarine cultivars are known to show symptoms:

Quetta, Early LaGrande, and Late LaGrande. Sweet and sour cherry and Shiro

plum are carriers of ABFV as are mazzard and mahaleb seedlings (H. K.

Wagnon and George Nyland, unpublished data).

Symptoms

Almond virus bud failure is characterized by failure of blossom and leaf buds

to grow and the constant association of the AlCs of PRSV spot virus with

the disorder in the field. Often no buds are produced in the axils of leaves of

the portions of current season shoots produced late in the season. Many lateral

buds that are formed die and are cast prior to budbreak or they may remain

attached to the shoot for several months. The terminal bud may be the only

surviving bud on the previous season's growth or a few basal buds may

also survive (ñg. 5). Often the terminal bud fails to grow, in which case the

shoot, over a period of weeks or several months, dies back to the uppermost

live lateral bud. Over a period of years, annual growth from only the terminal

bud and from a few basal buds of many twigs produces a dense brushy growth

of predominatly bare shoots with few lateral spurs in the portion of the tree

affected (fig. 6). Afiiected twigs usually have shorter internodes than unaffected

ones of the same tree or of healthy trees.

Symptoms of almond calico are seen in the leaves of some cultivars e.g.,

Nonpareil, IXL, Ne Plus Ultra, Peerless, Jordanolo) that also show virus bud

failure symptoms. Drake and Mission almonds in stabilized infections rarely

show calico leaf symptoms, but almond calico virus is readily recovered from trees

of these cultivars that show bud failure symptoms. Other leaf symptoms that

have been associated with almond virus bud failure in almond are a slightly

darker green, an erect rather than drooping posture, and retention of leaves

until very late in the fall.

Few blossoms and fruits are produced on affected branches after bud failure

symptoms become obvious. Not infrequently the disease is more severe on some

branches of a tree than on others although the infectious agent can be transmitted from any portion of the tree. Symptoms of almond calico are often

more prominent on the branches showing the most pronounced bud failure.

The symptoms of almond virus bud failure in peach have been referred to as

mule's ear (745) because of the erect leaves near the terminals of slender

v/illowy shoots (ñg. 7). These leaves are retained on the tree until long after

normal leaves have dropped in the fall. Failure of lateral buds of diseased shoots

to grow the spring following the year they are produced and the absence of buds

in the axils of leaves produced during the latter part of the growing season are

additional symptoms. Symptoms of almond calico are more or less evident in

leaves produced during the spring in peach trees with mule's ear symptoms.

Calico symptoms fade and may disappear entirely during the summer, but
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 35

almond calico virus is invariably associated with the disease (H. K. Wagnon and

George Nyland, unpublished data).

Fruit symptoms in peach trees infected with almond virus bud failure are

very striking (fig. 8). The cheeks of some fruits remain green and flattened,

and the stem and stylar ends are rounded and ripen with normal color. Other

fruits may be irregular in shape and ripen later than normal fruits. Fruits with

symptoms are seen usually on branches infected during the current season. In

old infections, few fruits are produced. The disease can reduce the crop significantly in some trees. Usually only limited portions of the trees show leaf symptoms; these are most evident late in the season. Normal pruning removes most

of the diseased shoots so that the disease in peach may be easily overlooked

during the first half of the growing season.

Transmission

ABFV has been transmitted by grafting to Drake, Nonpareil, Peerless, and

Jordanolo (744, 743) and to Mission and Ne Plus Ultra (George Nyland,

unpublished data) almond cultivars. Mission and Ne Plus Ultra do not develop

as conspicuous symptoms of bud failure as the other cultivars, but the virus

can be recovered from them. Virus from almond trees with symptoms of bud

failure was transmitted to peach that subsequently developed mule's ear syndrome {743) and to sweet and sour cherry, Shiro plum and mahaleb and mazzard cherry seedlings. The symptoms of mule's ear in peach and bud failure

in almond are produced 2 to 3 years after inoculation.

Mechanical transmission of virus to the common herbaceous hosts of PRSV

is readily effected from almonds with bud failure or from peach with mule's

ear. The virus obtained has been returned to Prunus hosts and has induced

symptoms typical for almond calico but not as yet the complete almond virus

bud failure—mule's ear syndrome (George Nyland, unpublished data).

Remarks

The AlCs of PRSV is invariably associated with both almond virus bud

failure and peach mule's ear wherever the diseases have been found. However,

although studies with pure cultures of this strain in almond and peach are in

progress, they have not yet shown conclusively that the AlCs is causally associated with the two diseases (George Nyland, unpublished data). The cherry

rugose mosaic strain of Prunus ring spot virus also induces bud failure and

calico leaf symptoms in several almond cultivars in addition to other symptoms

(%• 9).

Distortion of the leaves and a more pronounced mosaic associated with the

cherry rugose isolates in almond helps to differentiate rugose mosaic from almond

virus bud failure in field trees of almond.
36 VIRUS DISEASES OP STONE FRUIT
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 37

FIGURE 5.—Almond virus bud failure: Left, Drake almond branch showing the effect

of 3 years of bud failure. On four shoots produced the previous year, only two

terminal leaf buds, three lateral leaf buds, and one blossom bud grew; right, Gaume

peach branch showing failure of terminal and lateral buds and willowy shoots with

upright leaves (mule's ear symptoms). Many leaves have no macroscopically visible

buds in their axils.
38 VIRUS DISEASES OF STONE FRUIT

FIGURE 6.—A, Drake almond tree affected with almond virus bud failure, showing rigid,

upright leaves, bare twigs, and absence of fruit; B, comparable unaffected tree showing

normal growth and a good crop of fruit.
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 39

See legend on p. 40.
40 VIRUS DISEASES OF STONE FRUIT

FIGURE 7.—Almond virus bud failure: A, Gaume peach tree inoculated with tissue

from Peerless almond infected with almond bud failure virus (ABFV). Center shoot

shows erect leaves or mule's ear symptoms, that remain on the tree long after normal

time of leaf fall; B, shoot from Gaume peach tree showing calico leaf symptoms.
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 41

FIGURE 8.—^Almond vims bud failure. Peach fruit showing delayed ripening of

flattened cheeks.
42 VIRUS DISEASES OF STONE FRUIT

FIGURE 9-—Failure of buds of Nonpareil almond induced by cherry rugose mosaic

strain of Prunus ring spot virus, resembling almond virus bud failure and noninfectious

almond bud failure.
APRICOT PUCKER LEAF

BRYCE N. WADLEY

Apricot pucker leaf virus was found in 1957 in several orchards in Washington County, Utah (686). No additional infected trees have been found, indicating that natural spread has not taken place and that the disease is probably

of minor importance. Transmission by grafts was successful to apricot, peach,

Manchu cherry, and Marianna plum. Attempts to infect sweet cherry, sour

cherry, desert almond, Kwanzan flowering cherry, and mahaleb cherry were

not successful.

Symptoms first appear as chlorotic areas in the middle of young, developing

apricot leaves. As the leaves enlarge, they develop a marked puckering (figure

10). Much of the chlorotic tissue often becomes necrotic and falls out, giving

the leaves a tattered appearance at maturity. Fruit symptoms are mild and

consist of dark-green to reddish-brown spots on the surface of immature fruits.

Slightly deformed fruits are found occasionally. Symptoms were observed in

Moorpark seedling trees and in Perfected, Riland, Royal, Tilton, Moorpark, and

Sunglo.

Leaf symptoms were obscure and generally absent in Elberta and Gleason

Early Elberta peach cultivars. A few slightly deformed leaves and a few young

leaves with mild vein chlorosis were seen in infected peach trees growing in the

greenhouse. No fruit symptoms were seen in peach. Leaf symptoms were

usually as severe in Manchu cherry as in apricot, but no symptoms were detected

in Marianna plum. Transmission was readily achieved to host plants by budding

FIGURE 10.—Puckering, chlorotic spots and patterns, and tattered effect due to loss of

tissue on leaves of Moorpark apricot seedling affected by apricot pucker leaf.

43
44 VIRUS DISEASES OF STONE FRUIT

or tissue grafts, and the virus was recovered from inoculated apricots, peaches,

Manchu cherries, and Marianna plums the season following inoculation,

regardless of whether symptoms developed or not.

Symptoms of apricot pucker leaf somewhat resemble those of peach mosaic

and of apricot ring pox in apricot leaves. Both of these diseases have been found

in the same general area as pucker leaf. However, when symptoms were compared in greenhouse tests, those caused by apricot pucker leaf virus did not resemble those caused by the other viruses.
APRICOT RING POX

A. J. HANSEN, C. L. PARISH, and T. S. PINE

Causal Virus

Apricot ring pox virus (ARPV).

Synonyms

Apricot ring spot (83) ; apricot pox; ring pox. Local forms have been

named after typical symptoms, such as tatter leaf and pit pox.

History and Distribution

Apricot ring pox was reported first from Colorado (83) and has since been

found in Washington (334), British Columbia (403), Utah (682, 683), and

California (301). It is now known to occur in all the apricot-growing areas

west of the Rocky Mountains, but there is no substantiated report of its occurrence outside this region.

Economic Hosts

Apricot (Prunus armeniaca), all cultivars. Some are symptomless carriers of

ARPV (321, 339).

Other Hosts

The only known natural hosts of ARPV are apricot, western chokecherry,

hybrid plums (Prunus salicina x P. simonn), and sweet cherry. The virus can

be experimentally introduced into certain cultivars of almond, nectarine, Japanese plum, peach, sour cherry, desert peach, Bessey cherry, and black cherry.

Abundance plum (P. salicina), Shiro plum (hybrid), Italian Prune (P.

domestica), American plum, and bitter cherry are imiiiune to ARPV (696

and P. W. Cheney and C. L. Parish, unpublished data).

Symptoms

Symptoms of apricot ring pox occur in the fruit, leaves, and current season

twig bark of affected trees (83, 164). The first leaves to expand in the spring

may be without symptoms. Obscure spots develop in successively formed leaves,

particularly in the rapidly growing shoots. Simultaneously, veinbanding,

chlorotic spots, streaks, and rings appear at random and increase in size and

number (fig. 11). These symptoms become increasingly pronounced until

midsummer and are especially conspicuous in years of below normal temperature (164). When the entire border of a spot or ring becomes necrotic, the

center falls out, producing holes with a ragged or angular outline. On the

current season twigs of some cultivars, reddish spots appear at about midseason and eventually become necrotic.

Fruit of affected trees appear healthy until the pit-hardening stage. Then,

discolored or necrotic areas begin to develop on the fruit surface, under the skin,

or inside the flesh. These areas expand and coalesce, forming reddish-purple

45
VIRUS DISEASES OF STONE FRUIT

FIGURE 11.—Chlototk rings and ragged holes caused by apricot ring pox vims (ARPV)

in apricot leaves.

or black spots, rings, pits, and arcs. As the fruit reaches the soft-ripe stage, the

discolored areas may become slightly raised and may be surrounded by concentric lines or radial cracks (fig. 12). In some fruits, the discoloration and

necrosis extend deep into the flesh, where dry black pits are formed. In other

cases, symptoms are very mild, consisting of a light scurf, which may disappear

altogether by harvest time. The variation of symptoms which is found in field

trees is caused mainly by differences among virus strains and among reactions of

apricot cultivars.

Distribution of poxed fruit in diseased trees tends to be irregular; some

branches may produce fruit that are severely affected, whereas others produce

mostly healthy fruit. During the summer following infection, only a few fruits

may develop characteristic symptoms, but in subsequent years 30 to 100 percent

of all fruit is affected.

A marked fruit drop has been observed in British Columbia and Washington

at about the time other fruit symptoms begin to appear, but this symptom has

not been reported from south of the Washington-Oregon border. Under

Colorado growing conditions, developing fruit appears healthy until approx-
HANDBOOK NO. 437, U. S. DEPARTMENT OP AGRICULTURE 47

imately 2 weeks before ripening. After that time, protuberances develop on the

fruit and are followed by typical ring pox symptoms (83).

Of the major commercial apricot cultivars, Tilton and Wenatchee (Wenatchee

Moorpark) develop severe pox and leaf spots when infected by most forms of

ARPV. Royal (Blenheim), Reliable, Sunglo, and Blenril are usually symptomless. Responses to inoculation with ARPV in many other local and foreign

apricot cultivars have been cataloged and published (521, 539).

Foliage symptoms of apricot ring pox in plum are similar to those in Tilton

and Wenatchee apricots but are generally less severe. Plum fruit remains

unaffected (609, 696).

Various strains of ARPV have been distinguished on the basis of symptoms

in Tilton, Wenatchee, Royal, and Perfection. The common strain of ARPV

induces in apricot fruit a superficial black scurf or purple-to-black rings and

arcs, which may be elevated but never penetrate to the seed. Leaf symptoms are

generally present in Tilton but not always in Wenatchee or hybrid plum. The

common strain predominates from central Washington southward into California and eastward into Utah and Colorado.

The pit pox strain induces black cylindrical plugs which penetrate the fruit

flesh and reach the seed in most cases. These plugs are very pronounced in

Tilton, Riland, Perfection, and Wenatchee, but leaf symptoms are often absent

in these cultivars. In Hing sweet cherry, the pit pox strain tends to induce leaf

i^i^

• 1*

^

H>...

FIGURE 12.—Apricot ting pox. Discolored and necrotic tings and spots on Wenatchee

apricot fiuit.
48 VIRUS DISEASES OF STONE FRUIT

twisting similar to that caused by the cherry twisted leaf virus. This strain has

been found in Utah (B. N. Wadley, unpublished data), in the Yakima Valley

and north of Wenatchee in Washington, and in British Columbia. Experimental

transmission of the pit pox strain is more difficult than the common strain,

and field symptoms vary more from year to year. A strain of ARPV reported

from Cahfornia (301) and Utah (B. N. Wadley, unpublished data) differs

from common ring pox and from pit pox in causing leaf and fruit symptoms

in Royal, which is a symptomless host of all other known forms of the virus.

Isolates of the recently discovered spur cherry virus induce symptoms similar to

those of apricot ring pox in Tilton (E. C. Blodgett, unpublished data).

Transmission

Common apricot ring pox is easily graft-transmissible to healthy apricot trees

in budwood, scions, fruit, and leaf tissue (339). The pit pox strain is less

easily transmitted; five to seven buds should be used in each index tree.

Indicator trees infected through bud grafts usually develop symptoms the

following year, although an incubation period of 2 years has been observed

(83, 216). The virus is not seed-transmitted (131).

The pattern of natural spread of ARPV suggests that the virus is arthropodtransmitted (413) but no vector has been reported. Native chokeberry often is

naturally infected, even in locations far from apricot orchards, and this host is

the most likely source of infection in British Columbia.

ARPV has not been transmitted to herbaceous plants, has not been purified

directly from Prunus tissues, and has not been detected with the electron microscope. Therefore, nothing is known about its chemical or morphological characteristics. The virus was not inactivated in Prunus material exposed to 38 °C.

for 21 days or to 50° C. for 20 minutes (P. R. Fridlund, unpublished data).

Control Measures

Although no spectacular regional outbreaks of apricot ring pox have been

reported, the disease takes a constant toll in many western apricot-growing areas.

Until the natural vector of ARPV is discovered, and an adequate control is

established, the only means of preventing further spread of this disease is the

removal of affected trees. The present program is complicated in areas where

orchards are composed of mixed plantings of several apricot cultivars, or of

apricots and sweet cherries, because some of them may serve as symptomless

carriers of the virus. Trees infected with ARPV are commercially worthless if

they are a cultivar that develops fruit pox. Even if they do not exhibit symptoms,

they are reservoirs of the virus. In either case, infected trees should be removed.

Known virus-indexed stocks and scions should be used for new plantings.

Where native chokecherry occurs near apricot orchards, it should be removed.

Remarks

Diagnosis of apricot ring pox is made difficult by the varying degrees of

symptom development caused by strains of ARPV and by symptoms caused by

other viruses that closely resemble those of ring pox. Prunus ring spot virus
HANDBOOK NO. 437. U. S. DEPARTMENT OF AGRICULTURE 49

(516), peach mosaic virus (323), and pucker leaf virus (686) cause leaf symptoms in apricot which are almost identical to those caused by ARPV, but no fruit

symptoms develop. Because these viruses may be present in apricot material

suspected of carrying ARPV, it is essential to index for ARPV in a host

combination that produces fruit symptoms regularly (e.g., Tilton or Wenatchee).

Sarka (plum pox), a virus disease spreading at present in Europe, has symptoms

similar to apricot ring pox in some hosts (328). It can easily be distinguished

from apricot ring pox in Italian Prune, which has not become infected when

inoculated with ARPV. Ring poxlike fruit symptoms have been found on plum

in England (193) and on one apricot cultivar in Australia.

The relationship between ARPV and cherry twisted leaf virus (CTLV) has

not been investigated sufficiently. Extensive work in British Columbia (414,

413) indicated that a close relationship exists between the two viruses. A large

percentage of ARPV isolates were capable of inducing twisted leaflike symptoms

in Bing sweet cherry and, conversely, CTLV isolates from cherry induced ring

pox symptoms when budded into Wenatchee apricot. Similar results have been

obtained in Tilton apricot with isolates from Lambert sweet cherry from the Kettle Falls area of Washington. The data available at present are not sufficient to

determine whether one virus causes both diseases or whether two closely

associated viruses are involved in this syndrome.
VIRUS DISEASES OF PEACH

ASTEROID SPOT

H. E. WILLIAMS, BRYCE N. WADLEY, and H. K. WAGNON

Causal Virus

Asteroid spot virus (ASV).

Synonyms

Utah Dixie rusty mottle; stipple spot (in Texas).

History and Distribution

Asteroid spot in peach trees was reported first from California in 1938

(161) although the disease had been observed in Texas and California prior

to that time (162). Later the disease was recognized in peach in Colorado,

Oregon, Utah, Washington (^78), and Mexico (162). Two affected trees

reported in North Carolina were traced directly to infected nursery stock

originating in Texas (142). The virus is known to occur in native desert peach

trees in Nevada and California (699). A disease of sweet cherries in the Dixie

area of southern Utah was reported first in 1944 (^73) and later described

as Utah Dixie rusty mottle (383, 386). In 1949, what appeared to be a related

disease was found generally distributed in peaches growing near the infected

cherries (383). A virus, transmitted from these naturally infected peach trees,

produced symptoms of Dixie rusty mottle in sweet cherry and asteroid spot in

peach.

Economic Hosts

Peach, nectarine, and sweet cherry.

Other Hosts

Susceptible species are almond, desert almond, apricot, Japanese apricot, ansu

apricot, mahaleb cherry, Manchu cherry, desert peach, European plum, Japanese

plum. Damson plum. Prunus bokhariensis, P. angustifolia, and P. sp'mosa

(162, 682, 699; and T. S. Pine, unpublished data).

Symptoms

Peach and nectarine. — This disease was named for the small, star-shaped

spots that develop in infected peach leaves (fig. 13). Leaf symptoms appear

early in the spring on fully expanded leaves and become more pronounced as

the season progresses, particularly during periods of high temperatures. The

spots begin as small, translucent, light-green flecks in the fully expanded leaves.

Affected leaves gradually turn yellow, but the spots remain yellowish green,

thus reversing the color contrast. Spots vary in size, the size being inversely

proportional to the number present. Occasionally some of the larger spots have

green centers and are thus really rings. In some leaves, large, angular, chlorotic

50
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 5I

FIGURE 13.—Asteroid spot. Yellowish green angular or star shaped spots on yellowed

peach leaves.

blotches form along the veins. The chlorotic spots sometimes become necrotic

and drop out. The size, number, and character of the leaf spots varies among

cultivars and between isolates of the virus. Progressive defoliation of affected

trees often is encountered in the orchard, the older leaves dropping first. In

severe cases, peach and nectarine trees may be almost completely defoliated by

the end of summer. Affected trees show symptoms annually, but they are

usually more severe during the first year of infection.

White-fleshed peach and nectarine cultivars tend to develop more pronounced symptoms than yellow-fleshed cultivars. No fruit symptoms have been

reported but heavy defoliation seems to reduce the quality and quantity of fruit

on affected trees.

The presence of strains of ASV has been suggested {162, 699). The isolate

of ASV from desert peach (699) produces a much more severe reaction in

peach (e.g., Lovell and J. H. Hale) than isolates collected from other sources
52 VIRUS DISEASES OF STONE FRUIT

(699 and T. S. Pine, unpublished data). This isolate caused some dying of

twigs on inoculated limbs of peach trees, a symptom not found after inoculation

with other sources of the virus.

Sweet cherry. — Asteroid spot in sweet cherry was described originally as

Dixie rusty mottle, but the symptoms are distinct from those induced by other

viruses of the rusty mottle group. Symptoms vary considerably between cultivars

of sweet cherries and are influenced by climatic conditions (high temperatures).

The foliage appears healthy until 4 to 7 weeks after full bloom and then small

necrotic spots begin to appear in the leaves. A few days after the appearance

of leaf spots, many of the leaves begin to develop premature senescence, similar

to that which occurs with the rusty mottle diseases. As the chlorophyll

degenerates, islands of green remain on a background of yellow (fig. 14). The

yellow leaves may be cast within a week, and partial to complete defoliation

may result by mid- to late summer. Late fall symptoms differ from those produced earlier in that necrotic spots become larger and are surrounded by a halo

of yellow tissue with a green or reddish-brown outer margin (fig. 15).

Sometimes the necrotic spots are absent, but the yellow tissue and colored

rings remain.

Lateral buds and small branches of susceptible sweet cherry cultivars are

usually killed by ASV. Larger limbs also may be killed, and severely affected

trees may die in 2 to 5 years. Necrotic areas often form in the flesh of maturing

FIGURE 14.—Early season symptoms of asteroid spot on Lambert sweet cherry leaves—

small necrotic spots and green islands on a yellowing background.
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 53

FIGURE 15.—Late fall symptoms of asteroid spot on Lambert sweet cherry leaves—

large necrotic spots surrounded by halo of yellow tissue and outer green margin on a

yellow background.

fruits (fig. 16). The percentage of deformed fruits may be high enough to

cause complete loss of the crop. The heavy defoliation causes a reduction in

fruit size, a delay in maturity, and a lowering of fruit quality. Both leaf and

fruit symptoms in sweet cherry are most severe when summer temperatures

are high.

All sweet cherry cultivars are hosts of ASV, although some are more susceptible to damage than others. Lambert, Bing, Deacon, and Van are more

seriously damaged than Black Tartarian, Napoleon, or Windsor (682). Some

mazzard seedlings develop symptoms whereas others do not.

Apricot. — Symptoms of asteroid spot in apricot vary with cultivar and strain

of the virus, but they are essentially the same as those in peach. In a collection

of foreign and domestic apricot cultivars, ASV caused only delayed foliation

and retarded growth in many cultivars, but the virus was easily recovered in

peach or plum 4 years after inoculation (T. S. Pine, unpublished data). Some

cultivars in the collection underwent premature defoliation without displaying

foliar symptoms whereas others, such as Tilton and Royal, developed symptoms

as severe as those in peach and dropped most of their leaves by late summer.

Some apricot cultivars (e.g., Moorpark) may not develop symptoms until the

second year of infection.

The apparent presence of strains of ASV also can be detected in apricot.

Isolates of the virus from naturally infected Santa Rosa plum trees caused only
54 VIRUS DISEASES OF STONE FRUIT

mild symptoms in Tilton, but an isolate from an unknown peach cultivar

growing in a desert area of San Bernardino County, Calif., caused very severe

leaf symptoms and defoliation in Tilton (T. S. Pine, unpublished data).

Other hosts. — Symptoms caused by ASV in Japanese plums also vary with

cultivar and virus strain but generally resemble those in peach (fig. 17).

Defoliation is less common on plum than on peach and cherry. Symptoms in

inoculated French (Agen) prune and damson plum were obscure. ASV may

cause faint symptoms in almond but is known to remain latent in some cultivars.

The virus is completely latent in both desert almond and desert peach.

Transmission

ASV has been transmitted only through tissue grafts. The incubation period

varies from 4 weeks to 2 years, depending on the host cultivar and the time

of inoculation. The occurrence of ASV in widely separated geographic areas

and its recovery from native Prunus spp. is indicative of natural spread but

no vector is known.

Control Measures

Nursery trees should be grown only from inspected and indexed source trees.

Trees grown under provisions of official certification programs are highly

n

FIGURE 16.—Small necrotic spots and green islands on yellowing leaves and necrotic

spots on maturing fruits of Napoleon sweet cherry affected by asteroid spot.
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 55

FiGURB 17.—^Asteroid spot. Small chlorotic, angular or star shaped spots on leaves of

Late Santa Rosa plum.

recommended as planting stock. Diseased trees should be removed promptly

in those areas and orchards where infected trees occasionally appear. In areas

where the disease is widespread, and severe forms of the virus cause extensive

damage, attention should be directed toward the feasibility of an eradication

program.

Remarks

Asteroid spot cannot be considered economically important although ASV

occasionally causes the loss of fruit trees in limited areas. The more important

losses, which are usually overlooked, result from reduced yield and poor

quality of fruit from trees infected by mild forms of the virus. Leaf symptoms

of asteroid spot may be confused with those of Prunus ring spot, plum line

pattern, peach mosaic, apricot ring pox, and probably others, but the severe

defoliation of index peach seedlings inoculated with ASV is diagnostic.
PEACH BLOTCH

CARL W. NICHOLS

Peach blotch is a virus disease of minor importance that has been reported

from Ontario {730, 731), California {691, 694), Italy {168, 592), and possibly from Yugoslavia {592). It very likely occurs in many other peach-growing

areas but has not been reported because of the minimal damage it causes.

The primary symptom of peach blotch is a well-defined, pale-green to

yellow-green area in the leaves (fig. 18). These areas usually are large,

irregular blotches scattered over the leaf blade, but smaller, angular spots may

occur. Occasionally the chlorosis (light shades of green) is limited to bands

along both sides of the midrib and basal portions of the main veins, or to

one large chlorotic spot on one side or both sides of the midrib. While

the margins of the chlorotic areas are usually well defined, sometimes they are

■■feathered out" along the lateral veins. The usual pattern of chlorotic blotches

on a normal green background may be reversed, and dark-green islands occur

on a chlorotic background. Both patterns may occur on the same leaf. The

scorched margins and necrotic leaf spots reported in Canada {731) have not

been observed in California. In California, the symptoms are usually limited

FIGURE 18.—Peach blotch. Pale green blotches on peach leaves.

56
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 57

to leaves that are produced during the early and late parts of the growing

season (694). Mild symptoms of peach blotch have been detected late in

August in the terminal leaves of nursery stock propagated in the spring of

the same year with buds from virus-infected peach trees (691).

Peach is the only known host of this virus. Disease symptoms have been

observed in many peach cultivars in the orchard and have been produced on

others following graft inoculation. Apparently all peach cultivars that are

infected by the virus will develop symptoms, but the intensity of the symptoms

may vary widely (730, 731).
PEACH CALICO

H. KEITH WAGNON, JACK TRAYLOR, and HAROLD E. WILLIAMS

Causal Virus

Peach calico virus (PCV).

Synonyms

The term "peach cahco" was first appHed to peach variegation, a nonvirus

disorder, but later was reserved for use with peach calico virus disease (^-5),

History and Distribution

In the United States, the disease is known to occur only in California (689,

694), Idaho (33, 71), and Washington (334). It also has been reported in

Australia (306), Bulgaria (671), and New Zealand (132). Although PCV

is widely distributed, its incidence always has been low.

Economic Hosts

Peach and nectarine are the only known hosts. All cultivars of these fruits

are believed to be susceptible.

Symptoms

Symptoms of peach calico occur on the leaves, on stems of current year shoots,

and on the fruit. The most conspicuous symptoms are those found on leaves,

particularly those which develop during the spring and early summer. Occasionally, certain shoots will produce symptomatic leaves throughout the growing

season (ñg. 19). Usually, an affected twig will have both affected and nonaffected leaves.

The first leaf symptoms usually appear as the leaves unfold, and consist of a

mottle or mosaic pattern of green, pale green, yellow, cream, and white. As the

affected leaves age, the pale-green areas change to creamy yellow and even papery

white. The areas of the leaf lacking green pigmentation may follow along each

side of the midrib, often forming a symmetrical pattern. However, in many

instances, the pattern is spectacular in its nonuniformity. In extreme situations

all, or the greater part, of some individual leaves may be completely devoid of

green pigment. These leaves frequently become necrotic along their margins

during periods of hot weather.

Characteristic stem symptoms usually are confined to twigs having leaf

symptoms. Creamy white streaks or blotches, often with pink or reddish margins,

occur on stems of seriously affected shoots.

Fruits on affected branches may begin to show symptoms when they are

less than an inch in diameter. These symptoms are irregular patches of creamy

white or bleached tissue showing through the pubescence. As the fruit matures,

the affected areas may become orange or reddish. Affected fruits are smaller,

shorter, and more nearly round than healthy fruit.

58
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 59

[

FIGURE 19.—^Peach leaves affected by peach calico, showing mosaic patterns of pale green,

yellow, cream, and white.

Limited inoculation tests have failed to induce symptoms in Manchu cherry

and the following cultivars: Bing sweet cherry, Montmorency sour cherry, May

Duke semisweet cherry {Prunus avium X P- cerasus), Moorpark apricot, Italian

Prune, and Ne Plus Ultra and Peerless almonds.

Information on virus morphology and serological relationships is lacking.

Heat treatments in which growing plants were maintained for 40 days at 99° F.

had no apparent effect on the virus {132).

Transmission

Transmission of PCV has been accomplished only by grafting. Because the

virus moves very slowly in a tree, evidence of transmission is best attained by

the forcing of dormant or adventitious buds near the inoculum.

Control Measures

The potential hazard is in the propagation of nursery stock with infected

scions. Once PCV invades the apical meristem of a shoot, all subsequent
60 VIRUS DISEASES OF STONE FRUIT

shoot growth from that meristem is usually infected. Therefore it is important

to use virus-indexed budwood.

Remarks

Limited studies on the occurrence of the disease have provided no evidence

of natural spread. It is believed that the disease has been increased and distributed through the use of contaminated propagating materials. The erratic

occurrence of symptoms indicates that there may be more than one strain of

PCV. Mature trees infected by PCV, for the most part, have not been severely

affected by the disease. Because PCV spreads through a tree at such a slow

rate, natural spread of the virus in an orchard would be difficult to detect and

would not be of economic importance. The similarity of symptoms and occurrence of affected twigs in orchard trees causes some confusion with other

diseases, such as peach variegation, peach blotch, and almond calico.
PEACH MOSAIC

T. S. PINE

Causal Virus

Peach mosaic virus (PMV).

History and Distribution

In 1931, peach mosaic was found simultaneously in peach trees in Texas (322)

and Colorado (76, 77). Subsequently the disease was discovered in peaches in

Arizona, Arkansas, California, New Mexico, Oklahoma, and Utah, and in the

States of Baja California, Chihuahua, and Coahuila of the Republic of Mexico

(323). Today it is economically important only in western Colorado and southern California. It has been confused with peach calico, sarka, and other plum

virus diseases in Europe (328), but there is no substantiated report of its

occurrence outside the United States and Mexico. The widespread incidence of

peach mosaic in the Rio Grande Valley indicates that it has been present there

for a long time (323).

Economic Hosts

Peach and nectarine.

Other Hosts

The virus has been transmitted to peach from naturally infected almond,

tangut almond, apricot, ansu apricot, Japanese apricot, Manchu cherry, David

peach, flat peach, American plum, Bokar plum, beach plum, chickasaw plum,

damson plum, European plum, flatwoods plum, hog plum, hortulan plum,

Japanese plum, Mexican plum, myrobalan plum, and wildgoose plum. Western

sand cherry and Korean cherry (not true cherries) and Klamath plum can be

infected experimentally and will develop characteristic symptoms. PMV was

recovered from desert almond, desert apricot, and sweet cherry when these

species were grown on infected rootstocks but could not be recovered if they

were grown on their own roots or nonsusceptible rootstocks (82, 148, 138, 323).

Peach mosaic virus has not been found infecting, or has not been transmitted

to, fenzl almond, capollin cherry, bitter cherry, black cherry, hollyleaf cherry,

mahaleb cherry, pin cherry, sand cherry, sour cherry, sweet cherry, western

chokecherry, oriental flowering cherry, or Prunus kansuensis.

Peach mosaic virus was successfully inoculated into and recovered from 269

cultivars and 62 numbered selections of peaches and nectarines (138). Most

freestone cultivars are severely damaged but clingstones tolerate the virus with

little injury. Based on symptoms produced in J. H. Hale, peach cultivars can

be divided into three comparative classes. The most important commercial

cultivars are thus classified, in table 4, according to the relative severity of their

reactions to a severe strain of PMV. Forty-two horticultural plum cultivars

61
62 VIRUS DISEASES OF STONE FRUIT

TABLE 4.—Classification of commercially important peach and

nectarine cultivars according to the relative severity of their

reaction to peach mosaic virns

Severely damaged Moderately damaged Slightly damaged

cultivars cultivars cultivars

Alamar Babcock Andora

Ambergem Cardinal Carolyn

Blake Coronet Cortez

Dixired Early Babcock Gaume

Earlihale Early East Halford No. 2

Earlired Jerseyland Johnson

Elberta Keystone Nemaguard

Fay Elberta Merrill Fiesta Paloro

J. H. Hale Redglobe Peak

Le Grand (nectarine) Redskin Phillips

Loring Richaven Springtime

Maygold Redtop Stuart

Merrill 49'er Southland Sullivan No. 1

Ranger Sunhaven Sullivan No. 2

Redcap Suwanee Sullivan No. 4

Redhaven Wiser Suncrest

Regina Vivian

Rio Oso Gem

Sunhigh

Triogem

and 103 apricot cultivars tested were found to be hosts for at least one strain

of PMV, but not all susceptible cultivars developed foliar symptoms {78, 326).

Symptoms

Peach.—Diagnosis of peach mosaic often is difficult because the virus exists

in many forms which vary in virulence, and because peach cultivars differ in

tolerance to the virus (323). Symptoms of peach mosaic consist of blossom

break, retarded foliation, mottling and deformity of leaves, fruit deformity, and

abnormal tree growth. Symptoms in some cultivars may be so mild that they

are almost masked. Some virus cultures cause a pronounced shock stage during

the first year of infection, whereas others show no shock the first year but

increased symptom development the second year (320). In subsequent years,

affected trees usually enter a chronic stage of infection during which symptoms

are present in less severe forms (143).

Affected peach cultivars that normally produce large, solid-pink blossoms

(e.g.. Fay Elberta, Rio Oso Gem) often show an unusual color break in the

petals. Irregular streaks, spots, or lines of white break up the pink so that the

petals appear mottled (fig. 20). The affected petals sometimes become crinkled

and dwarfed. This symptom can be confused with a similar color break in peach
HANDBOOK NO. 437, U. S. DEPARTMENT OP AGRICULTURE 63

FIGURE 20.—-Petals from peach tree infeaed with peach mosaic virus,

showing color breaking.

petals caused occasionally by the Prunus ring spot vims. The number of

geminate buds produced on trees infected by PMV is substantially increased

{514).

Leaf growth and new twig growth on affected trees is retarded during the

spring and early summer. The degree of retardation depends on the virus form

present and may involve the whole tree or only one or two. branches (fig. 21).

Many of the early leaves are shed, but those formed later remain on the tree.

The retarded condition becomes less pronounced as the growing season progresses until, by late summer or autumn, the tree presents an almost normal

appearance. Reduced twig growth (shortened internodes) leads to a stubby

growth habit with the leaves crowded together to form rosettes (fig. 22). Some

severely affected trees are seriously dwarfed.

An important symptom of peach mosaic is the development of variously

shaped chlorotic patterns in the leaves during the spring and early summer.

These discolorations differ in size and form from tiny flecks to bold blotches,

streaks, or vein feathering (fig. 23). Severely affected cultivars may show

all these patterns at the same time. Cultivars infected with a mild strain of

PMV, or very tolerant cultivars, may show only vague veinlet clearing or yellow

flecking in the leaves. Leaf patterns of peach mosaic appear in both the early

formed leaves, which tend to drop, and those formed later. Many leaves on

severely affected trees are small, narrow, crinkled, or irregular in outline.

Chlorotic areas frequently become necrotic and fall out, resulting in a leaf shot
64 VIRUS DISEASES OF STONE FRUIT

Í^KÍ?!

^ tâ..

¥^1^^

FIGURE 21.—Peach mosaic. Retarded growth on part of a severely affected peach tree.

hole. As the season progresses, the foliage of affected trees becomes darker

green, and the leaf patterns become less distinct. The color change to darker

green is part of the normal development of the peach mosaic syndrome (326)

and probably results from high summer temperatures {119).

Many peach cultivars, particularly freestones, develop severe fruit symptoms

that make the fruit unmarketable. The surface becomes rough or bumpy (fig.

24) when fruit on diseased trees has exceeded an inch in diameter or at the

stone-hardening stage. The bumps appear as raised areas of normal tissue surrounded by depressions caused by failure of tissue to develop. Frequently, the

suture area is deformed. As the season advances, the bumpy character of the

fruits intensifies; the size of affected fruits fails to increase as rapidly as normal

fruits. Occasionally, affected fruits lose some of the bumpiness just prior to

maturity, but they never reach normal size or shape. Fruit of cultivars that

do not develop such severe symptoms tend to ripen several days to a week or

more later than healthy fruit. The flavor of affected fruit is only slightly

inferior, but the reduced size and irregular shape make it unmarketable.

Plum.—Horticultural plum cultivars are highly susceptible to PMV but only

occasionally are they found naturally infected {526). Symptoms in cultivars of

Prunus domestica (fig. 25) and P. sdicina usually are the same types found in
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 65

peach. Infected trees rarely show delayed foliation, dwarfing, or fruit injury.

Leaves of some affected trees are deformed but not as seriously as those of peach

trees. The severity of leaf symptoms in plum tends to remain more constant,

year after year, than in peach.

Apricot.—^Natural infections of peach mosaic occur more often in apricot than

in plum. Symptoms in most apricot cultivars are less severe than those in peach,

but some may be severely affected (fig. 26). The more sensitive cultivars

develop the same leaf patterns, leaf distortion, and short internodes associated

with peach mosaic in peach. Trees severely infected by PMV tend to be less

vigorous, produce less fruit, and have a higher percentage of sunburned fruit

than healthy trees.

FIGURE 22.—Peach mosaic. Stubby twig growth on affected branch, right; normal

growth on heahhy branch, left.
66 VIRUS DISEASES OF STONE FRUIT

FIGURE 23.—^Variations in chlorotic spotting and distortion of peach leaves affected by

peach mosaic.

Field diagnosis of peach mosaic in apricot often is complicated by dual

infections with apricot ring pox virus (ARPV) (-523). Early in the growing

season it is difficult to distinguish between the chlorotic leaf patterns caused by

PMV and those caused by ARPV. However, as the season advances, the leaf

patterns caused by ARPV redden and become necrotic, whereas those caused

by most strains of PMV remain constant and the leaves become cupped or

twisted. There is no synergism between PMV and ARPV in apricot trees with

respect to severity of leaf symptoms or fruit pox. Some cultures of Prunus ring

spot virus cause mosaic patterns in apricot leaves that are similar to those caused

by PMV, but the patterns fade more rapidly and usually do not reappear the

following year {516).

Other hosts.—Symptoms caused by PMV in almond usually are mild compared

with those in peach (fig. 27). Severe outbreaks of peach mosaic in almond

have occurred only when the almonds were grown near orchards with many

infected peach trees. Fruit on diseased almond trees may be bumpy, but there is

no appreciable reduction in yield or quality of the nuts (325). The incidence of

PMV is high in native Prunus spp., particularly plums, but foliar symptoms are

not always present.

Transmission

The natural vector of PMV is the eriophyid mite Eriophyes instdiosus Keifer

and Wilson {351, 747). The mite was collected first from peach in southern

California and subsequently from several Prunus spp. in California and in other

States where PMV is present. Range of the vector, however, does not coincide
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 67

with the present range of peach mosaic; the vector has been collected from

flowering peach trees as far north as Madera County in California's Central

Valley, 200 miles outside the limits of the known range of PMV. It has been

found in Georgia, Indiana, and Mississippi, where peach mosaic has never been

observed. The vector feeds and reproduces beneath the closely adhering leafbud scales, seeming to prefer the retarded or stunted buds that are commonly

found on peach trees late in the summer. However, the densest populations are

found in April in buds that have not yet expanded. On native plums, the mite

has been found not only under the scales of dormant or retarded buds but also

reproducing in leaf axils and among rudimentary leaves of expanding buds on

vigorously growing shoots. Bud retardation is characteristic of peach mosaic in

peach, hence the persistence of the vector is favored in diseased trees. A single

mite is capable of transmitting PMV from diseased to healthy peach seedlings.

Transportation in air currents is probably their means of dissemination.

PMV apparently spreads whenever the foliage is present and green; i.e., from

late March to October {33Í). When trees are infected before the leaves are

expanded in the spring, either by the vector or by artificial means, symptoms

usually develop in 21 to 30 days; if infection takes place later in the year, symptoms do not appear until the following spring (326). Natural spread of PMV

readily occurs from peach to peach and sometimes from peach to apricot and

FIGURE 24.—Fruit from peach trees affected by peach mosaic, showing reduced size,

bumpy surface, and uneven color development.
68 VIRUS DISEASES OF STONE FRUIT

\

FIGURE 25.—Chlorotic spotting and distortion of leaves of French (Agen) prune affected

by peach mosaic.

almond but rarely from apricot or almond to peach (163). This is probably

because the vector travels to hosts other than peach or plum and feeds on them

for short periods but does not colonize (reproduce) on them.

PMV has not been mechanically transmitted in expressed juice. The virus

has been transmitted in tissue grafts, using diseased fruit, leaf pieces, shootwood

and bark, and rootwood and bark (159). The virus is not transmitted by

dodder (32).

Because PMV has not been transmitted to any herbaceous plant and has not

been purified from Prunus tissue, nothing is known about its chemical or physical

properties. Based on differential symptoms in Prunus spp., cross-protection, and

consistent recovery from natural infections, it has been possible to show that

definable strains of PMV occur in nature {81, 144, 149, 154, 155, 160, 321,

520). The "hairy break" or mild strain of PMV has maintained its identity

through 25 years of research on peach mosaic. It provides good protection

against reinoculation as long as the challenging severe cultures of PMV are

obtained from peach trees, but it fails to protect completely against cultures

derived from other Prunus spp., especially plum (both P. domestica and P.

salic'ma) {79, 160, 520). The peach severe strain of PMV produces symptoms

in plum but not in almond or apricot. The plum strain, originally obtained from

French prune and Kelsey plum, causes symptoms in almond, apricot, and peach.

Control Measures

Peach mosaic has been contained within relatively limited areas since 1935

through a program of diseased-tree removal conducted by the Plant Protection
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE QQ

Division, USDA, in cooperation with the States, counties, and pest control

districts concerned. Infected areas are under Federal-State quarantines, and

tree removal is coordinated with nursery inspection to prevent spread of the

disease to noninfected areas. The use of tolerant peach cultivars in areas where

roguing of infected trees is used as a control measure is undesirable because of

greater difficulty of diagnosis, especially where the milder virus strains are

present. On the other hand, tolerant cultivars are desirable in areas where

roguing is not feasible and peach growers must operate in the presence of the

disease.

Peach mosaic virus was not inactivated by heat treatment (38.5). Oiemotherapy of peach trees infected by PMV has been attempted on a limited scale

without conclusive results {522).

Remarks

Because native plums seem to be the preferred host of the PMV vector and

because isolates of the virus from plums have a wider host range than those from

other Prunus spp., it seems plausible that this disease probably originated in the

native plum species of the Rio Grande Valley and ""escaped" to its economic

hosts, peach and nectarine. Long-range dissemination of PMV and its vector

from southwestern Texas (or northern Mexico) probably was in cuttings of

native P. americana and P. munsoniana, both valued for their fruit. Local

natural spread then took place wherever the vector and the virus were present.

The contagious nature of peach mosaic and the efficiency of the vector are shown

by the fact that only seven diseased trees were found in Colorado in 1931, but

30,467 were known to be diseased in 1935. During the first 5 years of the

tree-removal program in California, 204,193 diseased peach trees were destroyed.

Peach mosaic virus has seriously limited the culture of many popular freestone

cultivars (e.g., J. H. Hale and Elberta) in the southwestern United States. The

FIGURE 26.—Chlorotk patterns in leaves of Royal apricot afifected by peach mosaic.
70 VIRUS DISEASES OF STONE FRUIT

FIGURE 27.—Chlorotic spots and patterns in leaves of Ne Plus Ultra almond affected

by peach mosaic.

more tolerant cultivars, on which marketable fruit can be produced, are often an

economic threat to the industry in this region because of their ability to act as

reservoirs of virus for spread to susceptible cultivars. Control of the virus

vector, combined with diseased-tree removal and continued vigilance in the

selection of virus-free budwood for propagation, should continue to reduce the

incidence of peach mosaic.
PEACH MOTTLE

A. W. HELTON

Peach mottle was found in a few Elberta peach trees in Idaho between 1939

and 1943. The causal virus was transmitted by grafting to peach cultivars J.

H. Hale, Elberta, Slappey, and peach seedlings; to sweet cherry cultivars Bing,

Napoleon, Lambert, Black Republican, and mazzard seedlings; to sour cherry

cultivar Montmorency; and, to May Duke cherry (67). Trees inoculated in

the fall usually showed symptoms of peach mottle the following spring. No

natural spread of the virus has been reported, and the disease is of minor

economic importance.

Leaves of affected trees are slightly dwarfed and coarsely mottled, with the

margins tending to roll and pucker (fig. 28). Naturally infected trees are

ragged in appearance and generally lighter in color than healthy trees. Growth

is reduced but not enough to cause resetting. Foliar symptoms in artificially

infected peach trees are similar but vary markedly in severity among cultivars.

No symptoms of peach mottle have been noted on fruits or blossoms, but

infection at an early age often results in stunting or death. Foliar symptoms

tend to fade as the growing season progresses.

FIGURE 28.—Peach leaves showing m,ottling and puckering caused by peach mottle virus.

71
72 VIRUS DISEASES OF STONE FRUIT

Symptoms in artificially infected sweet cherry trees range from severe leaf

mottle and necrosis, shoot necrosis, and tree stunting in Bing, to a chlorotic

veinlet clearing in Lambert. Symptoms in Napoleon resemble those in Bing

but are less severe. Symptoms in Black Republican are similar to those in

Lambert but are somewhat more severe. Peach mottle virus in Montmorency

sour cherry causes variable leaf mottling, twig dieback, and formation of

gum pockets on the twigs, which are sometimes accompanied by stem swellings

or cracks in the bark. Infected May Duke trees produce leaf mottling and vein

clearing, stunting, and dieback of terminal shoots.

Infected trees should be removed. Only disease-free propagating materials

should be used for replanting.

Peach mottle virus induces severe symptoms in Black Republican and

Montmorency and is therefore distinguishable from the cherry mottle virus

which produces only mild symptoms in these hosts. Peach mottle is distinguished

from peach mosaic in that peach mosaic virus does not infect cherries.
PEACH ROSETTE

GLENN KENKNIGHT

Causal Virus

Peach rosette virus (PRV).

History and Distribution

Peach rosette was observed first in Georgia in 1881 (613, 614). Subsequently,

it was found in Alabama, Arkansas, Illinois, Indiana, Kansas, Kentucky, Mississippi, Missouri, Oklahoma, South Carolina, Tennessee, Texas, and West

Virginia (423 and author's unpublished data).

Economic Hosts

Peach; Japanese plum and plum hybrids; and wild plum species (Prunus

angustifoUa, P. hortulana, and P. munsoniand) and hybrids.

Other Hosts

Almond, apricot, flowering almond, damson plum, western sand cherry,

David peach, wild plums (Prunus mexicana and P. injucunda), Manchu

cherry, ma22ard cherry seedlings, mahaleb cherry, sour cherry, sand cherry,

common chokecherry, and red maple. Tobacco (Nicotiana glutinosa), tomato

(Lycopersicon esculentum), and periwinkle (Vinca rosea) have been

experimentally infected.

Symptoms

Peach.—The development of early spring symptoms in affected trees is both

rapid and striking. Leaves on part or all of a diseased tree are normal in size

but yellow and either folded inward or arched backward. Occasionally, the

first symptoms are the reddening of leaf veins and early defoliation. New shoot

growth has extremely short internodes. As leaves are formed on this growth,

they are appressed into distinct rosettes (fig. 29). Leaves on older portions of

the tree are shed by early summer, leaving only tufts of young leaves near the

tips of naked shoots. Blossoms on affected branches rarely develop or set fruit.

Most affected trees die during the first year of infection. Occasionally, an

affected tree will leaf-out the following spring but it dies quickly.

Plum.—Japanese plum cultivars and hybrids (e.g., Kelsey Ogon [Botan],

Maynard, and Red June) are very susceptible to natural infection by PRV.

Rosetting is less conspicuous than on peach, and affected trees may live 2 to

3 years after the appearance of symptoms. Some diseased plum trees are noticeably stunted. Inoculated damson plum trees develop symptoms similar to those

in Japanese plum. An Italian Prune tree (Prunus domestica) inoculated with

one source of PRV developed symptoms similar to those seen in Japanese plum,

but other Italian Prune trees inoculated from other virus sources showed no

signs of infection. The virus was transmitted from peach to Green Gage plum

and back to peach without the plum becoming permanently infected.

73
74 VIRUS DISEASES OP STONE FRUIT

FIGURE 29.—^Elbetta peach tree affected by peach rosette showing severely resetted

growth of all shoots.

Wild plum.—Prunus angustifolia is the principal native plum host of PRV.

Leaves on affected portions of trees often are larger than healthy leaves and

tend to become reddish rather than yellow. Rosetting of terminal leaves is

much less noticeable than on peach; shortened internodes are less prevalent,

and there is less premature defoliation. Most affected trees die the year of

infection; only a few live more than one full year. Naturally infected P.

injucunda is known in only one location in Georgia {5(>0'). Some affected

seedlings of this species die quickly while others become stunted and live

up to 5 years. They produce dense green foliage in the spring and the leaves

turn red in summer. Some clones of P. injucunda are symptomless carriers of

PRV.

Other hosts.—Symptoms in almond are similar to those in peadi {615).

Shoots of affected Royal apricot are weak and have shortened internodes, but

rosetting is not as severe as on peach. Growth may be stunted, and the leaves

often develop a yellow-green mottle. On Moorpark apricot, only stunting and

leaf mottle may appear (423). Wilson apricot develops very mild symptoms,

but there is a tendency toward proliferation of shoots on the main branches

which results in a witches'-broom effect (661). Leaves on affected trees are

slightly yellow and the petioles turn red. Some apricot seedlings, however,

may show very severe symptoms after inoculation with PRV.

The growth of ma2zard cherry trees infected by PRV is markedly reduced,

and the leaves are smaller and more rolled than healthy ones. The leaves are
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 75

yellowish and tufted, as on peach. Terminal buds fail to become dormant (423).

Symptoms resembling those of peach rosette were seen in seedlings of sour

cherry trees growing near infected peach (660). Affected sand cherry trees

develop a witches'-broom growth on the young shoots, and the leaves are

smaller and lighter green than those on healthy plants, but the trees are not

killed (423). In Georgia, when scions of an eastern chokecherry tree were

grafted to a diseased peach tree, they developed marked symptoms of peach

rosette, but similar scions of Bing and Black Tartarian sweet cherry. Montmorency sour cherry. Prunus serótina, P. mahaleb, and P. capulí, did not develop

symptoms (author's unpublished data).

Red maple trees, naturally infected by PRV, were found in Georgia (560).

The trees had developed shortened internodes, resulting in dense, rosetted

foliage. On periwinkle, PRV causes rosetting similar to that on peach. The

virus causes wilting and death of rapidly growing tomato and tobacco plants

(590).

Peach rosette virus has not been purified. The virus in budsticks was inactivated by hot water treatment, for 8 to 10 minutes at 50° C. (587) and in bark

patches for 18 minutes at 50° C. (539). The virus is known to move downward more rapidly than upward in diseased plants and will not pass a bark

ring (538). Neither peach yellows virus (586) nor phony virus protects peach

trees from infection by PRV, and no synergism between these viruses has

been observed. During host range studies, it was shown that apparently there

are three forms of PRV: one that causes overt symptoms in Marianna plum,

a second that infects Marianna plum without causing symptoms, and a third

that will not infect Marianna plum (author's unpublished data). The virus

apparently was inactivated in some peach seedlings by immersing the roots for

4 hours in 5 to 25 ppm of several tetracycline compounds (357). Similar

treatments with other antibiotics were not successful.

Transmission

Natural spread of PRV from wild plums to commercial plums and peaches

is well known although no vector has been identified (423). Attempted transmissions with sap and insects were unsuccessful (424). The virus can be

transmitted through tissue grafts from diseased to healthy peach or plum (613).

A bud-contact period of 8 to 14 days is necessary for transmission of PRV

from peach to peach (588). A single bark patch graft (3 cm. sq.) from diseased

plum or peach resulted in 80 percent transmission to 1-year-old peach seedlings

but seven patches the same size were needed to give 20 percent transmission

to 3-year-old peach trees. The virus was transmitted through dodder (Cuscuta

campestres) to periwinkle, tomato, and tobacco (590). The minimum incubation period of PRV in Burbank plum, approach grafted to diseased peach,

was 3 weeks but for transmission between diseased red maple trees and healthy

Methley plum (560), was 3 years.
76 VIRUS DISEASES OF STONE FRUIT

Control Measures

Eradication of infected orchard trees and wild Prunus growing near orchards,

as soon as symptoms are observed, has proved effective. If diseased trees are

allowed to remain in the orchard, peach rosette has been observed to reach

epidemic proportions, affecting whole orchards, in 3 to 5 years. Even under

these conditions, natural spread can be reduced to a few trees within 1 to 2

years by prompt diseased-tree removal in the spring (423).

Remarks

The presence of large populations of native Prunus hosts, particularly P.

cuigustifolia, which act as reservoirs of virus for spread to peach and plum,

continue to make the disease a threat to industry. Occasionally, winter-killing

of peach and cupping of leaves due to aphids on wild plums have been mistaken

for peach rosette. Zinc deficiency in peach is sometimes called rosette although

the symptoms do not resemble closely those caused by PRV.

Because PRV seems to be inactivated by certain antibiotics {357), peach

rosette possibly may be caused by one of the mycoplasmlike organisms and

not by a virus. This opinion has significance because peach rosette is one of

the yellows-type diseases that is not mechanically transmitted in expressed juice,

is inactivated during hot-water treatment, spreads rapidly in the field, and is

readily transmitted through dodder. However, it is not known to be transmitted

by leafhoppers. Until more information is known on the subject of mycoplasms

in plants, peach rosette will continue to be classified as a virus disease.
PEACH STEM PITTING

SRECKO M. MIRCETICH and H. W. FOGLE

Causal Virus

Peach stem pitting virus (PSPV).

History and Distribution

In i960, Christ (140) reported a new peach disorder in New Jersey and

attributed it to scion-stock incompatibihty, although the disorder later was

identified as peach stem pitting (470). In 1966, Barrât (23) reported the

occurrence of an obscure disorder characterized by wood pitting in young

orchard and nursery peach trees. The authors (unpublished data) have transmitted peach stem pitting from diseased to healthy peach trees in the greenhouse

and nursery by means of bud- and root-patch grafts.

Pitting of stems of Prunus spp. other than peach has been reported from

British Columbia (419), Maryland (469, 470), Pennsylvania (631), and

Oregon (113). The syndrome, as it occurs in British Columbia, is described

under ''Xylem aberration" (412).

Field surveys in 1967 and 1968 established the presence of stem pitting in

peach in New Jersey (140), West Virginia, Pennsylvania, Maryland, Virginia

(24, 396, 470), Ohio (334), Delaware (M. Sasser, personal communication).

North Carolina (C. N. Clayton, personal communication), South Carolina

(192), Michigan (A. L. Jones, personal communication), and California (J. H.

Weinberger, personal communication).

Economic Hosts

Peach stem pitting has been observed in 26 commercially important peach

cultivars and in peach seedlings (24, 140, 192, 396, 470). The same disease

was observed in naturally infected nectarine trees (470).

Symptoms

Peach trees affected by PSPV have the general appearance of being girdled

(fig. 30). The terminal growth is brachytic. Leaves droop, curl upwards lengthwise, and may be chlorotic. In late summer, leaves may become increasingly

chlorotic, often turning red or purple in the fall. Intensity of leaf color may

vary with the stage of disease, cultivar and climatic conditions during the

growing season. Unfolding of leaf buds in the early spring is delayed, but

leaf abscission in the fall occurs earlier than on comparable unaffected trees.

Fruits on affected trees may have insipid flavor, fail to size properly, be more

highly blushed than normal, and ripen and drop prematurely.

Marked enlargement of the trunk occurs at ground level or below. Occasionally, trunk enlargement in younger trees does not extend beyond the root

transition zone. This enlargement usually is noticeable as soon as foliar symptoms are recognized and becomes more marked as the disease progresses. The

77
78 VIRUS DISEASES OF STONE FRUIT

FIGURE 30.—^Peach stem pitting. A, Four-year-old peach seedling showing typical

drooping leaves with upward rolled margins; B, comparable healthy peach seedling.

enlarged portion has very thick, spongy bark that is often two to four times

the thickness of bark in a comparable unaffected tree (fig. 31, A, B). The

thick bark is usually detected at or below ground level. Removal of the bark

from the affected lower trunk reveals pits and grooves accompanied occasionally

by enations and necrotic areas within the cambium (fig. 31, C). Corresponding

ridges of inner bark are usually imbedded in the wood. Considerable variation

in symptom expression, particularly in the extent of pitting, enation, and

cambial necrosis, is found between cultivars—for example, Redhaven and

Redskin develop severe pitting, enations of assorted sizes, and necrosis of the

vascular cambium in the enlarged trunk areas (figs. 32, 33), whereas Elberta

develops short and very shallow pits in the wood. Only two cultivars, not

yet positively identified, among 26 surveyed developed neither pitting not

disoriented woody tissue, even though the rootstock was severely affected (fig.

32, C). However, these two cultivars showed foliar symptoms. It has not been

determined that these cultivars are symptomless carriers.
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 79

The wood pitting appears first below the ground level, then gradually spreads

into the roots and short distances into the aboveground trunk. The tissue within

the woody q^linder of the affected lower trunk may be highly disorganized

and may have wide xylem rays and inclusions of large phloem islands (fig. 33).

Lignification of the xylem cells appears to be incomplete, resulting in a weak

woody cylinder. Trees with a high proportion of such weakened tissue break

easily at ground level, exposing highly disorganized tissue in the woody

cylinder (fig. 34). The tendency to break is directly related to a high proportion

of disorganized woody tissue. The trees which are prone to break show fewer

normal annual growth rings than disorganized ones in the woody cylinder.

These trees are usually very stunted and have poorly developed root systems.

Affected peach trees that have developed a large number of normal annual

growth rings followed by a few disorganized ones (fig. 34, B), have excellent
80 VIRUS DISEASES OF STONE FRUIT

FIGURE 31.—Trunk symptoms in peach infected by peach stem pitting virus: A, Diseased

trunk—note thick bark (tb) and initial stage of wood pitting (p) extending to the ground

level (gl); B, healthy trunk—note normal bark (nb) and smooth woody cylinder;

C, pitting in woody cylinder accompanied by necrosis of vascular cambium (nvc).
HANDBOOK NO. 437, U. S. DEPARTMENT OP AGRICULTURE gl

¡^»^l 'n!k\
82 VIRUS DISEASES OF STONE FRUIT

FIGURE 32.—^Tmnk portions of 3 peach cultivais affected by peach stem pitting, showing

variation in symptom expression: A, Seven-year-old Redhaven tree with severe wood

pitting and enation; B, 20-year-old Elberta tree on undetermined rootstock—note mild

pitting on the scion (S) and distinct line of the union (U) formed by differential

pitting of the scion and rootstock (RS); C, 3-year-old tree of an unidentified cultivar—

note the scion portion (S) is free of pitting, whereas the rootstock (RS) is severely

pitted.

anchorage. Lateral roots are usually pitted when they develop from an affected

trunk (fig. 34, C). These roots may separate easily from the trunk, creating

a socketlike depression. Feeder roots of affected trees are usually decayed. The

severity of feeder root necrosis is determined by the stage of the disease. Foliar

and lower trunk symptoms in naturally infected nectarine trees are similar to

those in naturally infected peach trees.

Transmission

PSPV has been transmitted from infected peach to peach seedlings through

tissue grafts and field soil (authors' unpublished data). Elberta and Sunhigh

seedlings, inoculated by chip buds and root patches from naturally affected

peach trees, developed stem pitting in the greenhouse within 18 months and
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE §3

in the nursery within 11 months. Natural spread was observed in a densely

planted, 5- by 15-foot peach seedling orchard. Typical spread occurred within

the row from infected trees to adjacent trees 5 feet away. The number of

infected trees doubled within 1 year. However, the mode of spread and possible

vectors are not known.
84 VIRUS DISEASES OF STONE FRUIT

FIGURE 33.—Longitudinal section through lower trunk of 7-year-old Redskin tree severely

afferted by peach stem pitting. Note wood enations of various sizes and large phloem

inclusions within disorganized woody cylinder.

Control Measures

Infected trees should be removed promptly, and only budwood and seed

from healthy trees should be used for propagation. Good cultural practices

may be helpful in combating this disease. Because a disease similar to peach

stem pitting is found in many Prunus spp., eradication of wild Pmnus in the

vicinity of commercial orchards is advisable.

Remarks

Severe incidence of this disease in certain commercial peach and nectarine

orchards in southern Pennsylvania, Maryland, and West Virginia indicates

that stem pitting may become a limiting factor for peach production in these

areas. In some surveyed orchards, planted in 1966 and 1967, 12 to 25 percent

of the trees were affected by the disease. In several plantings of 4- to 13-year-old

trees, over 75 percent of the trees showed typical symptoms of the disease.

Affected peach trees become commercially worthless. Younger trees may die

within 2 or 3 years, but older trees may continue to produce fruit of inferior

quality for some time. Recovery of affected trees has not been observed.
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 85

FIGURE 34.—A, Seven-year-old Redskin peach tree, in an advanced stage of peach stem

pitting, broken off at enlarged area of affected lower trunk. Note highly disorganized

woody tissue throughout the trunk. B, Cross section through affected trunk of 7-yenold Redhaven peach tree. Note that only outer annual growth rings have disorganized

xylem tissue. C, Root of peach tree affected by peach stem pitting. Note thick bark,

pitted woody cylinder and outer annual growth rings composed of disorganized

xylem tissue.
86 VIRUS DISEASES OF STONE FRUIT

See legend on p. 85.
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE g7

A disorder resembling peach stem pitting has been observed in a number

of Prunus species other than peach. The following Prunus spp. and interspecific

hybrids are known to be affected by various forms of wood pitting in nature:

sour cherry seedlings and Montmorency and North Star {419, 469) \ sweet cherry

seedlings and Windsor (R. F. Stouiïer, personal communication) and Bing

{419) ; Shiro-fugen flowering cherry {651) \ mahaleb cherry {469) \ European

plum Stanley, Late Smith and NY H-2 selection {469), Bradshaw {651), and

Italian Prune {115)\ Japanese plum, Abundance, Santa Rosa {651) and

Burmosa {469) ; apricot, open-pollinated seedlings of several cultivars {419,

469) \ cherry plum-sloe plum hybrid seedlings {469) \ Chinese wild peach,

open-poUinated seedlings {469) \ hybrid Japanese plum, Redglow {469),

Shiro, and Wickson {651). In some naturally infected European plum trees

on myrobalan plum, the rootstock portion was without any pitting, whereas

the scion was severely affected {469).
PEACH WART

EARLE C. BLODGETT

Causal Virus

Peach wart virus (PWV).

Synonyms

This disease was first called blister (46) but usually it is known as wart

or peach wart.

History and Distribution

In 1939, Blodgett (46) described a peach disease present in Idaho that

was first recognized in 1938. In 1951 (70), it was recorded in Idaho, Oregon,

and Washington. Since then it has been reported in California (633) and

New Mexico (139). It has not been noted in any other country. Wartlike

symptoms have been observed on specimens of peach fruits from many areas

of the United States, but these probably were due to effects of environment,

insects, or other factors.

Economic Hosts

Peach (Prunus pérsica).

Other Hosts

The virus may be transmitted by bud inoculation to sweet cherry cultivars

Black Republican, Royal Ann (Napoleon), and Lambert (769). Fridlund

(220) tested a wide range of possible indicators including Bing, Lambert, and

Sam sweet cherry; Kwanzan and Shiro-fugen flowering cherry; Montmorency

sour cherry; Tilton apricot; and Shiro plum; plus 64 cultivars and selections

of peach and nectarine. All were infected by PWV.

In a later paper, Lazar and Fridlund (393) gave evidence that Shiro plum,

when inoculated with PWV, exhibited characteristic and abundant leaf symptoms

after 4 weeks when grown under temperature-controlled greenhouse conditions.

Fridlund (personal communication) stated that seedlings of Manchu cherry

(P. tomentosa), when used in the greenhouse, are also regarded as good

indicators for PWV.

Symptoms

The first symptoms in peach trees appear on the very young fruits, shortly

after the calyxes have fallen, as bleached bumps or raised welts on or near the

stylar end and often involve half or more of the fruit (31, 334). The fruits

are both dwarfed and misshapen if the disease is severe, but slightly affected

fruits are nearly normal in size. The surface of affected tissue varies from light

tan to dull red and may be rough with warty outgrowths conspicuously raised,

or it may be rather smooth (fig. 35). The fruits of some cultivars less severely

affected exhibit a cracked and russeted appearance. Gum is usually present and

88
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE gQ

may be abundant. The warty tissue is rather superficial, but the underlying

tissue is coarse and filled with gum pockets. In some cases, the warty tissue

is very hard and bonelike, but usually it is tough and leathery. Frequently,

the warts occur in ringlike patterns near the stylar end.

In the study of peach wart, certain variations were found and described

by such names as "smooth wart," ""crease wart," and "'beady wart." In tests

by Blodgett, it appeared that smooth wart was transmissible as such, that crease

wart was not caused by a virus but was associated largely with certain cultivars

(Rio Oso Gem in particular), and that beady wart was probably caused by

insects. Typically, there are no leaf symptoms and infected trees show no

reduction in size, vigor, or production.

Black Republican, Napoleon, and Lambert sweet cherries, when infected

experimentally, show leaf mottling in variable degrees, a tendency to dwarfness,

and dieback. Other Prunus spp. and cultivars (see "Other Hosts") tested

by Fridlund {220^ showed that Hing and Sam sweet cherry, Tilton apricot,

and Shiro plum produced mild symptoms, whereas Lambert sweet cherry,

Kwanzan and Shiro-fugen flowering cherry, and Montmorency sour cherry

did not, although all were carrying the virus. The 64 peach and nectarine

cultivars were rated according to symptoms and placed into six groups ranging

from no symptoms to very severe. None of the four nectarine cultivars showed

fruit symptoms, and none of the 64 cultivars in the test showed foliage

symptoms. Fridlund reported that clingstone peaches showed only mild fruit

symptoms.

FIGURE 35.—Peach fruits affected by peach watt, showing warty outgrowths on

immature fruit.
90 VIRUS DISEASES OF STONE FRUIT

Transmission

Peach wart virus may be transmitted by conventional budding, branch

approach grafting, and by "budding" 1-year-old nursery tree trunks with

wedge-shaped pieces of infected fruit tissue (36). Inoculation in the fall

may produce fruit symptoms the next spring.

In tests by Fridlund (222), PWV was transmitted from infected inoculum

buds to peach within 90 to 110 hours contact at 26° C. This time interval was

in his rate II group which, besides wart, included cherry mottle leaf, cherry

twisted leaf, apricot ring pox, green ring mottle, and Napoleon latent viruses.

A limited number of tests indicates that the virus is not seed transmitted

(6ß, 219) and no natural vector is known. However, healthy trees may become

diseased naturally in orchards (E. C. Blodgett, unpublished data).

Normally, to obtain proper index readings, fruit must be observed on the

peach indicator. Lazar and Fridlund (595) determined that Shiro plum is a

useful indicator for this virus, and, through its use, the testing time can be

greatly reduced. Fridlund (personal communication) regarded seedlings of

Prunus tomentosa as good indicators.

Control Measures

Diseased trees should be removed as soon as identified, and budwood for

propagation should be taken only from known healthy trees.

Remarks

Peach wart is rare, but the potential threat of spread is ever present. Fruit

from infected trees is of no value.
PEACH YELLOWS

T. S. PINE and R. M. GILMER

Causal Virus

Peach yellows virus (PYV).

Synonyms

Little peach and probably red suture (p. 133).

History and Distribution

Yellows first appeared as an unknown malady of peach trees on the farm of

Judge Richard Peters near Philadelphia in 1791 (^^3). The disease was

described in some detail by William Prince in 1828 {342). The history and

distribution, and much of the early research on peach yellows, was reported by

E. F. Smith during 1888-94 {612, 614, 616). Although severe outbreaks of

the disease occurred during the 19th and early 20th centuries, it has been of

minor importance in recent years {457). Peach yellows has been found in the

Atlantic Coastal States and the Appalachian States, from Massachusetts to the

Carolinas, and in Ontario, Canada, and southward through Michigan, Illinois,

Indiana, Kentucky, and Tennessee. It has never become established west of the

Mississippi River or in the South.

The little peach disease, described first by Taft in 1896 {641)/is encountered

more often today than peach yellows. It is found in approximately the same

area as peach yellows and on the same hosts {109, 117).

Economic Hosts

All cultivars of peach and nectarine, apricot, and almond.

Other Hosts

All Prmîus spp. that have been tested were found susceptible to infection,

including: American plum, David peach, myrobalan plum, European plum,

dwarf flowering almond, hortulan plum, Japanese apricot, wildgoose plum,

Japanese plum, and Manchu cherry. The plum cultivars Abundance, Chalco,

and Chabot (P. sal/dna), and myrobalan rootstocks are symptomless carriers

of the little peach strain {433).

Symptoms

Peach yellows.—In early spring, the leaf buds of an affected tree unfold

prematurely, and many normally latent buds fail to remain dormant. Leaves

produced from these buds are dwarfed and yellow. The tree rapidly develops

many slender, branched, willowy shoots that grow upright from the main limbs,

thus giving the tree a bushy appearance (fig. 36). Leaves on the abnormal shoots

are narrow, chlorotic, and develop red spots; they roll inward and tend to droop

downward. Terminal dieback of twigs and branches is common in advanced

stages of the disease. Severely affected trees die 2 to 3 years after the onset of

91
92 VIRUS DISEASES OF STONE FRUIT

symptoms, but those with mild infections may live 6 years or longer. Inoculated

greenhouse trees develop vein-clearing in the tip leaves, and the leaves tend to

droop or become sickle shaped. Such trees usually die 1 to 2 years after infection

Fruit produced on trees infected by PYV matures several days to 3 weeks

before healthy fruit and may be larger than normal (fig. 37). The fruit is of

poor quality, usually with a bitter taste (43). In cultivars that normally develop

FIGURE 36.—Peach tree affected by severe peach yellows, showing dense type of growth

and small leaves.
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 93

FIGURE 37.—Peach yellows. A, Normal immature fruits; B, comparable fruits aflFected

by peach yellows, showing early ripening.

red coloring in the skin and around the pit, the skin is abnormally highly

colored, spotted with red and purple, and the flesh is streaked or marbled

crimson with a pronounced red coloring around the pit (392).

PYV causes symptoms in apricot, almond, American plum, hortulan plum,

David peach, almond cherry, and Manchu cherry that are the same as those

produced in peach. In Abundance plum, German prune, wildgoose plum, and

Japanese apricot the symptoms are the same but milder than those in peach.

Some cultivars of plums and plum hybrids are symptomless carriers of the virus.

Little peach.—Infected peach trees have distinctly greener foliage than

healthy trees during the early part of the growing season and appear more

compact than normal. Proliferation of leaves on short lateral branches or spurs,

produced on 2- and 3-year-old wood, leads to a bushy appearance. The

branches are more upright than on healthy trees but are not as long and willowy

as those on trees with peach yellows. Leaves on affected trees are noticeably

leathery in texture and tend to droop or roll downward; they become progressively chlorotic as the growing season advances but do not develop the red

spotting common on trees with peach yellows. Symptoms are usually evident

first on a single branch or portion of a tree but spread to the whole tree within

2 or 3 years. Fruit produced on affected trees matures several days to 3 weeks

after healthy fruit and is reduced in size. The pits are small and the kernels

are either underdeveloped or fail to germinate. The fruit generally has an

insipid flavor. Symptoms on susceptible plum and apricot cultivars are similar

to those on peach but usually are milder.
94 VIRUS DISEASES OF STONE FRUIT

Designation of little peach virus as a strain of PYV is based on crossprotection; peach trees infected with little peach are immune from infection by

PYV, and trees with peach yellows are immune from infection by the little

peach strain (386, 387). However, exceptions to this pattern have been

recorded, in which the fruit on one branch of a diseased tree matured earlier

(peach yellows), whereas fruit on another branch matured later (little peach)

than fruit on healthy trees (43). When healthy bearing trees are inoculated

simultaneously near the growing points with one bud infected with PYV and

the other with the little peach strain, the yellows symptoms appear first but the

little peach symptoms eventually become dominant (435). When peach seedlings are simultaneously inoculated vertically in sequence with buds from both

sources, the bud placed in the top position determines the disease syndrome

(388).

Peach yellows virus, including the little peach strain, is inactivated by treatment with hot water—dormant trees by immersion for 10 minutes at 50° C.

and buds by immersion for 3 to 4 minutes at 50° (387). Because the virus

has not been purified, nothing more is known about its physical or morphological

characteristics.

Transmission

PYV and the little peach strain are transmitted through tissue grafts or by the

plum leafhopper (Macropsis trmaculata Fitch) (384, 388, 434, 614); they

have not been transmitted mechanically in expressed juice, are not pollen transmitted, and are not seedborne (612). The incubation period of the diseases in

field trees is usually 1 to 3 years but is less than 60 days in greenhouse plants

(388, 433). The virus moves downward more rapidly than upward in infected

trees (383). Hence, inoculations near the top of a tree cause symptoms to

appear much earlier than infections occurring at or near the ground level. The

incubation period of the virus in the leafhopper vector varies from 7 to 26 days,

with an average of 16 days (282, 283). Because plums are the preferred host

of the plum leafhopper, and because some plum cultivars are symptomless carriers of PYV, it has been assumed that natural spread of these diseases is largely

due to transfer of the virus from plum to peach in the vector (436).

Control Measures

Diseased trees should be removed as soon as they are discovered. Because

some plums and plum hybrids are either symptomless carriers of the virus or

develop only mild symptoms, they should not be planted near peach orchards.

Control of the plum leafhopper is essential.

Remarks

Although peach yellows and little peach are not economically important

today, the cyclic nature of these diseases in a large peach-growing region suggests that growers and agricultural technicians should be continually aware of

their presence and prepared to take appropriate action should the disease

incidence increase or the vector become prevalent.
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 95

Designation of peach yellows and little peach as virus diseases is based on

the best evidence gathered by the workers who originally described them. These

investigators concluded that a virus was the causal agent because no other

pathogenic entity could be implicated and because transmission could be obtained

only through tissue union or by means of an insect vector. Réévaluation of the

whole group of "virus yellows" diseases, exemplified by the aster yellows disease,

suggests that peach yellows may result from infection by one of the pleuropneumonialike organisms (331, 608). However, until more evidence is available on this subject, peach yellows and little peach will continue to be classified

as virus diseases.
PHONY

L. C. COCHRAN and LEE M. HUTCHINS

Causal Virus

Phony virus (PV).

Synonyms

In Georgia, the name "phony peach" was sometimes used by growers.

History and Geographic Distribution

Phony was first observed in two peach trees at Marshallville, Ga., about 1885

by Samuel Rumph, who discovered and introduced the Elberta peach. The

dwarfed specimens were called "phony trees" by Rumph and were regarded as

a curiosity. Their number increased, and, by 1915, thousands of peach trees

were affected in a limited district in central Georgia. Illustrated papers calling

attention to and describing the disease appeared in 1920 (482) and 1928 (318).

Research into the cause of phony was begun in 1921 by the Bureau of Plant

Industry, USDA. A fairly exhaustive, well-illustrated account of the research

and other information was published in 1933 (323). Additional information

may be found in other publications of that period (320, 321).

In 1928, phony was conclusively shown to be caused by a virus (319). At

that time the disease had spread over a large part of central Georgia and a

smaller area in eastern Alabama. A Federal quarantine was promulgated in

1929 which restricted the movement of peach and nectarine nursery stock and

peach roots from affected districts. Also, in 1929, a Federal-State cooperative

program for systematic survey and removal of phony-diseased peach trees was

inaugurated. By 1932, about 35 million orchard peach trees had been inspected.

The disease was found in all the South Atlantic States below Virginia, in all the

Gulf States, in Tennessee and Arkansas, and in a few locations in the southern

parts of Oklahoma, Missouri, and Illinois (672). Subsequent surveys added

isolated cases in Indiana, Kentucky, Maryland, and Pennsylvania. The disease

has now been eradicated from these last four States and from some other States

in the lightly affected area. The disease has not been positively identified elsewhere in this country or abroad.

Economic Hosts

All cultivars, races, and hybrids of peach (Prunus pérsica), including peach

trees propagated on rootstocks of other species, such as almond, apricot, Japanese

apricot, David peach, and hortulan plum.

Other Hosts

Seedlings of apricot, Japanese apricot, chickasaw plum, and Mexican plum.

Trees of all the abovenamed species on their own roots are also susceptible to

experimental infection through root grafts with root pieces from phony-diseased

96
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 97

peach trees. Peach is generally used as the test plant for verifying the presence

of phony virus in the other species.

Symptoms

The symptoms of phony are most striking when the trees are in full foliage

and in good vigor. Affected trees develop shortened internodes, profuse lateral

branches and flattened dark-green leaves, producing a compact appearance of

dense, luxuriant foliage. Decided dwarfing of new growth results and the

periphery of the upper crown tends to take on a uniform, rounded appearance

(fig. 38). Phony trees may live many years. However, after several years the

wood becomes brittle, and there may be notable dying back of the terminal twigs

and branches. Vigorous, new terminal growth cannot be forced. As large limbs

die or are broken down, they are not replaced and the tree takes on a ragged

appearance. Even on such trees, the foliage continues to be greener and flatter,

characteristic of the disease. In spring, phony trees flower and leaf cut earlier

than normal ones of the same cultivar, and they hold their foliage later in

the fall (fig. 39).

The fruits on phony trees are well formed and ripen a few days earlier than

healthy fruits, but they are reduced both in size and in number per tree (fig. 40).

They may be somewhat poorer m flavor than normal fruits, but they are generally more highly colored. Seeds from phony peaches average smaller than

normal seeds, but they give excellent germination and produce normal seedlings.

Infection by PV does not induce spindling growth or rosetting; does not cause

yellowing, rolling, or spotting of leaves; and does not induce lesions, galls, or

hypertrophies.

Identification of the disease in the afifected tree is made from the aspects of the

tree as a whole and should not be attempted from detached specimens. Phony

trees are most easily identified in cultivated orchards, where comparison with

vigorous healthy trees of the same age and cultivar can be made. Identification

of the disease in wild seedlings and in orchards of mixed cultivars may be difiîcult unless the symptoms are very pronounced. Pruning, fertilizing, and cultivating, in keeping with good horticultural practice, will induce vigor and growth

that intensify symptoms and bring out strong contrasts between the diseased and

the healthy trees.

No truly symptomless carriers of PV have been found, but some species, such

as chickasaw plum, are much less strikingly affected than peach. Such species

are also less strikingly affected when growing under competitive conditions in

natural thickets than under good cultural conditions. Visual identification of the

disease in native thickets is unreliable and highly uncertain. The occurrence

of PV in chickasaw plum growing in thickets near the sites of old phony-affected

peach orchards is also high (163).

Phony virus can be inactivated in dormant peach nursery trees by immersing

the trees for 40 minutes in water maintained at 48° C. (330).

Chemical idenùficaùoii test.—A simple, rapid chemical test, easily applied
98 VIRUS DISEASES OF STONE FRUIT

FIGURE 38.—A, Six-year-old Elberta peach tree affected by phony, showing the dense

shadow cast by the heavy, appressed foliage; B, comparable healthy tree in the same

orchard.
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 99

FIGURE 39.—Four nursery peach trees of same age: A and D, Healthy trees; B and C,

trees afifected by phony as a result of root-graft inoculation, showing dwarfing and

retention of foliage.

in the laboratory or field, can be used for confirming identification of the phony

disease of peach (323). The test reagent is prepared by acidulating 100 cc. of

absolute methyl alcohol with 15 to 20 drops of concentrated, chemically pure

hydrochloric acid.

For the test, select unblemished, whole-root sections 4 to 6 inches long, with

a woody cylinder I/2 to % of an inch in diameter remote from malformations or

injuries. Remove the bark and cut entire transverse sections of the woody

cylinder 0.5 to 1.0 mm. thick. Immerse these in 5 cc. of the reagent in a

shallow container. Before the test, the wood should be fresh, nearly white, and

in good condition. If numerous, well-distributed purplish spots up to 2 mm. in

diameter appear against a background of whitish or faintly purple wood after

a few minutes in the reagent, a positive test for phony is indicated (fig. 41).

Parallel tests should be run on roots of known healthy trees for comparison. If

acidulation is too strong or if the sections are allowed to remain too long in

the reagent, the entire surface of the sections (either healthy or phony) may be

purple.

In well-developed cases of phony, each suitable root will give a good positive

test throughout the year. In old cases of the disease, easily visible brown flecks

may occur in the wood sections. These will usually turn purple in the reagent,

and numerous additional purple spots will develop during the test. Only the

wood gives the test; the bark shows no reaction. In some cases, phony stem
100 VIRUS DISEASES OP STONE FRUIT

FIGURE 40.—A, Qsmmercial pack of best-grade Hiley peaches from a healthy tree; B, sim

ilar pack of fruits from a tree affected by phony, showing smaller size of fruit.

wood may show a positive reaction to the test, but it is much less satisfactory

than rootwood.

Prunus species other than peach give a somewhat variable reaction. Therefore, the chemical test is not considered definitive in tíiem.

Transmission

The phony disease is easily transmitted when roots of a diseased tree are

grafted onto roots of a healthy tree. If large root pieces are used as inoculum,

the incubation period may be only a few months, whereas with small pieces, 3

to 6 inches in length, symptom production requires 18 months or longer.

Transmission also can be effected by grafting diseased scions or root pieces into

the tops of trees. It is imperative that the inoculum contain infected wood along

with bark and that this wood be kept alive until a wood union has formed

between the inoculum and the inoculated tree.

Heel-spur scions (a bark shield subtending a short spur in place of a bud)
HANDBOOK NO. 437, U. S. DEPARTMENT OP AGRICULTURE IQl

were used effectively for transmitting phony from tops to tops (^328). The

freshly cut heel-spur bark shields are inserted in a T-cut in the same manner

as with budding. The shield placed directly against the cambium makes a

quick union which keeps the virus-infected wood in the spur alive until a new

union is formed. Straight scions cut to a long bevel inserted into a T-cut can

also be used but were less effective than the heel-spur type. The woody cylinder

of scions whipgrafted onto trees usually dies before a wood union is completed

even though the bark cylinder lives and the scion grows into a shoot. Such

scions were ineffective in transmitting phony.

When trees are inoculated in the roots, PV becomes distributed throughout

the root system, and the inoculated trees become characteristically phony, but

the virus does not move into the tops (328). If an infected scion is grafted

onto seedling roots at the ground level and develops into a new top, the virus

is carried along in new growth and becomes distributed throughout the top

from which it can be transmitted at will. If one arm of a growing tree is

infected through inoculation, PV moves rapidly to the roots. It may also be

carried to tissues of the inoculated tree immediately adjacent to the inoculation

point, but it will not become generally distributed to other parts of the tops.

PV is not generally well distributed in the tops of naturally diseased trees.

This fact indicates that insect vectors may feed on lower branches from which

the virus is translocated to roots. Roots contain approximately 20 times the

amount of living wood as tops (198). This larger amount of living wood

supports a greater amount of virus and, because the wood is interconnected, it

facilitates virus distribution. Living wood in trunks and branches exists mostly

as islands in medullary rays. PV is generally better distributed in the tops of

plum trees than in peaches.

No strains of PV have been demonstrated. However, six species of Cicadellidae have been reported as vectors of PV under experimental conditions (673,

674, 675). These are Draeculacephala sp., Homalodisca triquetra (F.), H.

FIGURE 4L—Chemical identification of phony in transverse sections of woody cylinder

of peach root: Left, before test; right, after test, showing color reaction.
102 VIRUS DISEASES OF STONE FRUIT

insólita (Walker), Oncometo-piä undata (F.)> Graphocephala versuta (Say),

and Cuerna costalis (F.). All are members of the subfamily Tettigellinae.

All are large, long-lived species, which overwinter as adults. Once they

acquire the virus, they can transmit it any time during the remainder of their

lives. On peach, they feed principally on the woody cylinder of 1- to 2-year-old

twigs and small branches. It is assumed that they place the virus directly into the

wood, but it is not known how the virus gets to the roots.

Control Measures

The phony disease reached a peak in the mid-1940's, and its incidence has

steadily declined since that time. Control is effected through a coordinated

program of roguing, general use of wide-spectrum insecticides, selection of

new orchard sites away from old, phony-affected orchards, and removal of wild

plums from the vicinity of orchard sites. The roguing program is carried on

jointly by the Agricultural Research Service, USDA, State regulatory officials,

and growers.

Remarks

Phony virus has unusual specific tissue relationships. Early work showed

that PV is largely limited to the roots of naturally infected trees; symptoms in

the tops are induced by effects of the virus on growth-controlling systems produced in the roots. Later work showed that the virus is restricted to the woody

cylinder {524) but could exist to a limited degree in the tops. If diseased trees

are developed from infected scions, PV is carried to all portions of such trees.

^'Tiere trees are infected by grafting diseased scions on branches, PV moves

rapidly downward, where it invades all portions of the roots. It also remains

in the inoculum scion and any growth from it. Sometimes it will invade other

branches near the inoculation point but does not invade other portions of the

tops of trees. If trees are infected by grafting diseased roots onto healthy roots,

PV will move throughout the root system but will not move into the tops of the

trees. General restriction to the roots is the result of restriction to living wood

and not the result of killing of the virus in tops exposed to high summer

temperatures.

Phony is first in importance among virus diseases of peach in Georgia and

some other Southern States. Over two million phony-diseased trees have been

removed by control agencies since 1929. Previously, an estimated million

orchard trees had been ruined by the disease and removed by growers in central

Georgia.

Phony does not cause early death of the affected trees, but it induces marked

dwarfing of new growth and of fruits, which results in a smaller crop of peaches,

most of which are undersized. The longer the tree has the disease, the more

pronounced this effect becomes. The bulk of the fruit from phony trees falls

in the smaller commercial grades or is graded out entirely. Trees that contract

the disease before bearing age never come into profitable bearing, and mature

trees that have had the disease several years produce no commercial crop of fruit.
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 103

The incidence of phony disease reached its peak in the 1940*s. At that time,

where the disease was prevalent and spread was rapid, it was not uncommon

for half the trees in an orchard to be phony by the fifth year in the orchard

and 99 percent at 10 to 12 years. During the last 15 years, with coordinated

control, the incidence of phony in well-cared for orchards has become negligible.

Local hot spots have developed in orchards in areas not receiving the standard

insect-control spray programs.
"PRUNUS" RING SPOT GROUP

GEORGE NYLAND, R. M. GILMER, and J. DUAIN MOORE

Causal Virus

Prunus ring spot virus (PRSV).

Synonyms and Relationship

Peach ring spot, peach necrotic leaf spot, necrotic ring spot, tatter leaf (in

part), lace leaf, cherry ring spot, and stone fruit ring spot are synonyms

of Prunus ring spot. Some of the isolates distinct enough {144) to be called

strains of PRSV are those that incite recurrent necrotic ring spot, necrotic ring

spot, cherry rugose mosaic, almond calico, and Stecklenberger disease. Typical

apple mosaic virus, rose mosaic virus, some virus isolates that incite plum line

pattern, and initial mosaic symptoms in hops show relatedness to PRSV; some

or all could be considered strains of PRSV. Each of these strains can be

recovered from naturally infected plants and identified. Variants that may be

designated as isolates or forms exist within each strain. Strains may be grouped

as serotypes {232). Serotype is a designation applied to virus groups that share

a minor proportion of common antigens {343). Thus, apple mosaic virus

(AMV) and rose mosaic virus (RMV) have a large proportion of common

antigens, and necrotic ring spot virus (NRSV) and Danish line pattern virus

(DLPV) have a large proportion of common antigens {232), but AMV and

RMV could be designated one serotype and NRSV and DLPV another serotype

of PRSV. The names for the diseases within the groups could be retained.

The final designation of particular isolates or groups of isolates of PRSV

associated with specific diseases as related strains or serotypes or as separate

but related viruses remains a matter to be settled in the future.

History and Distribution

PRSV occurs as many strains or forms that incite different diseases and is

the most commonly encountered virus in cultivated species of Prunus and some

other rosaceous plants. The virus was first named peach ring spot virus {156),

but earlier reports probably were also concerned with one or more strains {653,

679). PRSV was soon recognized to be a common contaminant of stone fruit

virus cultures {144), and transmission of it through seed was demonstrated

{123, 145, 147). One of the viruses first transmitted from sour cherry to

cucumber by sap {446, 473) was later identified as PRSV {227). Once the virus

was sap-transmitted some of its physical, chemical, and biological properties

were studied {228,231, 232, 233, 452).

PRSV and prune dwarf virus (PDV) both are spread by pollen from

plant to plant of sour cherry in the orchard {236). PRSV is carried in pollen

{196, 708, 725) and can infect seeds when infected pollen is applied to

emasculated flowers, even on healthy plants {666, 708). Seed and pollen trans104
HANDBOOK NO. 437, U.S. DEPARTMENT OF AGRICULTURE 105

mission and propagation of infected cultivars account for the worldwide

occurrence of PRSV. In spite of the general distribution and the means of

spread of PRSV, realistic nursery improvement programs have been exceptionally

successful in some areas in controlling the diseases incited by the many forms

of this virus. Spread is rapid in sour cherry in the Midwestern and Northeastern States, but relatively slow in sweet cherry, prune, and cling peach

in the Western States. Where natural spread is rapid, clean stock programs

must be combined with maximum isolation for control.

No arthropox vector of PRSV is known, nor has the place of origin of the

virus been established. PRSV has been isolated from native stands of pin cherry

in Wisconsin and from Prunus fasciculata in California, but native stands of

wild Prunus are not known to be generally infected in the United States or

Canada. Most evidence points to the Middle East or Western Asia as the

place of origin. Logically, there is where a search should be made for a vector.

The virus has many properties and characteristics of NEPO viruses which

have nematodes as vectors.

PRSV is a serious disease in the fruit-tree nursery causing poor bud and scion

"takes" and reducing growth of the trees {443, 449, 515, 318). It also reduces

growth and yield of trees in the orchard (378, 449, 508), but with some species

the effects may not be as great as with others (376, 537).

Economic Hosts

Almost all cultivated species and cultivars of Prunus that have been tested

are susceptible to one or more strains of PRSV (37, 152, 242, 475). Burbank

and Abundance plums were reported resistant to infection (474, 475) as was

P. cistena (242). However, later reports showed them to be susceptible to

some strains or isolates (761, 240). Symptoms induced by several strains in

some economic hosts are shown in figures 42 and 43.

Other Hosts

PRSV has a very wide host range among wild species of Prunus and

herbaceous plants (37, 152, 175, 225, 242). Some Prunus and herbaceous

hosts have been used successfully to separate certain viruses from a mixture with

PRSV (7, 225, 441).

Symptoms

Shock symptoms followed by chronic symptoms are produced after infection

in most hosts of the virus if they are not already infected with a latent isolate

or strain. Shock symptoms recur in some hosts intermittently in years subsequent

to infection and like chronic symptoms seem to be influenced by environmental

factors. The virus is extremely variable and exists as a multiplicity of forms

each slightly different in its effects on a standard host range. The differential

tolerance of host species and varieties, the variability of the virus, and the

effects of environment result in unlimited variations in symptoms encountered

in the field and in the test plot. General types of symptoms can be classified as

chlorosis, necrosis, leaf deformity, and stunting. Chlorosis occurs in patterns of
106 VIRUS DISEASES OF STONE FRUIT

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HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 107

rings, lines, bands, spot mottle, and mosaic. Buds, leaves, shoots, large branches,

and roots may become necrotic. Epinasty, twisting, rugosity, and enations are

leaf symptoms sometimes associated with infection. Entire plants may be

dwarfed or only portions of them may be stunted. Necrosis usually occurs only

during the initial acute stage. It may affect leaves, shoots, and shoot terminals

and may occur as small or large cankers on the limbs or trunks. In many hosts,

other conspicuous symptoms also become less obvious after the first year or two

of infection. In some hosts infected with certain strains of the virus (e.g.,

cherry rugose, almond calico, and recurrent ring spot), visual symptoms occur

annually and can be classed as chronic symptoms. In such cases, symptoms are

usually more severe a year or two following infection than they are later.

Symptoms on specific hosts will be discussed for each strain of the virus.

Necrotic ring spot strain (NRSs).—This strain can be classed as the ordinary

variety of ring spot and typically produces in its hosts shock or acute symptoms

followed by recovery and the absence of obvious visual symptoms. The extent

of recovery varies with the host, the isolate of the strain, and environmental

conditions. In peach trees, when infection occurs sometime during the previous

season, budbreak is retarded, many flower and leaf buds die when partially

open or before, and previous season's twigs are killed, or cankers form at the

nodes or extend vertically either below or above the point of infection on

branches that are not completely killed. Emerging leaves may show only a few

obscure rings or chlorotic areas or may develop severe necrosis or necrotic spotting of chlorotic areas (fig. 44). Leaves are often deformed as a result of

unilateral necrosis, and many leaves are cast when symptoms are severe (fig. 45).

Some forms of the strain kill small trees or trees up to 3 or 4 years old the year

following experimental inoculation or following natural infection in the

orchard (132).

As the season progresses, new growth of peach is essentially without symptoms,

except that in the nursery and orchard leaves of current season shoots that are

FIGURE 42.—Prunus ring spot. Symptoms incited by three strains of Prunus ring spot

virus (PRSV) on several Prunus hosts. A, Recurrent strain (RRSs) : upper left,

depressed rings on Montmorency cherry leaves; upper right, chlorotic spots and patterns

and mosaic on mahaleb cherry leaves; bottom, yellow Montmorency cherry leaves similar

to those with sour cherry yellows. B, Almond calico strain (AlCs) : Left, Calico, chlorotic patterns, and mosaic on mahaleb cherry leaves; center, calico on sweet cherry leaf;

right, chlorotic patterns and mosaic on Shiro plum. C-F, Cherry rugose mosaic strain

(CRMs) : C, Top row, sweet cherry leaves showing rugosity, lace leaf, and chlorotic

blotch; center row, left, two Montmorency cherry leaves with rugosity and ring spots;

right, three mahaleb cherry leaves with calico, mottle, and necrotic spots; bottom row,

yellow Montmorency cherry leaves similar to those with sour cherry yellows. D,

Chlorotic patterns in Shiro plum. E, Bare limbs and dieback in Napoleon cherry.

F, Closeup of Napoleon tree showing shoot development from latent buds, chlorotic

blotches in leaves, and leaf necrosis.
108 VIRUS DISEASES OP STONE FRUIT

FIGURE 43.—Prunus ring spot. A, Rose mosaic incited by inoculation with a pure culture

of recurrent ring spot strain (RRSs) of Prunus ring spot virus (PRSV) ; B, with a pure

culture of cherry rugose mosaic strain (CRMs); C, with a pure culture of necrotic

ring spot strain (NRSs). D, Mosaic on almond incited by CRMs. E, Mosaic on

Gravenstein apple incited by a strain of PRSV. F, Line pattern-type symptoms in

Shiro plum incited by an isolate of PRSV (spring mosaic, oak leaf patterns, and

vein netting).
HANDBOOK NO. 437, U. S. DEPARTMENT OP AGRICULTURE 109

growing rapidly may develop necrotic spotting as they emerge from the terminal

whorl (fig. 46). This phase of the disease, originally described as necrotic spot

(122), often follows short periods of excessively high temperature in the

Central Valley of California and is an important disease in the nursery {488,

692). Pure cultures of the other strains of the virus also 'ncite necrotic leaf

FIGURE 44.—A, Prunus ring spot afifected leaves of Lovell peach, showing tings, spots,

and chlorotic patterns. B, Affected leaves of July Elberta peach on which the symptoms

are predominantly chlorosis but on which rings and shot hole occasionally occur.
lio VIRUS DISEASES OF STONE FRUIT

spot as summer symptoms in peach (George Nyland, unpublished data). Leaf

casting and occasionally necrosis of cortical tissues of the young shoot or death

of the shoot tip reduce the growth of peach "June buds" and lower the grade of

infected trees.

In addition to necrotic leaf spot symptoms, mature peadi trees may show

other symptoms associated with necrotic ring spot infection. Color-breaking

of the blossoms of Rio Oso Gem and other unspecified cultivars of peach was

FIGURE 45.—^Elberta peach in midsummer after showing acute symptoms of Prunus

ring spot in the spring. Note bare twigs and thin foliage where buds died and

were shed.
HANDBOOK NO. 437, U. S. DEPARTMENT OP AGRICULTURE m

FIGURE 46.—^Young leaves of peach showing necrotic spots—the summet symptoms of

Prunus ting spot in peach.

attributed to ring spot virus in southern California {157). Up to 25 percent of

the blossoms on some trees showed symptoms, but no leaf symptoms were

seen. Blossom symptoms showed for 3 consecutive years that the trees were

observed. Other symptoms that are associated with necrotic ring spot in bearing

orchard peach trees are reduced vigor, death of lateral spurs and leaf buds on

older fruit-bearing hanging branches, rough bark of the trunk and main scaffold

branches, and reduced yield of fruit. Fruit yields of cling peaches may be

reduced as much as 5 tons per acre (H. A. Williams, personal communication).

All peach cultivars tested are susceptible to NRSs and show essentially a

similar range of symptoms, although the reactions to a particular isolate may

vary considerably. Freestone cultivars probably are damaged in an obvious way

more than clingstone cultivars. The tolerance of cultivars to individual isolates

varies: an isolate that may cause severe necrosis, splitting, and cracking of the

bark of Elberta may be relatively mild on Halford or on Lovell seedlings {152).

The NRSs in sweet and sour cherries is coextensive with these hosts. Most

trees in bearing orchards of cherries, which were established prior to clean stock

programs, are infected, and many show symptoms of some sort each year or

intermittently {291, 295). Although the NRSs is essentially symptomless in

some trees, careful inspection of trees in sweet and sour cherry orchards in late
112 VIRUS DISEASES OF STONE FRUIT

spring or early summer will detect some evidence of infection. In sour cherry,

scattered older leaves or entire spurs may show necrotic spotting or etched rings

early in the season. In sweet cherry, faint to prominent chlorotic rings or banded

chlorosis is evident, and often quite obvious symptoms of shot hole and lace

leaf are seen. It is not unusual to see one or more branches of a tree, known

to have been infected with PRSV for at least several years, develop tatter leaf

symptoms. Such trees observed in orchards in San Joaquin County, Calif., sometimes show symptoms of rugose mosaic on those same branches the following

year and subsequent years.

Symptoms in healthy cherry trees inoculated artificially with field cultures or

with pure cultures, of NRSs show symptoms characteristic of the isolate and the

host species. In Montmorency sour cherry, the initial effect of necrotic ring spot

is a pronounced delayed foliation of individual limbs or entire trees (37) (fig.

47 A, B, and C). Leaves on affected branches are reduced in size, and before

they unfold they may show light-green spots and dark rings, which vary in

size from 1 mm. or less up to 5 mm. in diameter and have a water-soaked

appearance (fig. ASB and C). Partial rings and sometimes concentric rings are

also present. The surface of affected leaves is roughened, and the margins tend

to be wavy (38). In the early stages, the ring symptoms are visible by reflected

light only. As the season advances, the affected areas may become necrotic, fall

out, and give a "shredded leaf" effect (fig. ASA). Symptom expression

usually is limited to the first leaves that unfold; leaves formed later generally

do not show symptoms (fig. A9A).

Sometimes, blossom symptoms also may be present on severely affected

branches of Montmorency. The pedicels may be shortened until they are

almost sessile, and the calyx and corolla may be twisted and distorted. Such

flowers usually do not set fruit. In subsequent years, branches that had shock

symptoms the previous year are essentially without symptoms, but infected trees

may be smaller and may have smaller leaves than healthy trees and show a

thinness of foliage as reported from Ontario (37), and confirmed in Oregon

and California by inoculation with pure cultures of the strain (J. A. Milbrath

and George Nyland, unpublished data). Details of symptoms may vary with

the isolate of the strain and with the clone of Montmorency.

The development of symptoms in sweet cherry and Stockton Morello is similar

to that in Montmorency in that most isolates of the strain produce initial

shock systems followed by recovery (fig. 50) to extreme necrosis involving buds,

shoot tips, and cortical tissues. Cankers that exude copious quantities of gum

may easily be confused with those incited by fungi or bacteria. Cankers usually

are produced in inoculated branches but not in other branches as the virus

spreads throughout the tree during the season of initial symptoms or in subsequent years. In some cases, leaf symptoms in subsequent years may be very mild;

in other cases, they may be as severe as initially. The lace leaf or tatter leaf

symptoms may be evident some years in one or more branches of trees known to
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE H^

FIGURE 47.—Prunus ring spot. A and B, Branches of Montmotenqf cherry showing

delayed foliarion, stunted leaves, and shortened blossom pedicels; C, comparable

healthy Montmorency branch. D and E, Italian Prune showing necrotic spotting and

shot hole; F, comparable healthy Italian Prune branch.
114 VIRUS DISEASES OF STONE FRUIT

FIGURE 48.—Montmorenqr cherry leaves with necrotic ring spot, showing A severe

necrotic shock and leaf shredding and B and C water-soaked rings and arcs.
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE US

jß^

FIGURE 49.—Prunus ring spot. A, Stockton Morello with shock symptoms of necrotic

ring spot on growth produced about 4 weeks after tree was removed from heattreatment chamber, followed by symptomless leaves. B, Chronic spring symptoms

of shot hole in Kwanzan cherry. C, Spur killing, an initial shock reaction in

Kwanzan cherry. D, Necrotic and chlorotic spots and rings in sweet cherry.
116 VIRUS DISEASES OF STONE FRUIT

have been infected with the NRSs for many years. Whether this is the resuU

of infection by another isolate or strain or by PDV or is an environmental effect

at the time symptoms are seen is not known. Trees known to have been infected

with the rugose mosaic strain for many years also have been observed with lace

leaf symptoms in certain other years. Most observers would agree with Helton

(29J) that annual fluctuations in symptoms in particular trees suggest environmental effects and that consistent variations among trees probably are due to

variations in the virus. NRSs may kill the shoot tip of infected nursery cherry

FIGURE 50.—Prunus ring spot. A, Leaves of mazzard cherry showing tings, shot hole,

and chlorotic and necrotic patterns. B, Nonpareil almond leaves showing chlorotic

rings and spots; unaffected leaves at left.
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 117

trees during the summer. This injury resembles insect damage with which it is

sometimes confused.

Almond reacts to infection with NRSs much the same as peach. Chlorotic or

necrotic rings, bands, and mottle are initial leaf symptoms (fig. 50ß), and the

amount of bud, stem, or bark necrosis varies with the isolate of the virus. Mild

mottle and mosaic in some leaves and occasionally recurrence of shock symptoms

in portions of the tree are seen in years subsequent to initial infection. Almond

may also show summer necrotic leaf spot similar to that on peach.

Other species of both cultivated and wild Vrtinus show symptoms of varying

severity. None has been found that is immune to all isolates of the strain. In

general, plums and prunes are affected less severely than peach or cherry in the

initial stage of infection and may show few or no symptoms in years subsequent

to initial infection. When symptoms are produced, they resemble those in peach

and cherry (J\g. 47, D-F). Prunus mahaleb and P. tomentosa develop good

symptoms that are diagnostic for some strains {202, 210). Symptoms in P.

mahaleb in the field may recur annually as chlorotic or necrotic rings, bands,

and oak-leaf patterns.

Recurrent ring spot strain (RRSsJ.—The very obvious chronic symptoms in

Montmorency associated with certain isolates of PRSV are consistently distinct

and probably justify strain status for these isolates. Fulton's virus A (227) is an

isolate of RRSs. The name "recurrent ring spot" implies that symptoms occur

on all the branches on a given tree of Montmorency year after year once the

virus becomes systemic. Almost all of the leaves formed in the spring and early

summer each year show symptoms in contrast with such leaves on a tree infected

with NRSs which would show only occasional symptoms in scattered leaves.

Initial symptoms are the same under similar conditions for necrotic and recurrent

ring spot. The severity will vary with the temperature at which the trees are

held and the isolate of the virus. If small potted ring-spot-free Montmorency

trees are inoculated at bud-break, 7 to 14 days later the first symptom consists

of a downward curvature of the growing shoots. This is followed within a few

days by a brownish, watersoaked spotting of leaves, usually evident first on the

lower surface. These spots become necrotic to form shotholes, or they may

coalesce and form large irregular necrotic areas that result in a tattered or lace

leaf effect. The typical dark-green to black watersoaked rings or areas usually

appear on later-formed leaves. The symptoms as described are essentially the

same up to this point for both necrotic and recurrent strains and occur on the

first three to five leaves to unfold. Field trees or potted trees infected the

previous season with either strain may show some additional symptoms as

described under necrotic ring spot. From here on the two strains react quite

differently in Montmorency. With necrotic ring spot, later leaves have few or

no symptoms as the "recovery stage' 'is reached. However, with recurrent ring

spot all or almost all later leaves may show the typical water soaked or etched

rings or have a pebbly, rough upper surface and smooth areas or scars on the
118 VIRUS DISEASES OF STONE FRUIT

lower surface (fig. 51; fig. 42, A). The specific symptoms may occur over most

of the leaf or in restricted areas of the leaf often either near the tip or base.

All symptoms except initial necrosis recur annually and with some strain-clone

combinations necrosis also may recur.

Other recurring symptoms seen in Montmorency trees infected with pure

cultures of RRSs are the presence of bract leaves that do not become yellow

uniformly as in healthy Montmorency trees but retain islands of green tissue.

These leaves are cast earlier than normal bract leaves. Trees which show bract

leaves of this type later develop yellow leaves that retain chlorophyll along

the main veins and resemble very closely leaves produced in Montmorency

trees that show symptoms of sour cherry yellows and rugose mosaic {486)

(fig. 42, A). One or more flushes of normal size, yellow leaves are produced

each spring in trees infected with recurrent ring spot about the same time that

other trees infected with PDV show symptoms of sour cherry yellows. The

total leaf fall on trees with recurrent ring spot is usually much less than that

on trees with sour cherry yellows.

Prunus to772entosa seedlings inoculated with RRSs show typical shock symptoms as with necrotic ring spot but also show chronic symptoms on both leaves

and fruit. The leaves may have calico bands and oak-leaf patterns, and the

fruits of some seedlings are deformed and necrotic internally when ripe.

Infected trees are stunted (George Nyland, unpublished data).

On peach, sweet cherry, and P. mahaleh, the symptoms of recurrent ring spot

are similar to those incited by the NRSs of PRSV, including the summer leaf

spot symptoms in peach.

Cherry rugose mosaic strain (CRMs).—This is designated a strain of PRSV

based on host reactions, cross-protection, and serological tests {A9^, 496).

CRMs can be isolated consistently from naturally and artificially infected trees,

from seed and from seedlings, and can be identified readily by symptoms produced in cherry and Gomphrena globosa (fig. 58, C). Certain isolates differ

from each other consistently and constitute mild and severe forms within the

strain {56, 486, 490) as is also the case with other strains of PRSV.

Initial shock symptoms of CRMs in a standard host range, free from other

strains of PRSV, are essentially the same as those incited by the NRSs and RRSs.

If inoculations are made in sweet cherry with CRMs during the summer or

fall, shock symptoms of ring spot are produced the following spring. If inoculations are made early in the summer, the portion of the tree near the inoculation site may produce only chronic symptoms the following spring as in the

case of an infection 2 years old or older. In sweet and sour cherry, acute shock

symptoms of ring spot are followed by rugose mosaic symptoms the same year

or the following year. The virus moves through mature trees not infected with

other strains of ring spot virus in 2 or 3 years but more slowly if infections

are mixed. The most obvious symptom occurs in the leaf blade and consists

primarily of chlorotic blotches that cause distortion of the leaves. Leaves so
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE HQ

FIGURE 51.—Prunus ring spot. Montmorency cherry infected with recurrent ring spot

strain (RRSs) of Prunus ring spot virus (PRSV) : A, Initial shock symptoms, showing

necrosis and the beginning of shot hole, B, recovery symptoms (depressed rings, arcs,

and etch) the same season as initial shock; C, chronic symptoms (depressed rings

and arcs evident by reflected light).
120 VIRUS DISEASES OP STONE FRUIT

affected often drop by late June or during July, but in some leaves the chlorotic

areas become necrotic and drop out, and the leaf remains on the tree. Trees

infected for several years with mild forms may show few leaves with symptoms

during most of the season. Most isolates produce enations on some leaves.

Enations may occur on any part of the abaxial surface of the leaf but are most

common immediately adjacent to the midrib near the base of the leaf. Leaves

on shoots that arise from latent buds on main scaffold limbs are most likely

to have enations (fig. 42, F).

Most isolates of CRMs incite yellow-to-white chlorotic speckling or mosaic

on scattered leaves of most seedlings and cultivars of sweet cherry. Trees of

sweet cherry with rugose mosaic usually bloom later and mature their fruit

later than healthy trees. Green, unripe fruits may be seen on scattered branches

when most of the unaffected fruits are fully ripe. Delay in ripening may vary

from a few days to several weeks. Affected fruits may be mildly to severely

deformed ; flattened or dimpled at the styler end, or lopsided or partially twisted.

Trees infected with severe forms of the strain slowly decline as a result of

dieback, death of lateral shoots and spurs, and lack of vigor. Symptoms incited

by the CRMs of PRSV are shown in figure 42, C-F; figure 43, B and D; and

figures 52, 53, and 54.

In peach, CRMs incites initial shock symptoms like those of necrotic ring

spot and also a rosette of some shoots produced from latent buds on the main

scaffold limbs. Trees usually recover from the initial severe symptoms but

continue to show some necrotic spotting of leaves in succeeding years in the

spring and in flushes of growth in summer as new leaves emerge from the

terminal whorl as is also the case with other strains of PRSV. Summer symptoms

in the Central Valley of California are most obvious a few days after a hot spell

of several days duration.

In almond, most isolates of CRMs incite severe leaf distortion; leaves with

yellow, white, or light-green mosaic or calico; and bud failure of lateral buds

of some shoots of most cultivars inoculated. Trees infected for several years

resemble, in gross appearance, those with Drake almond virus bud failure. Isolates obtained from almond trees in California, showing symptoms of "almond

mosaic" (fig. 42, D), incite extremely severe symptoms of rugose mosaic on

cherry and summer leaf spot symptoms in peach.

Sour cherry cultivar Montmorency reacts to inoculation with the CRMs with

initial symptoms that are much the same as those induced by isolates of NRSs

and RRSs of PRSV. Chronic symptoms of rugose mosaic are a twisting and

chlorotic blotch of leaves. Also, yellow leaves are produced 4 to 5 weeks after

full bloom, with some green retained along the veins, and very closely resemble

leaves of trees with sour cherry yellows. Yellow bract leaves that retain islands

of green tissue commonly occur prior to yellows of full-size leaves (fig. 42, C;

fig. 52, C).
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 121

FIGURE 52.—Prunus ring spot. Montmorency cherry infected with a pure culture of

cherry rugose mosaic strain (CRMs) of Prunus ring spot virus (PRSV) : A, Rugosity

and vein clearing, early season symptoms; B, calico spots and light-green mosaic,

spring and summer symptoms; C, yellow leaves with green retained along the veins,

similar to sour cherry yellows, midsummer.
122 VIRUS DISEASES OF STONE FRUIT

FIGURE 53.—Prunus ring spot. Napoleon sweet cherry infected with a pure culture of

cherry rugose mosaic strain (CRMs) of Prunus ring spot virus (PRSV). A, Left, severe

symptoms second year following inoculation; right, normal shoot. B, Individual leaves

from diseased shoot in A. Note the distortion, chlorotic blotches, rugosity, calico

mottle, and enations—all chronic symptoms of cherry rugose mosaic. C, Deformed

fruits on left compared with normal fruit at far right.
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 123

CRMs in Shiro plum incites calico blotches, lines, and oak-leaf patterns that

resemble plum line pattern symptoms in this cultivar. However, vein netting or

"fish net," a characteristic symptom of plum line pattern, has never been seen

associated with infection of CRMs in Shiro plum (fig. 42, D).

Almond calico strain (AlCs).—Infected trees of almond show variable

amounts of foliage with chlorotic spots or blotches {656). The calico spots or

blotches on individual leaves may be scattered or aggregated at the tip or base or

in a transverse band. The chlorotic areas are predominantly white or light yellow,

bleaching to white. Chlorosis in early spring may be quite conspicuous especially

on leaves of certain scaffold limbs that also show bud failure symptoms similar

to those described for almond virus bud failure. The intensity of the yellow-towhite chlorosis of the foliage varies from year to year and among almond

cultivars and seedlings (fig. 55, /4).

Lateral buds on shoots of affected branches often fail to grow the season

after they are produced, and those that do grow usually produce only flowers.

The failure of flower and leaf buds to grow is a prominent symptom associated

with almond calico in orchard trees of cultivars Peerless, Nonpareil, and Drake.

Chlorotic leaf symptoms are usually absent or inconspicuous in trees of Mission

FIGURE 54.—Prunus ring spot. Napoleon sweet cherry leaves naturally infeaed with a

moderate isolate of cherry rugose mosaic strain (CRMs) of Prunus ring spot virus

(PRSV), showing distortion and chlorotic blotching.
124 VIRUS DISEASES OF STONE FRUIT

and Drake, but the AlCs can be recovered from trees with bud failure symptoms

(George Nyland, unpublished data). Trees of Nonpareil inoculated with a pure

culture of AlCs showed typical leaf symptoms of ring spot and calico the

FIGURE 55.—Prunus ring spot. A, calico on leaves of Jordanola almond; Calico and

chlorotic flecks on leaves of Elberta peach B and mazzard cherry C infected with

almond calico strain (AlCs) of Prunus ring spot virus (PRSV).
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 125

following year but only mild bud failure symptoms after 3 years (George

Nyland, unpublished data). In time, Nonpareil trees in the field are seriously

damaged by AlCs. The coidentity of almond virus bud failure (744), almond

calico (636), and peach mule's ear (743) is suspected because of their constant

association, but research on this point is still in progress.

In sweet cherry, AlCs induces initial necrotic ring spot shock symptoms, and

in certain cultivars and seedlings AlCs produces striking light-yellow to white

chlorosis as lines, bands, rings, oak-leaf patterns or speckled mottle the season

following inoculation and intermittently in subsequent growing seasons (fig. 42,

B; fig. 45, C). Black Tartarian, Chapman, and Saylor show conspicuous calico

symptoms. In all sweet cherry cultivars, the calico and ring spot symptoms are

less obvious in older infections, but usually a few scattered individual leaves or

occasionally all the leaves on individual spurs show symptoms. Symptoms induced by the AlCs in sweet cherry resemble those of pinto leaf (367).

In peach, AlCs inoculated by tissue grafts induces initial shock symptoms

like those incited by the other strains of PRSV. Initial shock symptoms are

followed by the development of chronic symptoms of pale-yellow blotches on

leaves produced early in the spring. In older infections, these blotches may be

difficult to find later in the season or at all (fig. 53, B). In the Central Valley

of California, peach inoculated with AlCs shows summer leaf spot symptoms

like those described for other strains of PRSV.

In Shiro plum, AlCs produces a very conspicuous speckled, bright calico

spotting and prominent oak-leaf patterns (ñg. 42, B). However, almond calico

isolates react like those of cherry rugose mosaic and do not produce the "fish net"

symptom in Shiro plum characteristic of PRSV isolates associated with plum

line pattern. In Shiro-fugen flowering cherry, AlCs reacts the same as other

strains of PRSV, producing local necrosis around the inserted tissue.

Isolates of the AlCs vary considerably. Some incite stronger leaf symptoms

in almond and peach than other isolates, and they vary in the symptoms induced

on a standard herbaceous host range. A few isolates have incited conspicuous

chlorotic blotch symptoms in Gomphrena globosa that resemble those of cherry

rugose mosaic in this host but without distortion of the leaves (George Nyland,

unpublished data).

Other Strains of PRSV.—Several other strains of PRSV may exist, based on

published reports (30, 347, 349, 483, 394). Excluded from PRSV would be

those isolates that do not infect Chenopodium spp., but do incite dwarf symptoms on Italian Prune, yellow mosaic on squash, and tithonia, and local lesions

on Sesbania exaltata (706). Included as a strain of PRSV would be Stecklenberger virus, based on symptoms in herbaceous and stone fruit hosts and on

serological tests (348, 349, 483, 393). The virus described as chlorotic-necrotic

ring spot virus (349) shows some properties similar to PRSV and PDV; but,

based on host reactions, thermal inactivation point, and serology, it more nearly

resembles PDV.
126 VIRUS DISEASES OF STONE FRUIT

Transmission

PRSV is readily transmitted by tissue grafting. The virus is also transmitted

mechanically from sap and pollen and by plant contact (196, 226, 251, 639,

723, 736), The virus is carried in seed from infected plants (123, 143, 147)

and, at least in some cases, in seed produced on healthy trees (233, 666, 708).

PRSV is carried in pollen of infected cherry (196, 708) and other Prunus

hosts (723) and was transmitted from plant to plant by pollen of sour

cherry (236). Pollen from trees of sour cherry and plum infected with PRSV,

when applied to emasculated flowers on healthy trees, resulted in some infected

seeds (666, 708). Some infected seeds were produced on open-pollinated field

trees of mazzard and mahaleb in Oregon and Washington that presumably

tested virus-free (203). In P. pensylvanica, seed transmission occurred only

when both the ovule and the pollen parents were infected (227). Open pollinated trees in California's tree registration program have consistently produced

seedlings in which little or no virus has been detected so long as the ovule

parent tests free of PRSV. Environmental conditions as well as the host plant

may influence the incidence of seed transmission of virus.

PRSV and PDV spread from tree to tree of Montmorency grown in cages

or in the field in experimental treatments under conditions that strongly suggested pollen as the vector. PRSV did not spread into exposed field trees from

which all blossom buds had been removed. Rapid spread occurred in trees that

were permitted to flower normally (236, 237). Spread of PRSV can be accounted

for by tree-to-tree infection by pollen, by seed transmission, and by transmission through propagation practices. In spite of considerable effort devoted

to a search, no insect vector of the virus has been found (640). Some viruses

with characteristics similar to those of PRSV have nematodes vectors (104).

Buds or bark chips infected with PRSV often die soon after they are inserted

into healthy tissue of cherry, peach, and almond. Similar buds inserted into

apricot, plum, or some other species of Prunus may heal in normally. Whether

or not infected buds die depends on several factors such as the sensitivity of

the host, virulence of a partiailar isolate, or the time of year the virus is introduced into the plant. Even if the inoculum tissue dies, transmission usually occurs.

The time required for transmission is mostly a function of temperature (212),

but to some extent it is also a function of host dormancy (217). At 30° C.

transmission of PRSV occurred in 72 hours; at 18° C, 168 hours (212).

The time of infection influences the time of symptom appearance and severity.

With sour cherry, inoculation with the RRSs of PRSV in mid-May, June, or

July gave etch symptoms after bud-break on most of the trees except the inoculated branch, which had only mild secondary symptoms. Inoculation in late

fall resulted in severe shock symptoms the following spring (182). In later

experiments (181), trees inoculated at or near full bloom developed initial

shock symptoms a year later, except in the inoculated branch, which showed

only chronic symptoms. This is the usual condition seen in naturally infected
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE ^27

trees. When inoculations were made prior to full bloom, symptoms usually

showed on the inoculated branch the same year and on the remainder of the

tree the following year. This latter condition was not found in the orchards.

These results add evidence that infection takes place at flowering time.

Characteristics of the Virus

PRSV is a polyhedron of variable size depending on the strain and the

particular fraction of the virus measured. Isolates of the NRSs of PRSV had

particles averaging 17 m^x (60.5) and 23 m^ (228). Virus particles of CRMs,

AlCs, and apple mosaic strain measured 21.5 to 28.7 m/x, 20.4 to 23.3 m^n,

and 25.9 to 29.2 m^, respectively. Particles in the upper bands of sucrose

gradient columns were consistently smaller and less infectious than those in

the lower bands (422, 188). Two bands in a sucrose gradient seem to be

characteristic for several strains of PRSV. Sedimentation constants for the two

bands in sucrose gradient columns for several strains were 61, 72, 75, 88, and

95s for the upper zone and 87, 99, 105, and 117s for the lower zone (422, 188,

663).

PRSV is inactivated at 54° to 62° C. (227, 706) in vitro and 2 to 3 weeks

in vivo at 38° (488). It loses more than-one-half its infectivity in dilute

cucumber sap (1:80) in 1 hour at 24°. The virus is stabilized in 0.02 M phosphate buffer at pH 8.0 with 0.01 M diethyldithiocarbamate (226, 228) and

can be concentrated from buffered sap that is clarified with hydrated calcium

phosphate gel. Centrifuging for 2 hours at 78,480 g. produces a clear, highly

infectious pellet. Purified PRSV loses its infectivity rapidly in distilled wHer

or when shaken vigorously in buffer (228).

The dilution-infectivity curve of PRSV is steeper than a theoretical one-hit

curve. The slope of the curve is markedly in^uenced by adding infective or

noninfective related virus to a dilute PRSV extract. The host inoculated also

influences the slope. On DoUchos biflorus, each twofold dilution resulted in a

three- to fourfold decrease in infectivity ; on Momordica balsamina, an eightfold

to tenfold decrease. Adding related virus to PRSV extracts disproportionately

increased infectivity (229).

Strains of PRSV cross-react with each other in gel diffusion or microprecipitin tests (252, 422, 493). Spur formation between an isolate of the

apple mosaic strain of PRSV and PRSV from plum and cherry is reported

(188).

Indexing for PRSV

Several methods are available to index efiiciently for PRSV. Peach seedlings

and Montmorency sour cherry were among the first indicator plants used to

detect the virus in plants not showing symptoms (57, 132). Shiro-fugen flowering cherry (407, 443, 461) probably is the most reliable indicator host although

peach may be equally as good under the best conditions. The Shiro-fugen test

is made as follows (299, 300, 329) : One or more buds or bark chips from

the plant to be tested are inserted under the bark of a vigorously growing branch
128 VIRUS DISEASES OF STONE FRUIT

of Shiro-fugen in the manner of budding. Vigorous growth during the test is

very important to insure accuracy. The individual buds or chips are spaced

about 2 inches apart. Under favorable growing conditions the results can be

obtained about 30 days following budding. A necrosis of the tissue of Shirofugen around the inserted tissue indicates the presence of virus in the plant

from which the tissue came. (fig. 56). The test does not distinguish clearly

the strains of the virus or between PRSV and PDV. Indexing can be done as

soon as the leaves of Shiro-fugen trees are fully expanded in the spring and

can continue until growth ceases in the fall. Tests that are made just prior to

cessation of growth in the fall but while the bark is still slipping easily can be

read the following spring. So far as is known, only PRSV and PDV cause the

local necrotic reaction in Shiro-fugen.

FIGURE 56.—Prunus ring spot. A Shiro-fugen cherry stem budded with two sweet cherry

buds {upper virus-free and lower infected with Prunus ring spot virus) : A, Without

bark removed; B, with bark removed to show necrosis of the tissue adjacent to the

infected bud and normal color under virus-free bud.
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 129

Prunus tomentosa is another useful indicator plant for PRSV as well as some

other viruses {202, 210). Peach and P. tomentosa should be inoculated by

tissue grafts late in the growing season or just prior to bud-break. Symptoms

are best seen soon after bud-break. P. tomentosa can be used in the field but

may be more sensitive as a greenhouse test plant.

Another useful indexing method for PRSV is sap transmission to cucumber

or other herbaceous hosts (figs. 57 and 58). Leaves, roots, pollen, petals, or

seed have been used as sources of the virus {93, 233, 246, 446, 447, 668, 723),

Mechanical transfer of PRSV from leaves is most successful in early spring

and becomes less efficient as the season progresses. Identification of some strains

of the virus is possible by using selected herbaceous hosts {225, 493, 706).

Control Measures

Clean planting stock is the most important control-measure for diseases caused

by PRSV. In special cases, such as trees used for buds and scions or for seeds,

roguing diseased orchard trees as soon as possible after they are detected is

recommended. Spread of ring spot can be rapid in sour cherry and sometimes

in peach. Limited evidence is at hand that spread is more rapid in Alamar and

J. H. Hale than in Liberta or the common clingstone peaches. Alamar and J. H.

Líale are self-sterile and therefore require cross-pollination. Sweet cherries,

almonds, and some plums are also self-sterile; however, in the same areas that

spread in self-sterile peaches was very rapid, little or no spread occurred in

the other species (George Nyland, unpublished data).

Trees used as budwood sources or for seed production should be isolated as

far as possible from infected fruit trees. One-half mile isolation has proved

very effective in preventing spread of ring spot. In most cases, greater isolation

is difficult to find for commercial orchards. Planting solid blocks of virus-free

trees produced under some sort of certification scheme offers the best hope for

the future. Selection of self-fertile cultivars that are less apt to be infected

under field conditions offers some promise.

Remarks

The presence of PRSV as a contaminant of virus cultures obtained from

infected orchard trees and the variability of the virus have caused a great deal

of confusion among research workers in the past. The use of pure cultures

of isolates alone and in controlled combination is rapidly clarifying the confusion surrounding the Prunus ring spot virus complex. As accurate information is obtained, relatedness of isolates that incite different diseases is being

established. Thus, isolates inciting such diseases as cherry rugose, almond

calico, Stecklenberger disease, plum line pattern, almond mosaic, rose mosaic,

an initial symptom in hops, hop nettlehead, and apple mosaic all show relatedness of varying degrees. Questions about nomenclature remain, but these

probably will be resolved on the basis of convenience and common usage. In

the meantime, we need to learn more about the physical, chemical, and biological characteristics of particular isolates that incite the different diseases.
130 VIRUS DISEASES OF STONE FRUIT

FIGURE 57.—Prunus ring spot. Symptoms incited on herbaceous plants by inoculation

with Prunus ring spot virus (PRSV) : A, Local lesions on Momordica balsamina; B,

local lesions on cotyledons and systemic mosaic on leaves of cucumber; C, necrotic

local lesions on cotyledons of Buttercup squash; D, limited systemic invasion of

Buttercup squash leaves showing chlorotic blotches and deformed leaves; E, chlorotic

local lesions and green rings on cotyledons of Buttercup squash that became evident

2 to 3 weeks after inoculation; f, necrotic local lesions on leaf of Chenop

amaranticolor.
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE Jgl

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FIGURE 58.—Prunus ring spot. Symptoms incited on herbaceous hosts by inoculation

with the cherry rugose mosaic strain (CRMs) of Prunus ring spot virus (PRSV) :

A, Local lesions on primary leaf of Dolichus biflorus; B, vein necrosis on leaf of Pinto

bean; C, rings, blotches, and leaf distortion on leaves of Gomphrena globosa; D,

chlorotic lesions and distortion on systemically infected leaves of Chenopodium

amaranticolor; E, local lesions on cotyledons of Cyamopsis tetragonaloba. F, Local

lesions on cotyledons of Cyamopsis tetragonaloba inoculated with recurrent ring spot

strain (RRSs), left, and almond calico strain (AlCs), right, of PRSV.
132 VIRUS DISEASES OF STONE FRUIT

Also, we need to obtain and disseminate information about the advantages of

clean stock where these exist and develop practical programs based on biological

principles to minimize virus infection of clones during their development,

testing, maintenance, and distribution.
RED SUTURE

EDWARD J. KLOS

Red suture occurs in Michigan and Maryland (31, 702) ; records indicate it

was present in Michigan as early as 1911 (642). It was probably introduced into

Maryland on infected nursery stock (128).

Red suture has been found on peach and Abundance plum. All peach

cultivars tested were susceptible.

Red suture symptoms can be found on fruits and foliage (31, 117). Fruits

ripen and soften on the suture side several days prematurely, while the other side

is green and hard. Frequently, the suture side is swollen, rough, or bulged

(fig. 59). Red suture flesh is coarse, stringy, and watery. The early ripening

side of red fruited cultivars is blotched with dark red or purple, which is

evident on the apexes of the bumps. Yellow fruited cultivars, such as Gold Drop,

have a deeper yellow on the suture side. The fruit flavor is often insipid. The

suture side will bruise or break down more rapidly in transit or on the shelf.

Red suture leaves have a yellowish-green to greenish-bronze appearance,

which is often overcome by nitrogen fertilization. The color difference of

diseased and healthy trees is noted at certain times of the season, particularly

a few weeks after petal fall or just before harvest when diseased trees take on

early fall coloring. The buds of many 2-year-old branches grow into short,

spurlike outgrowths, resulting in a clustering of the leaves along the branch.

On normal trees, a few buds remain dormant, others grow long shoots, and

only a few develop into spurlike growths. A tree diseased for several years will

have an open center. Diseased trees may live for 8 years or more.

FIGURE 59.—Peach fruits showing enlarged, reddened suture characteristic of red suture.

133
134 VIRUS DISEASES OF STONE FRUIT

Cation and Bennett (128) noted on Abundance plum that the symptoms

of red suture are similar to those caused by peach yellows virus. Diseased trees

have lighter colored foliage and fruit ripens prematurely. Red June and

Wickson plum (P. salicina X P- simonii) also exhibit severe symptoms of

red suture when infected by peach yellows virus. Red suture virus (RSV)

alone had little effect on these cultivars.

Symptoms on mature trees appear in the second year after infection. Nursery

trees propagated from diseased buds do not show symptoms during the first

year of growth and only sporadically in the second year. Transmission has been

successful by grafting with bark tissue with or without buds from diseased trees.

Kunkel {587) found that red suture virus was inactivated when bud sticks

were immersed m a water bath at 50° C. for 3 minutes. Peach yellows and

little peach viruses have similar inactivation points. On the basis of disease

symptoms and virus inactivation temperature, red suture is probably related to

peach yellows and little peach. The restricted distribution of red suture would

indicate that, if it is a mutant of the peach yellows group, it rarely occurs in

nature.

Red suture can be controlled by periodic orchard inspection and eradication

of diseased trees. Virus-free budwood and rootstocks are recommended in peach

propagation. The disease has been of little economic importance in recent years.

Effects of 2, 4-D and 2, 4, 5-T on peach fruits frequently have been mistaken

for red suture.
ROSETTE MOSAIC

EDWARD J. KLOS

Causal Virus

Rosette mosaic virus (RMV).

Synonyms

Peach rosette mosaic. The name refers to two of the prominent symptoms

on this crop.

History and Distribution

This disease has been present in Berrien County in southwest Michigan since

at least 1917 (118, 121). It has been limited to a few scattered orchards in that

county. Similar diseases were reported in New York (303) and Italy (263).

Economic Hosts

Ali peach cultivars tested were susceptible, and the severity of the reaction

varied with the cultivar. The following peach cultivars are listed in the order

of the severity of effect of the disease: Sbuth Haven, Halehaven, J. H. Hale,

Elberta, Carmen, Golden Jubilee, Kalhaven, Ambergem, and Gold Drop.

Other Hosts

Italian Prune (Prunus domestica) and Wickson plum (P. salicina X Psimonn) developed symptoms following graft inoculation with RMV. Damson

plum, and Burbank, Red June, and Abundance plums (P. salicina) appear to

be symptomless carriers of the virus (124). Concord grape is now known to be

susceptible to infection by RMV (377 and H. Dias, unpubhshed data).

A number of herbaceous plants have been infected by sap transmission,

including Chenopodium amaranticolor, C. quinoa, Nicotiana tabacum, White

Burley tobacco, N. glutinosa, common bean, cowpea, petunia, and tomato.

Gomphrena globosa is a symptomless host (H. Dias, unpublished data).

Symptoms

The symptoms in peach may consist of delayed foliation; chlorotic mottling

of early formed leaves, generally accompanied by distortion (fig. 60) ; and a

shortening of internodes (fig. 61), which frequently crowds the leaves into

the rosettes from which the disease derives its name (fig. 62).

When chlorosis of the leaves occurs, it is evident early in the growing season.

Chlorotic areas vary in size and shape and range from yellow or cream color to

translucent. Tissue growth in these areas is retarded and distortion results.

Less definite retardation gives a wavy or undulating leaf margin. Leaves formed

later in the season on affected trees appear more normal in size and shape but

actually are about two-thirds as wide as leaves on unaffected trees. Affected trees

are darker green than normal trees. A variable number of normal branches

may be interspersed with affected ones on an infected tree. Inoculation of healthy

135
136 VIRUS DISEASES OF STONE FRUIT

FIGURE 60.—Misshapen leaves with chlorotic areas from a peach tree affected by

rosette mosaic.

trees with buds from such normal-appearing branches did not result in

transmission of RMV.

Italian Prune showed symptoms similar to those of prune dwarf when inoculated with RMV. Symptoms varied from strap-shaped to slightly dwarfed,

roughened, and thickened leaves. Wickson plum did not express symptoms

until the third or fourth year after inoculation. The leaves were smaller than

normal, and the twigs showed rosetting. Damson plum did not develop

definite symptoms.

Concord grape showed delayed foliation with small, distorted, chlorotic

leaves and vine decline. A berry-shelling symptom may be present. Many

affected vines die in a short time.

Mechanical transmission of RMV by using sap from young infected leaves

of Concord grape or peach gave the following symptoms on herbaceous plants:

Chenopodium amaranticolor and C. quinoa showed systemic mottle and leaf

deformity with stunting and distortion of the shoot tip 7 to 10 days after

inoculation; in C. quinoa, these symptoms are followed by severe stem twisting,

epinasty and frequently by death of the plant; in White Burley tobacco, systemic

mottling with chlorotic ring spots are apparent in 8 to 15 days; bean, cowpea,

Nicotiana glutinosa, petunia, and tomato are systemic hosts and show only mild

symptoms; although Gomphrena globosa is symptomless, the virus can be

recovered from inoculated and apical leaves.

Transmission

Transmission of RMV has been accomplished by grafting, by transfer of soil

from diseased to healthy trees, by planting healthy trees in a location previously
HANDBOOK NO. 437, U. S. DEPARTMENT OP AGRICULTURE I37

occupied by diseased plants, by the nematode Xiphenema atnericanum {568),

and by seed (H. Dias, unpublished data).

Dias has transmitted the virus from peach and grape to various herbaceous

hosts by mechanical sap inoculations.

The incubation period of RMV in peach varied from a few weeks under

optimum growing conditions in the greenhouse to 9 to 21 months in the field.

The length of time required depended on varietal susceptibility and growth

stage of the trees at the time of infection. Transmission in contaminated soil

took 10 months if transmission was attempted prior to July 15. Trees planted

in diseased soil in the spring showed symptoms the next spring, but trees

planted in the fall did not show symptoms until the second spring. On seedlings

18 to 24 inches tall, the shortest incubation period was 12 to 16 days when

rapid transmission techniques were used {306). With the defoliation technique,

14 to 19 days were required for symptom development, and with the shading

technique, 18 to 21 days {311).

Characteristics of the Virus

Dias (unpublished data) found that purified virus preparations of peach

rosette mosaic virus and grape decline have identical polyhedral particles of

approximately 28 m^a in diameter. Hildebrand was unable to inactivate RMV

by soaking the bud sticks in a hot-water bath at 50° C. for 20 to 22 minutes

(124), but Dias has shown that the thermal inactivation point is 10 minutes

at 65° to 68°.

FIGURE 61.—Dormant branch of peach tree affected by rosette mosaic showing severely

shortened internodes.
138 VIRUS DISEASES OF STONE FRUIT

FIGURE 62.—Peach branches with severe rosetting symptoms of peach rosette mosaic.

Control Measures

Removal of diseased trees and fumigation of tree sites for nematodes before

replanting is recommended {377). Planting of known virus-free stock of peach,

plum, and Concord grape is also suggested.

Remarks

Rosette mosaic reduces the production of individual trees. However, this

peach disease is found in a limited area in one township so that the total loss

is rather small.

The symptoms of peach rosette mosaic are similar in some respects to prune

dwarf and peach mosaic. Peach is more severely affected by rosette mosaic than

by prune dwarf, whereas Italian Prune is less markedly affected by rosette mosaic

and more severely affected by prune dwarf. Rosette mosaic does not cause

dieback or leaf spot symptoms in peach as does Prunus ring spot.

Infection by RMV has not resulted in blossom break, fruit distortion, shot

hole, or the marked and general chlorosis associated with peach mosaic.
STUBBY TWIG

H. KEITH WAGNON, HAROLD E. WILLIAMS, and JACK A. TRAYLOR

Causal Virus

Stubby twig virus (STV).

Synonyms

False yellow leaf roll.

History and Distribution

The disease was first noted in California in 1952 when its symptoms caused

confusion in diagnosing of the yellow leaf roll strain of western X-disease

(^63). In 1958, it was reported (693) to be a virus disease which was widespread in peach and nectarine plantings in California. Certain cultivars had

become infected prior to or shortly after their introduction, and the disease had

been spread by contaminated propagating stocks. Published reports on the disease have led to the belief that its occurrence is restricted to California, but

it has been noted also on trees in Missouri and Oregon and on trees propagated

in several other States and shipped to California. Symptoms of the disease also

have been observed on peach in both Italy and Turkey. The disease may go

undetected because peach and nectarine trees infected with the virus apparently

remain symptomless under certain weather conditions.

Economic Hosts

The virus is known to cause disease symptoms only in peach and nectarine.

Other Hosts

Transmission studies have shown that the following hosts could be symptomless carriers of the virus: Blenheim apricot; Jordanolo almond; Wickson,

Myrobalan 29C, marianna and damson plum; and desert almond.

Symptoms

The most conspicuous overall feature of an STV-infected tree is the scattered

occurrence of shoots or branches with pale-green to yellowish leaves, or both.

Three types of leaf symptoms and one type of twig symptom occur on infected

trees. Leaves of two of the symptom types, designated primary and secondary,

are chlorotic and are most evident in late spring and summer; leaves of a

third type are not chlorotic but chimaeralike and are seen only in the spring.

Because the chlorotic symptoms can be confused with symptoms due to other

causes, the spring leaf symptom, when present, is most reliable for diagnosis.

The leaf symptoms vary markedly with weather conditions, with the cultivars

involved, and with orchard care. Some symptomatic shoots and branches may be

removed by pruning. The three types of symptomatic leaves commonly are

retained until time of normal defoliation.

The primary chlorotic leaves which follow initial infection, and which may

recur annually, develop on somewhat vigorous, current season shoots (fig. 63).

139
140 VIRUS DISEASES OF STONE FRUIT

FIGURE 63.—Chlorosis and upward rolling of margins of peach leaves affected by

stubby twig.

These leaves, commonly associated with shortened internodes, are pale green to

light yellow with margins slightly rolled upward and inward toward the midrib.

Affected shoots may have normal-appearing foliage above and below symptomatic

leaves. The chlorosis first appears at the leaf apices and extends toward the

bases. As the season advances, the veins sometimes become swollen, the yellow

usually changes to reddish orange, and the leaf margin and some veins near the

apices become necrotic.

The spring chimaeralike chlorotic leaves develop on stems that are 1 year

old or older on trees infected 2 or more years. Foliation is retarded on affected

twigs and branches. The spring leaf symptoms become distinct in early April;

they may be of normal size and shape, but commonly they are subnormal in

size, are asymmetric, and have irregular margins (fig. 64). Contrasting paleand darker-green shades appear side by side in small sectors on angular areas

of the leaf blade, giving a marbled effect. This leaf sectoring, although diagnostic for STV, is transitory. As the season progresses, the marbling becomes

less distinct; by midsummer it is difficult to recognize. These leaves are seldom

produced in abundance and frequently are detected only after considerable

searching. Twigs and branches that bear these spring leaf symptoms may or

may not exhibit other symptoms of the disease. The secondary chlorotic leaf
HANDBOOK NO. 437, U. S. DEPARTMENT OP AGRICULTURE 141

symptom is the most common but does not become distinct before June. Twigs

and branches which bear the delayed, pale-green, and subnormal-sized leaves

are characterized by stubbiness, brittleness, lateral bud failure, and, sometimes,

dieback (fig. 65).

With the advance of the growing season, the small or subnormal-sized

chlorotic leaves become progressively more chlorotic, and those near the shoot

tip may develop red to reddish-brown spots, which may easily be mistaken for

symptoms of nitrogen deficiency. By July, afliected twigs or small branches

with their yellowish foliage become conspicuous, and, at first glance, may be

confused with damage resulting from girdling or simple mechanical breakage.

When affected twigs and branches are confined to one part, the tree may appear

lopsided. Vigorous, normal-appearing shoots often develop below the dead or

retarded terminals. The current season vigorous shoots tend to mask the older,

affected twigs, but before the end of the season, the primary chlorotic leaves

become evident.

Affected twigs bear fewer fruit buds. Mature fruits on these twigs are substandard in size and flavor. The total effect on fruit production depends upon the

number of affected twigs in a tree.

Transmission

The virus has been transmitted only by grafting. Attempts to mechanically

transmit STV to cucumbers by using pollen from infected trees have been

inconclusive.

Characteristics of the Virus

Information on virus morphology and serological relationships is lacking.

Stubby twig is caused by a yellows type of virus, which produces symptoms

FIGURE 64.—Chimaeralike spring symptoms in peach leaf affected by stubby twig.
142 VIRUS DISEASES OF STONE FRUIT

that resemble western X-disease. Young peach trees inoculated with both viruses

produced symptoms of both diseases, and the trees showed more decline than

did comparable trees inoculated with either virus alone..

Trials indicate that STV is inactivated within 5 but never less than 3 weeks

in air at 38°C. (George Nyland, unpublished data).

Control Measures

Observations indicate that there is probably no field spread of the disease in

peach and nectarine. The disease is best controlled by using STV-free propagating stock.

FIGURE 65.—Dormant peach branch affected by stubby twig, showing stubby growth

and terminal dieback.
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE I43

Remarks

STV is not lethal to a tree when present alone, but does, under some conditions in California, cause a debilitation of the tree. In commercial plantings,

its effects vary with cultural conditions. The severity of the disease can be

increased when STV occurs in combination with some strains of Prunus ring

spot virus. At least two commercial peach plantings have been removed because

of the reduction of salable fruit as a result of a high incidence of the disease.

Generally, the overall effect of the disease in the warm interior valleys of

California is to depress normal vegetative growth in varying portions of the

tree. Fruit production is reduced in proportion to the failure of flower buds and

blossoms. Although symptoms are restricted to certain parts of the tree, the

virus is completely systemic because progeny trees grown from buds of healthyappearing shoots have always been infected. The virus is symptomless in

growing nursery stock.

Superficially, symptoms of stubby twig resemble those produced by strains of

X-disease virus {^65). Pale-green to yellowish leaves may be produced by both

viruses; however, the development of necrotic spots from water-soaked areas,

which is symptomatic of X-disease, has not been observed with stubby twig. The

yellowing of affected leaves caused by STV can readily be distinguished from

the yellowing which is characteristic of peach leaf roll {500) \ yellowing in

stubby twig begins at the leaf tip and extends progressively toward the base; in

yellow leaf roll it develops more or less simultaneously and uniformly throughout the leaf. Vein swelling of affected leaves, a consistent symptom incited by

strains of X-disease virus, is much less prominent in stubby twig. Stubby twig is

readily distinguished from yellow leaf roll by the location of symptomatic leaves

on current season shoot growth. In stubby twig, the symptomatic leaves may

have normal-appearing foliage above and below them; in yellow leaf roll the

symptomatic leaves are not subtended by normal-appearing foliage. Leaves of

stubby twig trees never fall prematurely as with most X-disease. At least three

features in the symptomatology of stubby twig are not seen in X-disease—(1)

brittleness of infected twigs; (2) red to reddish-brown spots in some leaves,

which may be mistaken for nitrogen deficiency; and (3) the diagnostic leaf

sectoring that occurs on certain leaves that develop in early spring. The diseases

are very different in their reaction to heat therapy.
WEAK PEACH

GLENN KENKNIGHT

At Fort Valley, Ga., 142 weaker-than-average orchard peach trees {Prunus

pers/ca) were indexed in 1952. One tree of Erli-Red-Fre yielded a virus isolate

that, when transmitted by patch grafts or by scions, was able to induce a

"weakness" syndrome in trees of several peach cultivars grafted on Lovell peach

seedlings (362). The isolate was named weak peach virus (WPV).

Symptoms were induced within 1 to 4 years on trees of Early Hiley, Elberta,

I'airhaven, Prairie Rose, and Redcrest; but not on Cardinal, Hiland, Keystone,

and Redcap peach. Prunus mahaleh can be infected. Symptoms similar to those

caused by WPV have been induced in peach by graft transmission from a stunted narrow leaf plum (P. angustijolia) and a Concord grape {Vitis labrusca).

Symptoms have been recognized only in peach. Trees on peach rootstocks

show annual delayed onset of growth in spring, progressive stunting, dieback,

and summer chlorosis. Trees on mahaleb rootstocks show only delayed onset

of growth in the spring.

The disease apparently is not soil borne. Percentage transmission by grafting

is very high. Incubation periods appear to vary with age of inoculated tree.

WPV-inoculated, first-year Early Hiley trees showed symptoms in 3 to 4 years;

6-year-old trees, in 2 years; and 8-year-old trees, in 8 months. Transmission by

bark-patch grafts was not affected by treatment of scions in hot water for as

much as 30 minutes at 50° C.

Peach orchards in central Georgia now last half as long as they did early in

the history of commercial fruit production in this region. Inadequate investigation has been made of the possible role of debilitating viruses in the short life

of peach orchards growing on land that has been replanted to peaches many

times. The symptoms induced by WPV closely resemble those caused by the

root rot fungus, Clitocybe tabescens (Scop, ex Fr.) Bres., which has been

detected in as many as 80 percent of stumps in uprooted orchards. When

nursery-stock peach trees were inoculated by placing Clitocybe-mYSLdeà peach

stumps in the planting holes, the trees developed symptoms strikingly similar

to those caused by WPV, whereas control trees, with sound peach stumps in

the planting holes, grew normally. The similarity of symptoms induced by

WPV and C. tabescens provides uncertainty about the degree to which WPV

contributes to the problem of orchard debilitation.

144
X-DISEASE

R. M. GiLMER and E. C. BLODGETT

Causal Virus

X-disease virus (XDV).

Synonyms

XDV is a highly variable virus, and its numerous strains vary considerably

in their severity and symptomatology in economic hosts. Because of this

variability and the wide range of environments in which the virus occurs, the

diseases incited have been described under numerous names: X-disease (628),

yellow-red disease or virosis (313, ^04), western X-disease (367), western X

little cherry (379, 383), western X red leaf (373) wilt and decHne (381),

red leaf (373), cherry buckskin (348), peach leaf casting yellows (637),

peach yellow leaf roll (398), and small bitter cherry (410).

History and Distribution

Detailed accounts of the history and general distribution of the disease have

been presented previously (363, 630). X-disease was initially discovered in

Cahfornia in 1931, where it was described as cherry buckskin (348). In 1933,

the disease was observed on peach in Connecticut, where it had probably been

present for several years before discovery (628, 629). Blodgett (43) observed

X-disease of peach in Idaho in 1936. Within a few years, the disease was

found in all of the New England States, New York, New Jersey, Pennsylvania,

Ohio, Indiana, Illinois, Michigan, Wisconsin, North Dakota, Cahfornia,

Oregon, Washington, Idaho, Colorado, Arizona, Utah, British Columbia,

Ontario, and New Brunswick (43, 111, 208, 313, 346, 410, 348, 367, 378,

607). The disease has been observed in chokecherry in western North Carolina

and eastern Tennessee (R. M. Gilmer, unpublished data), but does not occur

in the peach-growing areas of South Carolina, Georgia, Arkansas, or Texas.

Earlier publications maintained a distinction between the eastern and western

forms of X-disease (363, 378, 630). The only direct comparisons of eastern

and western X-disease were made by Hildebrand (308), who concluded that

the causal viruses were distinct but probably related because of variations in

the rates of symptom development and in type of symptoms. This distinction

v/as apparently supported by differences in orchard epidemiology. Spread of

X-disease in eastern orchards was closely linked with the presence of diseased

chokecherry, but in western orchards spread occurred even in locations where

chokecherry did not occur.

Reeves et al. (363), however, pointed out the wide range of symptoms

present in different forms of western X-disease; these differences were as

marked as those between the western and eastern forms of the disease. These

authors also suggested that differences in orchard epidemiology could be

145
146 VIRUS DISEASES OF STONE FRUIT

explained most plausibly by differences in vectors in the two areas. These same

conclusions were reached independently in Eastern United States (260).

Historically, identification of X-disease in new localities has been based on

its appearance in chokecherry. This relationship was noted by Stoddard (629)

in the East and by Richards et al. (-578, 379) in the West. The disease is

widely distributed in chokecherry and occurs in this host even in areas where

peaches and cherries are not grown (363). In Santa Barbara County, Calif.,

X-disease occurs naturally in hollyleaf cherry (H. E. Williams, unpublished

data).

Economic Hosts

Peach, nectarine, Japanese plum, sour cherry, and sweet cherry.

Other Hosts

X-disease occurs naturally or has been transmitted experimentally to almond,

apricot, mahaleb cherry, Korean cherry, western sand cherry, bitter cherry,

hollyleaf cherry, Manchu cherry, wildgoose plum, and several plum hybrids

(239, 330, 363, 629, and H. E. Williams, unpublished data). Its important

wild reservoir hosts are common and western chokecherry. The disease occurs

without evident symptoms in flowering cherry (239, 360), pin cherry, American

plum, damson plum, and European plum (239).

Species apparently immune to some strains of the virus are fenzl almond,

desert apricot, desert peach, David peach, black cherry, myrobalan plum,

Klamath plum, and beach plum (239, 330, 629, 630).

XDV has been transmitted experimentally through dodder to carrot, celery,

parsley, periwinkle, strawberry, tobacco, and tomato (98, 260, 332) and has

been recovered from naturally infected milkweed (243).

Symptoms

Peach.—In the East, the foliage of infected peach trees appears normal for

about 6 weeks after growth commences in the spring. At that time, yellow

or red irregular blotches develop in the leaf blades, and affected leaves roll

upward longitudinally (figs. 66 and 67). Discolored blotches may occur

anywhere on the leaf lamina and are not restricted by the veins; there may be

few to several blotches per leaf. Shortly after blotches appear, the remainder

of the leaf blade becomes chlorotic and brittle; many of the discolored areas

drop out, giving the affected foliage a tattered appearance. At this stage, the

diseased trees appear distinctly pale green. Somewhat later, the affected leaves

abscise and drop, leaving the terminals bare with only a small persistent rosetted

tuft of leaves at the ends.

In the West, the syndrome is generally similar, but the irregular blotches

are often pale green or slightly watersoaked and drop from the leaf blade

before any red or yellow coloration develops. The affected leaves remain pale

green and are cast, the older leaves falling first. Later in the season, newly

developed blotches may become necrotic and may or may not fall from the
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE I47

lamina. In some cultivars, foliage of affected branches or trees may become

distinctly red.

The yellow leaf roll strain of XDV incites the same initial symptoms as the

common strain, but summer symptoms are more conspicuous. The affected

shoots continue to grow throughout the summer with only slight defoliation.

Infected trees are conspicuous for their yellow, upward-rolled leaves often with

enlarged prominent veins (fig. 68). Trees rarely survive for more than 3 years

after infection.

In trees newly infected with the common strain of XDV, only one or two

branches commonly develop symptoms, and the foliage and fruits on the

remainder of the tree may be normal. In succeeding years, branches with symptoms appear at random throughout the tree, often interspersed with branches

with normal foliage and fruits. Branches with symptoms usually show considerable dieback from low temperature injury during the dormant period.

Large trees may persist in a generally unthrifty condition for several years

following infection, but smaller trees often die within 1 to 3 years after the

appearance of the initial symptoms.

FIGURE 66.—Elberta peach leaves showing irregular yellow and red blotches,

early season symptoms of X-disease.
148 VIRUS DISEASES OP STONE FRUIT

FIGURE 67.—Terminal rosetting and leaf rolling in peach infected with X-disease virus

in New York.
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE I49

FIGURE 68.—Peach tree, foreground, infected with yellow leaf roll strain of X-disease

virus, showing yellowing and upward-rolling of leaves.

The fruits on branches with symptoms commonly abort and drop soon after

the fohage symptoms appear. If the fruits persist, they are usually more pointed

than normal (fig. 69), with shrivelled nonviable seeds and internal discoloration around the pits. Although such fruits often color prematurely, their flavor

is bitter and unpalatable. Large trees with chronic infections set few or no

fruits.

Sour cherry.—The initial symptoms of X-disease are apparent in the fruits,

which are smaller than normal, often distinctly pointed, and pale red or

greenish white. Some normal fruits are often interspersed with fruits with

obvious symptoms on the same branches. Affected fruits persist in a half-ripe

stage long after normal fruits have matured.

In the early stages of infection, distinctive foliage symptoms are not apparent.

In late summer, a few leaves on infected branches may be rusty in color and

develop traces of red or orange along the midrib. In the chronic stage of the
150 VIRUS DISEASES OP STONE FRUIT

FIGURE 69.—Small and misshapen fruit from Elberta peach tree affected by X-disease,

bottom; normal Elberta fruit, top.

disease, terminals are rosetted, the foliage is a pale green, and considerable

dieback of twigs and branches is evident.

As in peach, the initial symptoms of X-disease are often confined to only

a few branches, but in succeeding years symptoms gradually appear in the

remaining portions of the tree.

Trees on mazzard rootstocks may persist for a number of years with chronic

infections of XDV but are economically worthless. Trees on mahaleb rootstocks are generally short-lived after infection. They frequently wilt and die

in midsummer under conditions of temperature and moisture stress.

Sweet cherry.—The X-disease syndrome in sweet cherry is quite similar to

that described in sour cherry. The initial symptoms are usually evident on the

fruits, which are small, pointed, often flat-sided, and pale red to greenish

white (fig. 70). Affected fruits are often initially confined to a few branches,

while the remainder of the tree bears normal fruits.

Terminals of affected branches are commonly slightly rosetted; in late summer their leaves, which may be slightly undersized, become bronze or rusty

green. A few leaves may become red or orange along the midrib. In Utah,

the leaf stipules are more broad and elongate than normal {566), but this

symptom is less common or entirely absent in other areas. A late flush of growth

may develop from normally dormant terminal buds on infected trees.

In California, two well-defined strains of XDV occur in sweet cherry, the

Green Valley strain and the Napa Valley strain. The Green Valley strain is
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 151

apparently identical with the common strain of XDV present elsewhere in

the West. The Napa Valley strain differs in that many of the fruits on infected

sweet cherry trees on mazzard roots are cast just before or at the time normal

fruits are ripe. These affected fruits are almost normal in shape and are borne

on pedicels of normal length.

Leaves on trees infected with the Napa Valley strain roll upward at the

margins, and a prominent bronze coloration develops on the exposed abaxial

surfaces by early June. Infected limbs are apparent at considerable distances.

The Napa Valley strain of XDV is restricted to Napa and Sonoma counties

of California.

Trees on mazzard rootstocks may survive for a number of years after they

are infected with X-disease virus, but the virus gradually spreads throughout the

tree and affects most of its fruits. The infected trees are generally unthrifty

and more subject to dieback from winter injury. Trees on mahaleb rootstocks

decline rapidly when infected and often wilt and die in midseason.

Chokecherry.—^Newly infected chokecherry trees show a definite but transient

delay of growth initiation in the early spring but appear almost normal until

about 6 to 8 weeks after growth commences: At this time, the foliage gradually

becomes bright orange or red (fig. 71). Many of the affected leaves drop but

others are retained. A second flush of growth may appear in late July or August

FIGURE 70.—Top, immature fruits of May Duke cherry infected with X-disease virus.

Bottom, healthy fruits of May Duke cherry from an uninvaded portion of the same tree.
152 VIRUS DISEASES OF STONE FRUIT

from terminal and axillary buds that break dormanq^. This growth is initially

yellowish-green, but gradually turns red as the season progresses.

Fruits on newly infected trees are pointed and remain pale red without

maturing.

In succeeding years, growth of infected trees is very rosetted, and the foliage

is duller in color, often yellow instead of red. Leaves are fewer in number and

smaller in size. Many twigs and branches die, and few or no fruits are produced.

Infected chokecherry trees decline rapidly and commonly die within 3 to 4 years

after infection, although they may survive slightly longer in areas with mild

winters.

Transmission

XDV usually is readily transmitted by budding or grafting, although a fairly

high percentage of buds from peach trees infected with the common strain

may not carry the virus, possibly because of irregular distribution of XDV

in the infected trees. The yellow leaf roll strain of XDV is very invasive and

usually completely systemic in infected peach trees, so that transmission is easily

accomplished by budding. Besides differences in the invasiveness of XDV

strains in peach, other factors may influence ease of transmission. Successful

FIGURE 71.—Chokecherry tree affected by X-disease, showing characteristic bright orange

to red foliage in the second year of symptoms.
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE I53

transmissions decline markedly if infected peach buds are not used promptly

(E. L. Reeves and E. C. Blodgett, unpublished data). Transmissions from buds

of trees with longstanding chronic infections is often difficult, probably because

of the failure of the debilitated tissue to unite (R. M. Gilmer, unpublished

data). The presence of Pmnus ring spot virus in XDV inoculum may also

prevent tissue union and transmission of XDV.

XDV may be transmitted from infected stone fruits to a variety of herbaceous

hosts with dodder {Cuscuta spp.) {260, 591, and D. A. Slack, unpublished

data). Transmission from one herbaceous host to a second is also readily

achieved with dodder. But, in spite of repeated attempts by several workers

{260, 391), transmissions between stone fruits or from herbaceous plants to

stone fruits with dodder has not been achieved.

Although Stoddard (629) and Hildebrand (308) suspected that XDV was

transmitted in the field by insects, Wolfe et al. (730, 731) were the first to

demonstrate unequivocal transmission of XDV by a leafhopper. Colladonus

geminatus (Van D.). Jensen et al. (333) confirmed transmission by this insect.

Anthon and Wolfe (17) later discovered three additional leafhopper vectors:

Scaphytopius acutus (Say), Fteberiella flor/i (Stal), and Keonolla confluens

(Uhl). Several other leafhoppers also may serve as vectors of XDV: Osbornellus horealis Del. & M. (332), Collandonus montanus (Van D.) (749), C.

clitellarius (Say) (260, 662), Gyponana lamina DeL., Paraphlepsius irroratus

(Say), and Norvellina seminuda (Say) (260).

The most important vector in the West appears to be C. geminatus, although

Jensen (332) considered F. florii to be an important vector in California. In

the East, S. acutus is probably the most important economic vector, but other

species occasionally may be of local importance (260).

In the northeastern United States, serious outbreaks of X-disease are cyclic

in occurrence at intervals of about 8 to 10 years. Serious damage occurred

during 1942-45 and 1954-1957. A new cycle began in I968. Although the

ecology of the insect vectors has not been worked out thoroughly, these cycles

appear to coincide with heavy vector populations.

XDV is not mechanically transmissible so relatively little is known of the

characteristics of the virus itself. XDV is heat labile in woody plants (Prunus) ;

Hildebrand (308) reported that XDV was inactivated in infected peach buds

by immersing them in water at 50° C. for 6 to 7 minutes. Stoddard (629)

reported that a range of hot water treatments fromi 48° for 16 minutes to 53°

for 2 minutes inactivated XDV in peach buds. Nichols and Nyland (483)

found that the yellow leaf roll strain of XDV was considerably more tolerant

of heat than the common strain; in their best treatment the YLR strain was

inactivated in only 50 percent of the buds. R. M. Gilmer (unpublished data)

found that XDV was inactivated in experimentally infected sweet cherry budlings exposed at 37° for 15 days or more, but many of the trees died as a

result of treatment.

The incubation period of X-disease in peach or chokecherry depends largely
154 VIRUS DISEASES OF STONE FRUIT

upon the stage of growth at which inoculation occurs. Bud-inoculations made

in late July or early August result in the appearance of symptoms about 6 weeks

after growth begins the following spring. If trees are inoculated just as growth

begins, symptoms often develop within 6 to 8 weeks.

The latent (incubation) period of XDV in leafhopper vectors is rather

lengthy: 22 to 35 days in Colladonus geminatus {751'), 45 days in Scophytopius dcutus (731), and 20 to 40 days in Fieberiella florii (260). Transmission

by infective leafhoppers is often erratic, i.e., many suscepts on which infective

leafhoppers feed may escape infection (260). Peach is apparently a rather

poor host for XDV acquisition by leafhoppers (260, 333), perhaps because

the virus is often irregularly distributed in this host. Although periwinkle is

easily infected by leafhoppers, it, likewise, is a poor host for XDV acquisition

by vectors (260). Celery (333), chokecherry (260), and sour cherry (260)

are good virus sources for leafhopper acquisition.

Control Measures

In the East, outbreaks of X-disease in peach or cherry orchards are invariably

associated with the presence of diseased chokecherries nearby. Eradication of

chokecherries within 500 feet of orchards generally provided acceptable commercial control of the disease in New York (504). Although there is no

indication of significant spread of XDV within the orchard from infected

orchard trees, the latter are commercially worthless and should be removed.

Chokecherry is readily reseeded by birds, so continued vigilance in its removal

is required. Distance does not appear to be an effective barrier in the spread

of XDV from chokecherry to chokecherry where the rate of spread is much

more rapid than in peach or cherry.

In the West, XDV spreads from- peach to peach or cherry to cherry, and the

presence of infected chokecherry as a reservoir host is not necessary. Chokecherry should be eradicated, and infected orchard trees should be removed as

soon as they are identified. In Washington, a survey and eradication program

(1947-51) was effective in reducing the threat of X-disease.

In areas where the disease is important and spread is rapid, topworking

cherry on a mahaleb framework is recommended (378). Individual cherry

limbs may become infected, but the spread of XDV into the remaining portions

of the tree is limited by the mahaleb frame. Cherry trees on mahaleb rootstocks

appear less likely to be infected than those on mazzard rootstocks. Several

sweet cherry cultivars are highly resistant to infection even when propagated

on mazzard rootstocks. Among these are Napa Long Stem Bing, Dicki Braune,

Blakenburger, and Coop's Special (349 and B. N. Wadley, unpublished data).

Although X-diseased peach or cherry nursery trees grow poorly with obvious

symptoms, XDV can occasionally be carried for a short time in a latent form

in nursery trees. Scionwood for propagation should be selected from healthy

trees, and chokecherry near nursery planting should be completely eradicated.

Since seeds from infected trees abort or fail to germinate, there is little danger

of XDV transmission in seedling rootstocks.
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE I55

Remarks

Most stone fruit virologists now consider that the eastern and western forms

of X-disease are caused by very similar if not identical viruses. Both forms

attack the same economic hosts—peach, sweet cherry, and sour cherry (30^,

330, 363, 630). The symptoms of buckskin disease on sweet cherry on mahaleb

rootstock in California were very similar to the cherry wilt and decline syndrome induced by western X-disease in Utah (363). Zeller and Milbrath (771)

demonstrated that buckskin of sweet cherry and X-disease of peach were induced

by the same strain of XDV, and the similarity of cherry buckskin and leaf

casting yellows of peach in California to both eastern and western X-disease

has been described (349, 657). Considerable strain variation of XDV also

occurs in the East (239, 260, 308).

The leafhopper vectors of XDV are members of a single subfamily, Deltocephalinae, with the exception of Gypo?iana lamina, which belongs to subfamily

lassinae. There is a single report of transmission by Keonolla confluens (subfamily Tettigellinae) (17), but confirmation would be highly desirable because

numerous other members of this subfamily were unable to transmit XDV (260).

Gilmer et al. (260) pointed out that many of the leafhoppers that transmit

XDV are also vectors of western aster yellows virus. Although the symptoms

of X-disease in herbaceous plants are distinct from those of aster yellows or

western aster yellows, they are basically similar. These facts suggest that XDV

and aster yellows virus may be related. Yellows-type diseases are associated

with mycoplasms rather than viruses (330), and X-disease may also be induced

by a mycoplasm. This hypothesis is supported by recent investigations (George

Nyland and T. S. Pine, unpublished data) in which remission of foliage symptoms occurred in peach trees infected with the yellow leaf roll strain of XDV

when these were treated with terramycin by trunk injection, foliar sprays, or

soil drenches. Individual branches of infected mature peach trees injected with

terramycin during dormancy produced normal-appearing fruits the year following treatment, while nontreated branches of the same trees produced no fruits.

Stoddard (629) reported that X-disease could be controlled in infected peach

trees by injection or soil drenches with a number of chemicals, including

P aminosulfonamide, P-toluenesulfonamide, maltose, hydroquinone, calcium

chloride, and zinc sulfate. A repetition of some of his experiments showed

the preinoculation treatments of calcium chloride, zinc sulfate, and hydroquinone

were effective, perhaps because these materials caused sufficient injury to prevent

union of inoculum (R. M. Gilmer, unpublished data). If inoculum had united,

postinoculation treatments with these chemicals were not effective in preventing

the disease.

Note: Several reports have appeared (Virology 41: 583, Phytopathology 60:

1534, and 61: 1036) that demonstrate the association of mycoplasmas with

X-disease.
YELLOW BUD MOSAIC

ARCHIE SCHLOCKER and JACK A. TRAYLOR

Causal Virus

Yellow bud mosaic (YBMV) strain of tomato ring spot virus (TomRSV).

Synonyms

Winters' disease; Winters' peach mosaic; Eola rasp leaf.

History and Distribution

Yellow bud mosaic was found affecting peach and almond trees in the

Winters area of Solano and Yolo Counties, Calif., in 1936 and was described

for the first time in 1939 (6J3). Inspections showed its presence in at least

40 orchards in the two-county area. Between 1950 and 1964, the disease was

found in peach in all the peach-growing areas of northern and southern California and in cherry in the cherry-growing areas of San Joaquin and Stanislaus

Counties. The disease has not been found in peach or cherry in the southern

portion of the San Joaquin Valley. The disease has not been reported in peach

outside of California. The disease in cherry in California is the same as that

described in Oregon as Eola rasp leaf. All evidence indicates that the disease

spreads from native wild plants to fruit trees grown in infested soil (498).

Economic Hosts

Yellow bud mosaic is a serious disease of peach, nectarine, sweet cherry,

almond (principally the Texas cultivar), and Wickson plum (636, 653, 698).

Other Hosts

Apricot is a natural host but is not seriously damaged. Infected trees may

be symptomless carriers of YBMV and are capable of supplying the virus to

the nematode vector (Xiphinema americanum), which can carry it to more

susceptible hosts (638). Some brambles and a number of weeds have been

reported as natural hosts of YBMV in California, including Himalaya blackberry (Rubus procerus), red raspberry (R. ¿daeus), red currant (Ribes sat/vum),

sand strawberry (Fragaria chiloensis), cheeseweed (Malva parviflora), seaside

daisy (Erigeron glaucus). Fuller's teasel (Dipsacus jullorum), bristly ox tongue

(Vieris echioides), plantain (Plantago spp.) and hedge nettle (Stachys bullata)

(13, 209, 341 and H. E. Williams and Q. L. Holdeman, unpublished data).

Thomas and Rawlins reported transmission of YBMV to Portugese laurel,

Japanese apricot, rose (Rosa sp. cv. 'Ragged Robin'), Japanese kerria (Kerria

japónica), desert peach and myrobalan plum—the last by passage through desert

almond (653, 654). YBMV also has been graft-transmitted to Manchu cherry

(^99).

The virus was transmitted to cowpea, tobacco, bean, and cucumber in

expressed juice in 1954 (755, 760). Karle (341) extended the herbaceous

host range to include some members of each of the following plant families:

156
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE I57

Amaranthaceae, Caryophyllaceae, Chenopodiaceae, Compositae, Cucurbitaceae,

Geraniaceae, Leguminosae, Malvaceae, Solanaceae, and Rosaceae. He reported

that the best herbaceous indicators for YBMV were Bountiful bean {Phaseolus

vulgaris), Virginia blackeye cowpea {Vigna sinensts), tobacco {Nicotiana rustica

and N. tabacum), and National Pickling cucumber {Cucumis sativum).

Symptoms

Peach and fiectarine.—Symptoms are most clearly expressed in the spring as

soon as the earliest leaves have expanded. Growth from some of the leaf buds

is either arrested or severely retarded, producing very short tufts of tiny, paleyellow leaves. The tufts often turn brown and die before attaining a length

of more than 2 to 5 mm., but some may grow slowly to a length of 5 to 10 mm.

and appear to remain in an arrested state of development. This severely

retarded growth stands out in sharp contrast to normal-appearing leaves on

the same branch or in other parts of the tree. However, as the season progresses,

many of these retarded, partially developed yellow leaves expand into small

rosettes of dwarfed, distorted, yellow-green leaves (figs. 72, 73).

Many tufts die with the onset of hot weather, leaving many bare shoots

on the affected limbs. The reduced current-season growth and relatively sparse

foliage give the diseased tree an open or thin appearance so that it is possible

to see through the lower half of the tree.

The first symptom to appear in the leaves of a newly infected tree are chlorotic

blotches or spots in the leaf blades—the "mosaic" phase. These chlorotic

blotches and spots are produced on shoots into which YBMV has recently

moved. They are irregular in outline, feather-edged, and almost without

exception follow along the main veins. The blotches commonly occur toward

the base of the leaf and predominantly on one side of the midrib. When the

blotches involve smaller veins, they appear to leak out into the green portions

of the leaf. They are accompanied by a leaf blade distortion which often takes

the form of a pinching, puckering, and corkscrewing, and lateral bending of

the leaf blade toward the chlorotic areas. Sometimes the yellow spots consist of

small chlorotic flecks approximately 1 mm. in diameter. The chlorotic areas

frequently die and drop out, resulting in holes and tattering (fig. 74).

In the second year of infection, yellowish, severely retarded growth from

the buds—the "yellow bud" phase—predominates, and the twigs bearing these

buds usually die by mid-July. Both types of symptoms may occur on the same

twig, but often only yellow buds will be present in a tree. The "mosaic"

phase may be observed in leaves in various stages of development. In very

mild cases, and on trees which are in the early stages of infection, the only

symptoms to be found may be a few mottled leaves which may or may not

be distorted. In such cases, painstaking and thorough examination of the tree

is necessary to detect these symptoms.

The virus moves slowly upward in infected trees so that, after several years,

fruit is produced only on shoots at the branch extremities. The limbs, and
158 VIRUS DISEASES OF STONE FRUIT

larger branches become sunburned because of sparse foliage and often succumb

to wood-boring insects. Infected trees progressively decline into worthless

snags (fig. 75).

Symptoms of yellow bud mosaic in infected trees may vary depending on

the age of the trees at the time of infection and how long the trees have been

FIGURE 72.—Peach shoot affected by yellow bud mosaic showing retarded buds and

two almost normal spurs on right; healthy shoot on left.
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE I59

infected. Young, thrifty trees, 3 to 8 years old, that become infected are the

best indicators for the presence of YBMV in the soil. They usually show

symptoms better than trees that are inoculated at a later age. Any particular

infected tree may express strong and abundant diagnostic symptoms one year

and mild and sparse symptoms the next year. Symptoms apparently are influenced

by environmental conditions, particularly moisture and temperature.

Spread of YBMV within an orchard occurs slowly and mostly to trees

adjacent to infected ones, gradually enlarging the original area of infection.

FIGURE 73.—^Peach shoots affected by yellow bud mosaic, some dying and others

developing rosettes of small leaves.
160 VIRUS DISEASES OF STONE FRUIT

FIGURE 74.—Chlorotic spots and blotches, vein feathering, and distortion in leaves

of Elberta peach afîeaed by yellow bud mosaic.

In some orchards, spread occurs more rapidly in the direction of flowing irrigation water rather than at right angles to it. Frequently, a focus of infection

in an orchard occurs at or near the outside row, and the spread to adjacent

trees affects areas in a more or less semicircular shape with eventual enlargement

of the area in an irregular pattern.

Replants in old infected orchards may become infected by the second or

third year after planting. Sometimes, seedlings 2 years of age or older,

originating from peach pits under bearing trees, escape destruction from

cultivation tools and become infected from soil and develop typical symptoms

of yellow bud mosaic. Sometimes symptoms can be found only on these

seedlings and not in the old trees above them, although the latter are known

to be infected with the virus.

S. H. Smith and J. A. Traylor (unpublished data) have observed stem pitting

and bark thickening in yellow bud mosaic infected trees examined in the

Sacramento and San Joaquin Valleys. This was the first report associating these

symptoms with this disease in peach.

No flower symptoms are known. Flower buds commonly drop from severely

affected branches and few, if any, fruit are set. Consequently, fruit production

is seriously reduced in severely affected trees.

Almond—Symptoms of yellow bud mosaic in almond consist mainly of sparse

foliation, tufting, and lack of terminal growth. Some affected trees show considerable killing of spurs and of the lateral buds and shoots along the branches,

giving the trees an open or thin appearance (fig. 76.) Texas almond is most

severely affected by YBMV, often showing symptoms extending into the upper-
HANDBOOK NO. 437, U. s. DEPARTMENT OF AGRICULTURE 161

most portions of the tree. In this cultivar, one or more normal shoots are frequently produced on otherwise completely diseased branches. Sprouts from the

trunks of infected trees usually show rosette-type growth. Unusually wrinkled,

rough fruits with hulls abnormally thickened have been observed on diseased

branches of Texas almond (fig. 77). Reduction in yield is directly proportional

to severity of symptoms (342). In trees of Nonpareil and Ne Plus Ultra, yellow

bud mosaic symptoms seldom show above the main trunks or bases of the

scaffold limbs. Occasionally, leaf symptoms resembling those in peach have been

seen on almond leaves.

Sweet cherry.—Affected trees are characterized by a bare-limb appearance

which starts in the lower portion of the tree and advances slowly upward.

The disease kills spurs, twigs, and small branches as it moves. Leaves on

affected spurs are undersized with prominent whitish secondary veins that branch

off from the midrib almost at right angles, resembling those of elm leaves.

Initial shock symptoms from YBMV inoculation may appear in some cherry

leaves in the form of chlorotic blotches associated with the veins, resembling the

leaf blotches observed in peach leaves infected with the virus. Enations develop

on the underside of affected leaves, most commonly adjacent to the midrib.

They are smaller, fewer, and accompanied by less leaf distortion than the

enations caused by cherry rasp leaf virus.

FIGURE 75.—^Lovell peach tree in advanced stage of yellow bud mosaic.
162 VIRUS DISEASES OF STONE FRUIT

Transmission

Xjphinema americanum Cobb, the dagger nematode, is the natural vector of

YBMV {645, 646). The virus can be transmitted through grafts and mechanically in expressed sap (340, 341, 735, 757, 760). Peach, almond, mahaleb, and

FIGURE 76.—Yellow bud mosaic in Texas almond: A, healthy branch; B, affected branch

with dead and sparsely foliaged spurs.
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 163

mazzard rootstocks become infected when grown in infested soil. In limited

trials in the orchard, Myrobalan 29C, myrobalan seedlings, and Marianna 2624

did not become infected for 3 years when planted in infested soil (George

Nyland, personal communication). Teliz et al. (646) succeeded in transmitting

YBMV to the roots of Royal apricot and damson plum seedlings by X.

iimericanum.

B
164 VIRUS DISEASES OF STONE FRUIT

FIGURE 77.—^Yellow bud mosaic in Texas almond: healthy fruit on left; diseased fruit

on right. Note roughness and larger size of diseased fruit due to thicker hulls.

Characteristics of the Virus

The YBMV particle is spherical with a diameter close to 25 m^i. (107, 108,

711). Cadman and Lister {107) reported that the virus lost its infectivity when

infective plant sap, diluted one-fifth with distilled water, was heated for 10

minutes at 60° C. but not at 58°, or when diluted more than 10* with distilled

water. Sap lost little infectivity when kept at —10° for 24 hours but lost

SO to 90 percent in 5 days at this temperature. They considered YBMV to be

less stable than other viruses of the ring spot type, such as arabis mosaic and

tomato black ring, because its infectivity was destroyed by most of the customary

means of clarifying sap. The virus was inactivated in vivo in buds of infected

peach trees exposed to 38° for 21 days (George Nyland and A. C. Goheen,

unpublished data).

Control Measures

Strict adherence to quarantine regulations, which restrict the movement of

susceptible host material and soil from infested properties and areas, and the

use of propagating stock free from all known viruses are the primary preventative measures for controlling yellow bud mosaic.

To suppress or eradicate the disease in infested orchards, the following steps

are recommended: (1) If the affected area involves only a small part of the

orchard, the infected trees and adjacent trees in at least two rows beyond

should be removed. If several areas of diseased trees are present in a contiguous
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 165

planting, complete removal of the block may be advisable. Trees to be removed

should be pretreated with a herbicide applied into cuts made with an ax into the

bark and well into the wood around the tree trunks near the ground to aid in

killing the roots. As many roots as possible should be removed with the trees.

(2) The infested soil should be fallowed for at least two growing seasons,

preferably three, after tree removal. The fallow period must be long enough

for all tree roots to die, plus an additional year for the nematodes feeding on

the roots to die. The land should be kept free of weeds during the entire

fallow period because many weeds are hosts for both the virus and the nematode

vector. (3) Fumigate soil with a nematocide. Specific dosages will depend on

soil type and material. (4) Replant with nonhosts where fumigation is not

to be done. These include most plums and prunes on plum rootstocks, and

probably walnuts, although specific tests have not been made.

Remarks

Gooding et al. {267) showed that the grape yellow vein disease found in

California vineyards was caused by a soil-borne virus serologically related but

distinct from TomRSV. Teliz et al. {643) demonstrated that Xiphinema

dmericanum was the natural vector of grape yellow vein virus. Cadman and

Lister {101, 108) compared isolates of YBMV, TomRSV, and tobacco ring

spot virus (TRSV). Based on plant protection and serological tests, they concluded that YBMV and TomRSV were closely related and should be regarded

as synonymous. They found no relationship between YBMV-TomRSV and

TRSV.

Eola rasp leaf of cherry, a soil-borne virus disease described from the

Willamette Valley, Oreg., is caused by TomRSV {437), with symptoms very

similar to those found in YBMV-infected cherry trees in the San Joaquin Valley

of California (George Nyland, personal communication). A Lovell peach

seedling bud-inoculated with Eola rasp leaf in Oregon developed typical yellow

buds in the second season after inoculation {437).
VIRUS DISEASES OF PLUM AND PRUNE

PLUM LINE PATTERN

H. C KIRKPATRICK and R. W. FULTON

Causal Virus

Plum line pattern virus (PLV).

Synonyms

Shiro line pattern, plum mosaic, peach line pattern, and banded chlorosis of

oriental flowering cherry.

History and Distribution

Line pattern has been reported on plum, plum nursery stock, peach and

oriental flowering cherry in Canada, and throughout the United States (33, 120,

130, 679, 729) \ on plum, peach, and apricot in New Zealand {131) \ and on

plum in Great Britain {341), Italy {116), India {19), and Germany {28).

Line pattern probably is widely distributed in most of the plum-growing areas

of the world.

Economic Hosts

Line pattern occurs in nature frequently on Red June and Abundance Japanese

plum; on Amanogawa, Shirotae (Mount Fuji), Naden, Kwanzan, and Temari

oriental flowering cherry; and, to a lesser extent, on peach seedlings {130). It

occurs on myrobalan plum rootstocks in nurseries, on a number of European

plum and greengage cultivars, and on damson plum and mahaleb cherry in

New Zealand {131).

Other Hosts

Prunus spp. and cultivars that have been experimentally infected include:

Liberta, J. H. Hale, Rochester, and Carman peach; David peach; Becky Smith

Japanese plum; Shiro, First, Ember, LaCrescent, Climax, Duarte, and Marianna

2624 hybrid plum; Italian Prune, Early Golden Drop, German, Imperial Gage,

Reine Claude, Lombard, Grand Duke, and Richards Italian European plum;

Fviamath plum; sweet cherry seedlings and cultivars Black Tartarian, Napoleon,

Gil Peck, and Seneca; Montmorency sour cherry; Amur cherry; pin cherry;

Bessey cherry; Yoshino flowering cherry; common chokecherry; desert peach;

sloe plum; flowering almond; and Drake, Nonpareil, and Mission almond {28,

130, 211, and P. W. Cheney and E. L. Reeves, unpublished data). Niagara

apricot appeared to be a symptomless host. The virus has been transmitted

mechanically to 86 herbaceous species representing eight families {372, 312).

Symptoms

Symptoms are invariably confined to leaves emerging in the spring when the

daily mean temperatures are below 13° to 15° C, and they persist in these leaves

166
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 167

throughout the season. Therefore, in the summer, most of the leaves on

infected trees are symptomless.

Plum.—Commercial plum cultivars are variable in disease expression. Symptoms in leaves consist of lines, bands, and oak-leaf patterns. Vein-banding and

small chlorotic rings also may be present. In Shiro plum (fig. 78, A) and

myrobalan plum (fig. 79, D), the patterns are conspicuously yellow or yellowgreen in the spring and become a vivid creamy white early in the summer. In

Abundance plum, the patterns resemble those in Shiro but are less conspicuous

and more transient. The symptoms consist of chlorotic rings, spots, and line

patterns bordered with a white to bright golden band. In Italian Prune, Reine

Claude, and First plums, very faint oak-leaf patterns may appear although in

Italian Prune they may be absent in some seasons. In German and Grand Duke

fine, irregular yellowish lines predominate.

Willison and Berkeley {150) found that Imperial Gage and Early Golden

Drop plum and some myrobalan plum seedlings carried the virus without

developing symptoms. Other myrobalan seedlings showed a golden net pattern

bordering the veins and veinlets (768). In Lombard plum only a few leaves

are affected. In these, faint markings of the Shiro type may be noted, but the

more characteristic symptom is a regular, chlorotic, and eventually necrotic, line

outlining the marginal triangular section of the lamina and usually distorting

the leaf.

Peach.—No differential reaction of peach cultivars to infection by PLV was

detected by Willison (130). The characteristic symptom is a fine, irregular,

wavy band on each half of the lamina, usually forming a symmetrical pattern

(fig. 78, B). Some leaves are marked with a network of fine lines, or a golden

net pattern, fine confluent rings, vein-banding, or an oak leaf pattern, or both of

the last two. Markings on peach leaves are generally pale green or more rarely

yellow-green, and usually disappear during the summer. The number of affected

leaves and the predominant type of symptom varies from year to year in

response to the temperature conditions in the spring (130).

Sour cherry.—In Montmorency sour cherry, the symptoms in the early stages

of infection are inconspicuous pale-green bands, spots, and coarse rings; a few

necrotic spots also may be present. In the following year, sharply defined lines

do not appear until early June (fig. 79, B). These lines are sometimes chlorotic,

but more commonly they appear as watermarks seen best by transmitted light

(130). Symptoms observed by P. W. Cheney and E. L. Reeves (unpublished

data) in Washington were vein-banding, mosaic mottle (light-green mottle

developing to a yellow or orange mottle with large necrotic areas resembling

those of rusty mottle), and some leaf cast.

Mdhaleb cherry.—Symptoms in mahaleb consist of oak-leaf patterns, coarse

lines, and rings sometimes darker and sometimes paler than the rest of the leaf

(hg. 19, C). Short, narrow, yellow bands along the larger veins are of diagnostic value. In these areas the veins, and frequently part of the yellow-band
168 VIRUS DISEASES OF STONE FRUIT

FIGURE 78.—Plum line pattern. A, Chlorotic lines and patterns and vein netting on

Shiro plum leaves; B, chlorotic lines and patterns on peach leaves.
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE Igg

tissue, eventually become necrotic and either split or drop out. The severity of

symptoms varies with individual trees. One strain of PLV from Michigan

produces a golden blotch mottle with some ring spots, whereas a strain from

Oregon, from Amanogawa flowering cherry, produces a banded oak-leaf patFlGURE 79.—^Plum line pattern. Chlorotic rings, patterns, or vein netting in A, Amanogawa oriental flowering cherry; B, Montmorency cherry; C, mahaleb cherry; and

D, myrobalan plum.
J^YO VIRUS DISEASES OF STONE FRUIT

tern in some leaves and banded circular spots or irregular line patterns in others.

The majority of leaves show no symptoms (130).

Sweet cherry.—Symptoms in Napoleon and Black Tartarian sweet cherry are

divided into two groups. The first is made up of tiny rings, larger coarser rings,

and faint oak-leaf patterns which are more or less transient. The second group

consists of persistent watermark lines and more conspicuous yellow or creamy

white hnes, up to 1 mm. in width, which form striking irregular patterns (130).

Black Tartarian is considered resistant to PLV in Washington (P. W. Cheney

and E. L. Reeves, unpublished data). In the young foliage of Bing and Black

Republican, PLV causes faint line pattern symptoms, which later become pronounced. Chlorotic mottle develops as the trees become older. Zeller and

Milbrath (768) found that mazzard seedlings vary greatly in disease expression.

Some seedlings may show a well-formed, banded oak-leaf pattern while others

show an irregular chlorotic or red mottle. In some seedlings, affected tissue

becomes necrotic and falls out (130).

Oriental flowermg cherry.—Symptoms are similar in all affected cultivars of

Oriental flowering cherry. Leaf borders are faintly chlorotic to pronounced

golden or white (fig. 79, A). The patterns are sometimes made up of large

rings but more often are an oak-leaf type (130).

Almond.—Drake, Mission, and Nonpareil all have line pattern symptoms

similar to those in peach. A fine light-green, vein-banding network is a

prominent symptom, with some irregular oak-leaf or chlorotic areas in a few

leaves.

Herbaceous hosts.—Plum line pattern virus, originally from Myrobalan 29C,

was mechanically transmitted from Shiro plum to Chicago Pickling cucumber

and other herbaceous plants (372). The herbaceous host range for PLV was

extended by using another source of the virus, which was separated from other

Prumis viruses by passage through Abundance plum (474, ^'>12). Some differences were noted in the herbaceous host ranges of these two isolates. However,

evidence based on serology indicates the strains react to the same antiserum (A.

Q. Paulsen and R. W. Fulton, unpublished data). The originally described

PLV culture, while not a lineal propagation, was related in host range and

symptom data with the PLV culture used by Paulsen and Fulton and was

closely related serologically. The symptoms on four herbaceous hosts, which

can be used for an index or for greenhouse culture of PLV, are presented rather

than the entire herbaceous host range.

Physalis floridana. Symptoms of plum line pattern develop in new growth

following juice inoculation. A light-green or chlorotic interveinal blotching is

noticed first, followed by leaves which develop chlorotic vein-banding or ring

spots. Some leaves show a chlorotic or light-green, oak-leaf pattern (fig. 80, A).

No other stone fruit virus has been transmitted to P. floridana, and this host is

considered part of a selective host range to isolate PLV from cultures of mixed

content (374).
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 171

Nicotiana megalosipbon. Chlorotic or necrotic local lesions and ring spots

occur as primary symptoms in inoculated leaves. Systemic chlorotic or light-green

mottle with necrosis develops in the new growth (fig. 80, B). This host is

commonly used for propagating PLV (312).

Vigna cylindrica. Inoculated leaves develop necrotic local lesions or rings

followed by a systemic mottle and necrosis of new growth (fig. 80, C). The

primary symptom is effective for local lesion assay studies (312).

Cucumis sativus. Chicago Pickling cucumber cotyledons, inoculated as the first

primary leaf is expanding, will develop some chlorotic lesions. When the

cotyledons are cleared of chlorophyll and stained in iodine-potassium iodide

solution, starch rings or broken rings are revealed (fig. 80, D). PLV does

not become systemic in cucumber (372).

Transmission

The virus is easily transmitted in tree hosts by budding and bark-patch

grafting. No evidence of an insect vector has yet been found.

Mechanical transmission from young Shiro or mahaleb leaves with line

pattern symptoms to herbaceous hosts has been accomplished by homogenizing

infected tissue at 1:10 (w/v) dilution in 0.001 M neutral phosphate buffer

containing 3 percent nicotine sulfate (40 percent solution), the slurry centrifuged

at 6,000 g. for 15 minutes to remove cell debris, and the supernatant centrifuged at 74,000 g. for 1 hour to sediment the virus from the nicotine sulfate

solution (372). Alternatively, inoculum may be prepared in 0.03 M phosphate

buffer, pH 8.0, containing 2-mercaptoethanol, 0.01 to 0.02 M. Sodium

diethyldithiocarbamate, 0.01 M, is added when inoculum is prepared from

rosaceous species (A. Q. Paulsen and R. W. Fulton, unpublished data).

Mechanical transmission from PLV-infected P. floridana to mahaleb cherry

seedlings was positive when the inoculum had been partially purified and concentrated by homogenizing at 1:10 (w/v) in 0.001 M neutral phosphate buffer

including 0.001 M cysteine HCI, centrifuging at 6,000 g. for 15 minutes, and

ccntrifuging the supernatant at 85,000 g. for 1 hour. The pellet was suspended

in the buffer at a concentration of 1:2 (original w/v). The inoculum v/as

applied with an airbrush to the leaves of vigorously growing mahaleb seedlings

in the 8- to 12-leaf stage. Symptoms of plum line pattern in the new leaves

developed within 16 to 20 days after inoculation (372).

Cuscuta campestris and C. subinclusa failed to transmit PLV from infected to

healthy Nicotiana megalosipbon. C. campestris did transmit PLV from N.

megalosipbon to petunia but C. subinclusa did not. Attempts to transmit PLV

from petunia to mahaleb or from mahaleb to Italian Prune through C. campestris

were negative. PLV could not be recovered in mechanical inoculations from

dodder tissue (R. W. Fulton, unpublished data).

Attempts to transmit PLV with apterous adults of Myzus persicae from infected petunia or Vigna cylindrica were negative (312).
172 VIRUS DISEASES OF STONE FRUIT

FIGURE 80.—Plum line pattern. Herbaceous hosts inferted with plum line pattern virus

(PLV) : Leaves of A, Physalis floridana showing chlorotic spots, rings and patterns;

B, Nicotiana megalosiphon showing chlorotic mottle and necrosis; C, Vigna cylindrica

showing necrotic local lesions; and D, Chicago Pickling cucumber cotyledon, cleared

of chlorophyll and staineU with iodine-potassium iodide solution to show starch lesions.
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE I73

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174 VIRUS DISEASES OF STONE FRUIT

Characteristics of the Virus

A. Q. Paulsen and R. W. Fulton (unpublished data) have purified PLV with

two cycles of high- and low-speed centrifugation. Inoculated leaves of Nicotiana

megdosiphon were homogenized in 0.02 M phosphate buffer, pH 8.0 (1.5

ml./g. leaf), containing 0.02 M 2-mercaptoethanol. Clarification of the first

supernatant was made by adjusting the pH to 4.8 with 0.1 M citric acid. The

green coagulum was removed by centrifugation and the extract adjusted to pH

6.5. After concentrating the virus by centrifugation, the remaining host protein

was precipitated with the gamma-globulin fraction of antiserum to N.

megdosiphon protein.

Purified PLV had an A2eo/A28o ratio of ca. 1.7 and formed two zones in

density gradients at pH 6.0-7.0. The virus was about 30 m|u. in diameter in

negatively stained preparations, and the particles are easily disrupted (fig. 81).

PLV is quite unstable in crude sap but infectivity can be maintained if

infected tissue is ground in buffer with 0.02 M 2-mercaptoethanol. Under

optimum conditions, sap of some infected species is still infectious when

diluted 1:6400. Infectivity is greater in diluted than in undiluted sap of most

FIGURE 81.—^Negatívely stained plum line pattern virus, X 94,000 (tobacco mosaic virus

was added as a standard of size).
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE I75

species. The thermal inactivation point of PLV in diluted sap is 66° C. for a

10-minute exposure.

Control Measures

It is doubtful whether roguing diseased trees should be recommended {150).

Use of disease-free stock and scion material for nursery propagation is suggested.

Remarks

The combination of PLV with prune dwarf virus increased the virulence

of prune dwarf in some hosts and of line pattern in others {150).

The similarity of symptoms in peach and plum caused by PLV and apple

mosaic virus (AMV) has been a confusing issue. AMV was transmitted from

apple to peach and from peach to apple {570). The symptoms in peach were

similar to those induced by PLV. Apple mosaic symptoms were induced in

apples by PLV, and plum line pattern symptoms were induced in Shiro plum by

AMV {245 ). Two isolates from plum showing line pattern, and AMV isolates

from apple, produced similar symptoms in peach and apple {^41). A. F.

Posnette (unpublished data) has now shown one of the line pattern isolates in

plum to be serologically identical to AMV, whereas the second isolate is

serologically Prunus ring spot virus. A vein-banding strain of AMV causes

what appears to be line pattern in plum {481). Fulton {252) presented

serological evidence that a line pattern of plum (DLPV) reacted only weakly

with AMV antiserum. Host range and symptom data indicate Cation's originally

described PLV culture to be similar to the PLV culture purified by Paulsen

and Fulton, but both differ somewhat from the PLV culture of Kirkpatrick.

All three PLV cultures, but not DLPV, reacted with antiserum to PLV made

after the development of methods of the purification of PLV were determined

(A. Q. Paulsen and R. W. Fulton, unpublished data). This indicates strain

variation of PLV. AMV cultures were not serologically related to PLV. It is

clear that line pattern symptoms in plum and peach can -be induced by viruses

other than PLV.
PRUNE DIAMOND CANKER

H. KEITH WAGNON and HAROLD E. WILLIAMS

Only an occasional tree with prune diamond canker was noted prior to 1915

(619), but during the following 20 years its increased occurrence in newer

plantings attracted considerable attention. Extensive investigations on the disease

were started about 1927 by R. E. Smith and culminated in a report in 1941

with evidence of its virus nature (620). Although the disease has been observed

during the years following this report (691, 701), there has been very little

investigative work on it. The disease is known only in California and affects

only the French (Agen) prune cultivar (Prunus domestica.) It was of particular

concern in Napa and Santa Clara Counties (622) and was rare in the Sacramento and San Joaquin Valleys. When it was found to be associated with the

use of infected propagating budwood, nurseries became more selective in their

dioice of budwood (620, 701), and as a result the incidence of the disease

has decreased in newer plantings in Napa and Santa Clara Counties. The

disease has not been observed during the last 25 years in the Sacramento and

San Joaquin Valleys, where higher temperatures are believed to suppress the

development of symptoms. Many new, large plantings of French prune are

being made in California, particularly in the Sacramento Valley, with stock

propagated from selected budwood sources free of Prune diamond canker virus

(PDCV).

Recognition of prune diamond canker depends on the occurrence of bark

cankers on the trunk and older branches of a tree. No fruit or leaf symptoms

are recognized. The cankers become apparent as the bark becomes thickened

and roughened in a somewhat diamond-shaped area frequently observed around

such wounds as pruning cuts (iig. 82). The wood may or may not be exposed.

In some infected trees, the cankers may not be distinct, but the symptoms may

consist of roughened bark on older parts of the tree. Slight roughening of bark

is sometimes seen on bark only a year or so old.

PDCV has been transmitted only by grafting (620). Symptoms may develop

in 2 years, but generally do not do so until several years later. Young trees

propagated from infected buds may not develop symptoms in the orchard until

5 to 8 years of age. When diseased prune scions are grown on apricot, almond,

peach, myrobalan plum, and Marianna 2624, these understocks do not

develop symptoms. In at least one of these (myrobalan plum), the disease

was demonstrated to move through the rootstock from an infected scion on one

side to a healthy scion on the other side of the tree.

Information on virus morphology, properties, and serological relationships is

lacking. Graft-inoculation tests on Shiro-fugen flowering cherry made with buds

from different infected French prune orchard trees indicate that there is no

176
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE I77

relationship between the occurrence of PDCV and strains of Prunus ring

spot virus complex.

Prune diamond canker is of economic importance only in French prune.

Affected trees at first may show stimulated growth, but they will decline in

vigor as they grow older. Secondary causes may contribute to a more rapid

decline of the tree. Fruitfulness also declines, although the individual fruits may

FIGURE 82.—French (Agen) prune tree affected by prune diamond canker showing

discrete cankers above and general rough bark below.
178 VIRUS DISEASES OF STONE FRUIT

be large. The disease is best controlled by using PDCV-free planting stock. If

tested budwood source clones are not available, young trees should be avoided

as budwood sources, because they may be infected but have not yet developed

symptoms.
PRUNE DWARF

R. M. GiLMER, GEORGE NYLAND and J. DUAIN MOORE

Causal Virus

Prune dwarf virus (PDV),

Synonyms

Diseases incited by PDV in economically important stone fruits have been

described under a variety of names. In plums and prunes, the disease has been

termed prune dwarf, prune mosaic, willows, and shoestring (312). In peach,

Muir peach dwarf (329) and peach stunt (432) are incited by PDV, and some

strains incite gummosis of apricot (214 and P. R. Fridlund, unpublished data).

In sweet cherry, PDV may induce symptoms indistinguishable from tatterleaf

(733) and some other ring spotlike symptoms, or it may be present without

symptoms (312).

In sour cherry, the names sour cherry yellows (333) yellow leaf, physiological

yellow leaf (626), physiological leaf drop (264), and boarder tree (334) have

been applied to the disease. The initial acute symptoms in sour cherry have

been called chlorotic mottle and chlorotic ring spot (233). These symptoms

were undoubtedly often described as Prunus ring spot, an entirely different

disease, in much of the literature before I960.

The virus itself also has several synonyms (249) ; sour cherry yellows virus

(333), "yellows" strain of ring spot virus (447, 432), peach stunt virus

(432), Muir peach dwarf virus (329), and virus B (22:5, 226, 227). A proposal to conserve the name sour cherry yellows virus against the earlier name

prune dwarf virus (249) has not been generally accepted, although the former

term is preferred by some authors (182, 184, 246, 248, 249, 709).

History and Distribution

Chronic effects of PDV infection on the tree habit and fruit production of

sour cherry were perhaps observed in France in 1768 and in England in 1839

(248). The virus may have been introduced into North America early in

the 19th century in the cherry cultivar Large Montmorency (248).

Yellows of sour cherry was observed in New York in 1919 by Stewart (626)

and again in 1928 by Gloyer and Glasgow (264), who suggested that the

symptoms resulted from winter injury.

In 1936, Thomas and Hildebrand (631) described prune dwarf in Italian

Prune in New York and Ontario and demonstrated the virus etiology of the

disease. Keitt and Clayton (332, 333) soon afterwards showed that sour cherry

yellows was a virus disease. Concurrently, Hutchins et al. (329) demonstrated

that Muir peach dwarf, observed in California as early as 1920, was also caused

by a virus. As will be shown later, each of these diseases is induced by PDV.

PDV was perhaps the first of the tree fruit viruses to be transmitted

179
180 VIRUS DISEASES OF STONE FRUIT

mechanically to herbaceous plants (93, 475, 680), a fact that has greatly

facilitated research on it and many other viruses of tree fruits. Although PDV

was demonstrated to be graft transmitted quite early {552, 631), its method

of spread in the orchard was not discovered until 1963 (256, 257, 230, 261).

PDV is prevalent and widely distributed in sweet and sour cherries throughout North America and appears equally common in Europe {340, 762^ and

Australia {307). It undoubtedly occurs in all areas where these fruits are

grown. In plums and prunes, where the virus was first discovered, prune dwarf

is a rare disease, although a few infected trees have been found in New York,

Ontario, and British Columbia {631).

Natural infections in peach occur in California {529) but have not been

reported elsewhere.

Economic Hosts

PDV is very prevalent in sour cherry and sweet cherry, and natural infections

occur in peach and occasionally in European plum. Damson plum is a symptomless carrier of PDV {72S and R. M. Gilmer, unpublished data). Mazzard and

mahaleb, the common cherry rootstocks, are frequently infected without

evident symptoms {125, 123, 236).

Thomas and Hilderbrand {631) transmitted PDV to Japanese plum, apricot,

and myrobalan plum with few or no evident symptoms. Fridlund {214) found

that some apricot cultivars developed severe gummosis when infected with PDV,

but others were symptomless carriers. Moore and Keitt (In 534) considered

that Burbank and Abundance plums {Prunus salichía) were immune, but these

cultivars were reported susceptible by Gilmer {242).

All isolates of PDV tested induce a severe localized bark necrosis and gummosis in Shiro-fugen flowering cherry (P. serrulata) ; this host is widely used

as an indicator of PDV and of Prunus ring spot virus (PRSV). Similar symptoms developed in Krassa Severa, a duke cherry, with each of eight PDV

isolates but not with isolates of PRSV {273).

Other Hosts

Moore and Keitt (In 534) inoculated wild American plum, wild black cherry,

common chokeberry, and pin cherry with PDV and recovered PDV from each

of them. Fulton {227) has shown that PDV is readily transmitted to pin cherry

mechanically. Nearly all of 122 Prunus spp. inoculated with virus isolates containing PRSV and PDV (as sour cherry yellows virus) showed symptoms

(242). It was not clear that the symptoms on all the hosts were the result of

PDV infection, but PDV was recovered from a number of species, including:

P. davidiana, P. jasciculata, P. fruticosa, P. glandulosa, P. lyoni, P. maackii, P.

munsoniana, P. mume, P. pensylvanica, P. ssiori, P. tenella, P. tomentosa, P.

triloba, and P. virginiana (R M. Gilmer, unpublished data).

PDV infects a number of herbaceous plant species; Fulton (223) recorded

infection of 86 of 227 species by virus B (PDV), including a number of species

not infected by PRSV. Momordica balsamina and Cyamopis tetragonaloba were
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE Igl

differential hosts for PDV (706). Several squash cultivars—Butternut {246),

Buttercup (447), and Cocozelle (244)—are good diagnostic hosts of PDV

(fig. 83). THhonia speciosa, a composite, is commonly used as a diagnostic

indicator for PDV (246, 589), but is not infected by some isolates (706).

Symptoms

As Keitt et al. (554) suggest, many of the early descriptions of the symptoms

of PDV infections were complicated by the presence of such other contaminating

viruses as PRSV or green ring mottle virus (GRMV). For the most part, the

syndromes described below in sour and sweet cherry are based on inoculations

with PDV isolates purified by single lesion selection in cucurbits or inoculations

by graft transmission from trees in which PRSV and GRMV were absent.

Sour cheiry.—Davidson and George (1S2) have demonstrated that the

severity of acute or "shock" symptoms in Montmorency is governed by the stage

of tree growth at which the inoculations are made. Inoculations in the early

stages of growth result in severe symptoms, and those made late in the season

induce severe symptoms the following year, but those made in midseason just

after terminal growth has ceased, may result in the introduction of the virus

without symptoms.

In newly infected Montmorency trees, chlorotic mottle or chlorotic rings and

flecks develop in the foliage (227, 255). Tissues in portions of the chlorotic

areas may become necrotic and fall from the lamina, resulting in a tattered

appearance (227, 255). As additional leaves develop, the amount of chlorotic

mottle becomes progressively less, and it is often entirely absent in the last

leaves formed. In succeeding years, these acute symptoms are absent or affect

only an occasional leaf. This phase of the prune dwarf syndrome is much like

FIGURE 83.— Bright yellow mottle and vein-banding of Butternut squash induced by

prune dwarf virus.
182 VIRUS DISEASES OF STONE FRUIT

that of ring spot {227), but the etched appearance of ring spot lesions is

absent, and the degree of necrosis is commonly much less {227 and R. M. Gilmer

and K. G. Parker, unpublished data).

Chronic symptoms—leaf yellowing and leaf casting—may appear in the

same year as the acute symptoms, but more commonly do not develop until 1

to 3 years later. Moore and Keitt {476, 477) and Mills {466) have shown that

temperature is a critical factor in the development and severity of leaf casting

yellows symptoms; symptoms are favored by temperatures of about 16° C.

during the postbloom period and are limited or absent at higher temperatures.

In the West, low night temperatures (10° to 16°) alternating with relatively

high day temperatures (30° to 35°) seem particularly favorable for leaf

casting symptoms. With favorable temperatures, leaf casting yellows may recur

each year.

A striking yellow and green mottle appears in the foliage about 3 to 4 weeks

after petal fall. The mottle pattern may be irregular, but more commonly

green is retained along the midrib and larger veins, with the interveinal areas

becoming yellow (fig. 84, A and B). Leaves with these symptoms are soon

cast; many leaves may drop even before any significant degree of chlorosis is

evident.

Older leaves are usually the first to develop mottle, which is often initially

evident on the scale leaves. If temperature conditions are favorable, younger

leaves may develop symptoms in the order of their age. Successive waves of

yellowing and leaf casting may occur in varying severity throughout the early

portion of the growing season, but these gradually decrease in severity and

finally cease as temperatures increase. Under favorable conditions for symptom

development, 30 to 50 percent of the leaves may drop.

On fruiting trees with infections of some duration, the leaves are fewer in

number and somewhat larger in size than on healthy trees. The number of

fruiting spurs is much reduced; those which persist tend to grow into shoots, so

that infected trees eventually develop a willowy growth habit with long bare

spaces on the twigs (fig. 84, C and D). Fruit yields may be reduced by 50 percent or more {184, 578). Although the fruits are fewer in number, they are

large and of excellent quality. If young trees are infected, their growth is

markedly checked {184).

Symptoms in Early Richmond cherry are identical with those just described.

In English Morello sour cherry, the yellow color of leaves is less pronounced

and often is restricted to the leaf margins, and the amount of defoliation is

considerably less than in Montmorency, but the absence of fruiting spurs,

FIGURE 84.—Á-C, Sour cherry yellows in Montmorency cherry; A, Leaf showing irregular

pale-green or yellowish mottling; B, leaf showing retention of green along main veins;

C, affected branch showing willowy type of growth. D, Comparable normal branch

with fruit spurs.
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 183
184 VIRUS DISEASES OF STONE FRUIT

willowy growth habit, stunting of the trees, and reduction in fruiting are as

pronounced.

Sweet cherry.—The initial symptoms of infection are the appearance of large

chlorotic rings or mottle and varying degrees of necrosis and shot-holing of

the foliage (fig. 85), symptoms identical with those described as "tatterleaf"

{755). In some cultivars (Yellow Glass, Giant, Ebony, and Van), chlorotic

rings and mottle, usually with little or no necrosis, recur each year; these

symptoms are generally more prominent in the early leaves and absent in later

leaves. In other cultivars (Emperor Francis, Windsor, Noble, and Hedelfingen),

the recurrence of chlorotic mottle is rare or completely absent, and infected trees

cannot be identified by visual inspection. Yields may be seriously reduced

{540, 709), but some varieties are more tolerant of infection than others. A

strain of PDV, recently described in California {493), induces narrow roughtextured leaves in sweet cherry and reduction in tree growth. Similar symptoms

have been observed in New York (K. G. Parker, unpublished data).

Plum and prune.—In trees of Italian Prune infected with PDV, the leaves

are narrow and straplike in shape, rugose, and somewhat thickened (fig. 86).

Early in the season, the terminals are rosetted with shortened internodes and

narrow leaves, but as temperatures increase, terminal growth may be almost

normal, with normal leaves. In large trees, symptoms may be restricted to a

FIGURE 85.—Chlorotic ring spot and mottle on Yellow Glass sweet cherry leaves induced

by experimental pollination with pmne dwarf vims—infected pollen.
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 185

FIGURE 86.—Strap-shaped rugose leaves of Italian Prune affected by prune dwarf.

portion of the tree, or occasional branches with normal foliage are interspersed

among those with severe symptoms. Hildebrand et al. (312) indicated that the

flower petals were elongated and pistils frequently aborted, but that the fruits

that matured were large and of excellent quality. In Lombard plum (312),

symptoms were similar to those of Italian Prune but considerably milder, and

yield reduction was slight.

In addition to Italian Prune and Lombard, experimental inoculation has produced prune dwarf symptoms on the following cultivars: Giant, Standard,

Emilie, President, Tragedy, Green Gage, and Albion (130 and R. M. Gilmer,

unpublished data). No symptoms are produced on cultivars of Prunus salicina

except by the cherry narrow leaf strain (493).

In controlled temperature experiments in the greenhouse and growth chambers,

a constant temperature of 22° C, beginning at budbreak and continuing until

new growth ceased, completely masked prune dwarf symptoms in Italian Prune.

Exposures of infected potted trees to a constant temperature of 22° for 48 to 72

hours reduced symptom severity or masked symptoms completely on certain

leaves, whereas exposure to 12° for at least 10 hours every 48 hours resulted

in development of typical prune dwarf symptoms. It was immaterial if the low

temperature exposure was during tlie dark period or the light period (J. Duain

Moore, unpublished data).

Peach.—In peach seedlings inoculated in New York, varying degrees of

budkill and terminal dieback appeared in the spring after inoculation the
186 VIRUS DISEASES OF STONE FRUIT

previous fall. Foliation was delayed, and chlorotic rings, mottle, or oak-leaf

patterns appeared in the early foliage. These symptoms were probably caused

by a PRSV contaminant. The seedlings were dwarfed, and their foliage was

an intense deep green. Partial recovery occurred by midseason.

Inoculations of 2-year-old peach trees in the field in California with pure cultures of PDV produced only mild symptoms of stunting in inoculated branches

and rootstock suckers in the spring following fall inoculation, and mild stunting

persisted during the 4 years the trees were observed. Italian Prune growing on

the inoculated peach trees showed severe symptoms of prune dwarf. However,

when PDV was introduced into trees already infected with a pure culture of

PRSV, moderate to severe symptoms of peach stunt were produced in succeeding

years. In all cases, symptoms became less obvious as the season progressed but

recurred each spring (George Nyland and J. A. Milbrath, unpublished data).

The severity of symptoms on mature trees in the orchard varies among infected

trees and is influenced by the pruning system used. The internodes of spring

shoot growth are short, and the leaves on these shoots are more erect and darker

green than those on normal shoots. In older infections, failure of many leaf

buds to grow results in thinly foliated trees and bare branches with few lateral

shoots. The shortened internodes and erect leaves are obvious until late May or

early June after which shoot growth is nearly normal. Infected trees are smaller

than healthy trees and yield less fruit. The disease is very conspicuous in the

Muir peach (329).

Flowering cherry.—Inoculation by T-budding Shiro-fugen flowering cherry

with tissue infected with PDV results in the development of an initially localized

bark necrosis and gumming at the point where the tissue was inserted (fig. 87).

In inoculations at midseason (July), these symptoms are evident in 4 to 6 weeks.

If the infected shoots are not removed, the virus moves down the inoculated

shoot and kills large branches and finally the entire tree. Hampton {275) indicated that the rate of movement averaged about 2 to 5 cm. per day.

Transmission

PDV is readily transmitted by budding or grafting. Gilmer and Brase {234)

reported that the virus was irregularly distributed in sweet cherry and that some

buds from infected trees were free of virus. Hampton {274) recorded some

"false" negatives in indexing buds of infected sweet cherry on Shiro-fugen but

concluded that the virus was present in too low titre for detection rather than

being irregularly distributed.

PDV is readily transmitted through seeds of several stone fruits: mahaleb

{123, 236), sweet cherry {236), and sour cherry {261). One almost certain

instance of transmission through myrobalan seeds has been observed (R. M.

Gilmer, unpublished data). In sour cherry, the percentage of infected seeds may

range from 20 to 70 percent {261), and incidences of PDV infections of 15

to 30 percent have been found in commercial lots of mahaleb and mazzard

seedlings {236). The infection of rootstocks through seed transmission un-
HANDBOOK NO. 437, U. S. DEPARTMENT OP AGRICULTURE JgY

FIGURE 87.—Gumming and necrosis of Shiro-fugen oriental flowering cherry about

6 weeks after insertion of a sweet cherry bud infected with prune dwarf virus (PDV).

doubtedly accounts for much of the prevalence of PDV in sweet and sour

cherries.

PDV also spreads naturally in the orchard. The spread in sour cherry is

much more rapid than in sweet cherry (247). Little or no natural spread occurs

in plum (631).

Typically, the rate of spread in sour cherry orchards is low for the first 2 to

4 years after planting but increases rapidly in trees 5 to 15 years of age until all

or nearly all of the trees are infected. The initial spread is often concentrated

around individual infected trees, but occasional trees some distance from an

infection locus may become diseased. There is a rather pronounced tendency

for new infections to occur downwind from sources of inoculum, and the same

tendency has also been observed in the spread of peach stunt and Muir peach

dwarf (329).
188 VIRUS DISEASES OF STONE FRUIT

In 1961, Gilmer and Way (262) demonstrated that PDV was transmitted by

pollen to seeds of sour cherry. Das and Milbrath (180) demonstrated plantto-plant transmission of PDV in squash by pollen. George and Davidson

(236, 237) soon afterwards showed that PDV was transmitted from tree to

tree in sour cherry by pollen. Tree-to-tree transmission in sweet cherry and

Prunus fruticosa also occurs via pollen (230). Deblossomed sour cherry trees

remained noninfected in the field under conditions where rapid spread of PDV

occurred in controls (236, 231, and J. A. Milbrath, unpublished data). These

data suggest that pollen transmission is responsible for the spread of PDV in

the orchard and that bees and other pollinating insects are indirect vectors.

The reasons for the very slow rate of spread of PDV in sweet cherry (2Al)

and the virtual absence of spread in plum remain obscure, particularly since

sweet cherry cultivars are obligately cross-pollinated. Some limited and inconclusive data (R. M. Gilmer, unpublished data) suggest that in the sweet cherry

cultivars. Van and Hedelfingen, most of the ovules fertilized with infected

pollen abort quickly, perhaps before the virus can be translocated from the

flower. In the cultivars Windsor and Yellow Glass, such ovule abortion is

limited or absent, and these cultivars are rather easily infected experimentally

by pollen. Field trees of cherry, peach, and plum that index negative for PDV

or PRSV may produce some infected seed (205). Ehlers and Moore (196)

and Williams et al. (126) showed that pollen from infected trees contains virus.

The latter workers successfully transmitted PDV to peach by inserting infected

pollen beneath the bark (126).

Characteristics of the Virus

Fulton and his coworkers (226, 221, 211, 106) have determined the properties and morphology of PDV. PDV particles are isodiametric "spheres" about

22 m/x in diameter; it is thus one of the smaller plant viruses (228). The UV

adsorption spectra are typical of nucleoproteins (228).

In cucumber sap, the thermal inactivation point was 44° C. (226), but in

squash extracts stabilized with DIECA and thioglycolate, some isolates were

inactivated at 44°, whereas others remained infective at 54° (106).

At 1:80 dilution, PDV retained about half of the original infectivity after

3 hours at 24° C; there was essentially no loss of infectivity after 3 hours at

0° (226). Polyphenol oxidase completely inactivated PDV, and oxidized

catechol partially inactivated it (211).

The dilution end point is 10-2— 10-^ (R. M. Gilmer, unpublished data).

PDV is rather easily inactivated in infected stone fruits by thermotherapy

at 36° to 37° C for 15 days or longer (488 and R. M. Gilmer and R. D. Way,

unpublished data; P. R. Fridlund, unpublished data).

Control Measures

The first ess£ntial step in control is to provide nursery trees free of the

virus. Both scion and rootstock must be free of PDV, and the seed-source trees
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE IgQ

for seedling rootstocks must be maintained free of PDV and protected from

infected pollen.

In New York, the incidence of PDV in certified cherry nursery trees was

reduced from about 40 percent to a level of 1 to 2 percent by the use of indexed

scionwood, procurement of clean rootstocks, and roguing (233). Elimination

of PDV from the nursery will only be possible when virus-free rootstocks are

available.

Orchards should be planted with certified nursery trees and well isolated

from older infected trees. In the early years of the orchard (age 1 to 5 years),

the trees should be visually inspected when leaf casting occurs (3 to 4 weeks

after petal fall) and any infected trees should be removed. Vacant sites may

be replanted safely. At tree ages of 6 to 10 years, continued removal of infected

trees is probably advisable, even though replanting of vacant sites may not be

economical. In orchards over 10 years of age, roguing of infected trees is

probably useless, and the entire orchard may be left undisturbed until it becomes

uneconomic and is removed entirely.

Replanting vacant sites in old orchards with virus-free trees is not recommended because the young trees will be infected as soon as they reach fruiting

age.

Remarks

Because of its prevalence and the serious yield reductions that accompany

the disease, sour cherry yellows is the most economically serious virus disease

of sour cherries in midwestern and eastern North America. In orchards 12 to 15

years of age, which should be near peak production, the incidence of sour cherry

yellows commonly approaches 100 percent, and the expected yields are reduced

by half or more (184, 378).

In sweet cherries, where the presence of PDV is more difficult to determine,

the effects of the disease in reducing the crop are not as well known. Yield

losses are undoubtedly considerable. Way and Gilmer (709) showed that pollination with infected pollen may reduce fruit sets in sweet cherry by 25 to

90 percent. Posnette et al. (340) have estimated that the complex of virus

diseases in England, of which PDV is an important component, reduces cherry

yields by an estimated 30 percent or more. PDV in peach, especially when

mixed with PRSV, is of considerable economic importance. Tree size and

yields are markedly reduced.

Earlier publications (333, 334) on sour cherry yellows suggested that the

disease resulted from infection by two viruses, PRSV and PDV. Dual infections are common in orchard trees (247, 389, 706)^ but the absence of PRSV

from many trees with yellows (247, 706) and the development of sour cherry

yellows following experimental inoculations with pure PDV isolates (223, 227,

228, 432, and R. M. Gilmer, unpublished data) indicate that PDV alone is

capable of causing the disease. The added presence of PRSV, however, probably

increases the severity of yellows symptoms ( 173, 223 ). Both the. recurrent
190 VIRUS DISEASES OF STONE FRUIT

pxecrotic ring spot and rugose mosaic strains of PRSV can duplicate the

"yellows" symptoms in Montmorency induced by PDV (496). This suggests

caution in identifying the disease solely on the basis of yellow leaves.

PDV exists naturally in a wide spectrum of strains that differ in properties

(226, 706), herbaceous host range (223, 706), rate of movement (234, 433,

728), and symptomatology in Prunus (493, 706). Milbrath (432) has suggested that PRSV and "y^^^^^ws" strains of ring spot virus (=: PDV) may be

strains of a single virus. This hypothesis is not supported by available information on some of the properties of the viruses or serological evidence (226, 227,

233, 669). Although PDV and PRSV are morphologically similar in size and

shape (228) and the symptoms each induces in many Prunus spp. are similar,

these viruses differ in herbaceous host range (22:5) and in some properties (226,

706). Some evidence for the relationship is that there is interference in Montmorency trees between the recurrent ring spot strain of PRSV and PDV. When

healthy scions of Montmorency were grafted on mahaleb rootstocks previously

infected with the recurrent ring spot strain, symptoms showed in the tops the

following year. If Montmorency scions infected with PDV were grafted on

similar mahaleb rootstocks, symptoms of recurrent ring spot did not appear

fully distributed in the tops even after 3 years (J. A. Milbrath and George

Nyland, unpublished data).

PRSV and PDV have many characteristics in common with the NEPO viruses,

the soil-borne polyhedral viruses vectored by nematodes. The individual viruses

of the NEPO group do not share common antigens, but there is clear evidence

of natural affinity among members of the group (104). There is no evidence

that PRSV or PDV are soil-borne, but it is conceivable that the viruses have

become separated from a vector that may exist in the area of origin.
VIRUS DISEASES OF SOUR CHERRY

BARK SPLITTING IN MONTMORENCY CHERRY

H. R. CAMERON

The bark splitting virus (BSV) was first reported in Montmorency sour

cherry in 1954 (112). There are no known synonyms, but the symptoms incited

in apricot by this virus are similar to those reported by Blodgett and Twomey

(73) for apricot gummosis. The BSV was discovered in Montmorency trees

budded with Napoleon sweet cherry from Oregon.

Symptoms incited by the virus have been described on Montmorency sour

cherry and apricot. In Montmorency, narrow, brown stripes appear on the

new shoots in midsummer. The bark usually splits for several inches or more

along these stripes and gum may be exuded (fig. 88). Symptoms recur in

succeeding years but usually not on all shoots and only on the current season's

growth. Affected shoots tend to bend away from the trunk. In subsequent years,

the areas of original splitting are somewhat flattened, and the limbs are

weakened at these points. Symptoms on apricot are more striking and consist

of gum pockets breaking through the bark. The gum flow is excessive, and

all of the new growth dies back. A new flush of growth starts at about the

time the tree appears to be dead. The gumming and dieback appear again, and

the process is repeated until the tree dies. The virus has not incited symptoms

on sweet cherry, Italian Prune (Prunus domestica), Shiro-fugen and Kwanzan

flowering cherry (P. serrulata), or Abundance and Burbank plum (P. salicind).

The virus was recovered from symptomless peach seedlings 13 years after

they had been inoculated (J. Duain Moore, unpublished data).

The virus is easily transmitted by grafting, and symptoms are usually observed

on the new growth the year following inoculation. Even though the bark

splitting virus is widespread in Oregon sweet cherry orchards, it has not been

known to spread to adjacent Montmorency trees.

191
192 VIRUS DISEASES OF STONE FRUIT

FIGURE 88.—Splitting and necrosis of the bark of current-season growth on Montmorency

cherry inoculated with bark splitting virus (BSV).
GREEN RING MOTTLE

K. G. PARKER, P. R. FRIDLUND, and R. M. GILMER

Causal Virus

Green ring mottle virus (GRMV).

Synonyms

Green ring yellows; constricting chlorosis; rough bark of oriental flowering

cherry; epinasty of oriental flowering cherry.

History and Distribution

Green ring mottle of sour cherry was first reported in Michigan in 1937;

by 1942, the disease was also observed in New York, Wisconsin, and Ontario

(347). In 1945, GRMV was transmitted from symptomless sweet cherry trees

in Oregon (461 ) and has since been recovered from symptomless sweet cherries

in Washington (223), New York (247), and Switzerland (600). Leaf symptoms resembling those in sour cherry were reported in duke cherry in Idaho

in 1955 (291).

A rough bark of oriental flowering cherry was observed in New York in

1937 (309) and in Oregon in 1942 (460). In 1959, a virus-induced epinasty

of oriental flowering cherry was reported in New Zealand, and the same virus

was recovered from symptomless sweet cherry and mazzard clonal rootstocks

(1). Subsequent investigations (21, 223, 431) demonstrated that rough bark

and epinasty were induced by GRMV and not by Prunus ring spot virus

(PRSV) as previously supposed. This point should be kept in mind when referring to the early literature.

Economic Hosts

Natural infections of GRMV occur in Montmorency and English Morello

cultivars of sour cherry (Prunus cerasus) and in oriental flowering cherry (P.

serrulata) (1, 309, 460).

Other Hosts

Infections without symptoms are common in sweet cherry (P. avium) (213,

213, 223, 247, 443, 467, 600); the cultivars Bing, Lambert, Black Republican, Napoleon, and Deacon are often infected with GRMV. Foliage symptoms

like those in sour cherry have been observed in duke cherry (P. cerasus x P.

avmm) cultivars Late Duke (291), May Duke, and Reine Hortense (R. M.

Gilmer, unpublished data).

Peach, nectarine, and apricot are symptomless carriers of GRMV (213).

The peach cultivars Halehaven, Sunhaven, Richaven, Glohaven, Suncling, and

Rio Oso Gem appear to be universally infected (127 and P. R. Fridlund,

unpubhshed data).

Preliminary results (P. R. Fridlund, unpublished data) indicate that P.

tomentosa is susceptible to infection and P. cistena is immune. GRMV was

193
194 VIRUS DISEASES OF STONE FRUIT

transmitted experimentally to P. mahaleb (547) and has been recovered from

a symptomless mahaleb clone of German origin (R. M. Gilmer, unpublished

data). Milkweed {Asclepias syriaca) has been suggested as a possible host of

GRMV and other cherry viruses {336), without later confirmation.

Symptoms

Sour cherry.—In mature leaves of Montmorency, a yellow and green mottle

(persistent green islands or ringlike bands) appears about 4 to 6 weeks after

petal fall (fig. 89). Some GRMV strains may also induce irregular necrotic

spots of varying size in Montmorency leaves (P. R. Fridlund, unpublished data).

The yellow and green mottle develops predominantly over a 2 to 3 week

period, and leaves with these symptoms soon drop. Mottle may continue to

appear in an occasional leaf as late as September in some areas. Mottle symptoms

do not necessarily occur each year, and some GRMV strains may incite no

symptoms in infected Montmorency trees (P. R. Fridlund, unpublished data).

An additional foliage symptom, constricting chlorosis {247), appears to result

from the failure of sections of the leaf lamina to develop normally in areas

along the midribs or major lateral veins. Linear areas of chlorotic and distorted

tissue appear along these veins (fig. 89). Constricting chlorosis appears during

the period of leaf expansion, and the affected leaves persist indefinitely.

FIGURE 89.—Green ring mottle in Montmorenqi cherry. Right, a yellowing leaf with

persistent green rings and islands; center, constricting chlorosis along a lateral vein;

left, a normal leaf.
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE I95

FIGURE 90.-

i

-Left, pitting and necrosis of Montmorency cherry fruit affected by green

ring mottle; right, normal Montmorency fruit.

In fruits on infected trees, some GRMV strains induce necrotic pits or rings

in the epidermis with ring-shaped areas of necrosis deep in the flesh (fig. 90).

The aiïected fruits are bitter and off-flavor {454, 510). Other GRMV strains

may induce subepidermal netlike patterns of necrosis in fruits, visible only by

transmitted light {454 and P. R. Fridlund, unpublished data).

Leaves with the yellow and green mottle are most abundant in the interior,

shaded portions of infected trees, but fruit symptoms and constricting chlorosis

are randomly distributed throughout the tree (27).

In infected English Morello trees, the green and yellow mottle of leaves and

necrosis of fruits are lacking. In English Morello trees inoculated with a mixture

of GRMV and PRSV, scattered symptoms of constricting chlorosis were

observed, suggesting that some GRMV strains may incite symptoms in this

cultivar {20).

Duke cherry.—The characteristic green and yellow leaf mottle occurs in at

least three cultivars: Late Duke, May Duke, and Reine Hortense.

Oriental flowering cherry.—Infected trees of Shirofugen and Kwanzan show

epinasty of the foliage that may rarige from very mild to severe, depending on
196 VIRUS DISEASES OF STONE FRUIT

the GRMV strain (434 and P.R. Fridlund, unpublished data). Portions of the

midrib or lateral veins become necrotic, resulting in a twisting and curling of

aiïected leaves hke that caused by aphid feeding (fig. 91). The internodes of

elongating terminals are shortened, and as the bark matures it is often roughened

by the development of longitudinal fissures (fig. 91). Considerable terminal

dieback usually occurs in infected Kwanzan trees in New York, but at Prosser,

Wash., dieback is apparent only when GRMV is contaminated with certain

PRSV strains.

Symptoms are mild in Naden and completely absent in Shirotae (460).

Sweet cherry, peach, and apricot.—Naturally infected trees of these species

are symptomless carriers of GRMV (1, 208, 213, 247, 443, 434, 467, 389,

600). No differences in symptoms were observed between peach and sweet

cherry trees inoculated with PRSV and others inoculated with PRSV and

GRMV; the symptoms that developed were attributed to PRSV (20, 21, 318).

The development and severity of symptoms of GRMV infections in various

Prunus hosts is influenced by environmental conditions. In the oriental flowering

cherries, leaf epinasty and veinal necrosis are most pronounced at cool temperatures (18° C). At higher temperatures (22° and 26°), a mild, limited veinal

necrosis was the only symptom in Kwanzan (P. R. Fridlund, unpublished data).

Conversely, the characteristic yellow and green leaf mottle does not appear in

the foliage of infected Montmorency sour cherry until about midseason, when

ambient temperatures are relatively high.

In experimentally shaded Montmorency trees in the field, Barksdale (21)

found that low light intensity favored the development of leaf mottle and that

low light intensity at a temperature regime of 21° C or a diurnal regime of

24"^ to 16° resulted in pronounced leaf symptoms. In other experiments (P. R.

Fridlund, unpublished data), symptoms were very pronounced in infected

Montmorency trees at 26° to 30°; mottle symptoms were absent in infected

trees at 18°. Large necrotic spots appeared in leaves at 22°; these spots were

considerably smaller at 30°.

Transmission

GRMV is readily carried in scionwood used in propagation, particularly in

symptomless carriers such as sweet cherry, peach, and apricot. GRMV appears

to be completely systemic in infected peach and sweet cherry. However, there is

preliminary evidence that GRMV may not be completely systemic in some

infected Montmorency trees (P. R. Fridlund, unpublished data).

Natural spread of GRMV in sour cherry orchards has been observed repeatedly (21, 434). The grouping of infected sour cherry trees is often in a

pattern suggesting spread from a central locus. Because the rate of spread is

relatively slow, some of the local spread may result from root grafts between

adjacent trees.
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE I97

FIGURE 91.—A, Current-season growth of Kwanzan oriental flowering cherry infected

with green ring mottle virus (GRMV), showing charaaeristic twisting and curling

of leaves; B, older infected branch showing severe splitting and rough bark symptoms.
IQg VIRUS DISEASES OF STONE FRUIT

Evidence against transmission of GRMV through cherry seeds appears conclusive (127, 219, 233). Attempts to transmit GRMV mechanically to woody

or herbaceous plants have been unsuccessful. No vectors are known.

Characteristics of the Virus

Because GRMV has not been transmitted mechanically, very little is known

of its properties. GRMV is highly resistant to heat therapy. An exposure at

36° to 37° C. for 13 days or more inactivated PRSV but not GRMV in sweet

cherry (431). P. R. Fridlund (unpublished data) did not eliminate GRMV

from infected sweet cherry or peach buds exposed to 38° C. for 21 days or from

sweet cherry buds after hot-water treatment at 50° C. for 20 minutes. Nyland

(491), however, reported eliminating GRMV from Stockton Morello cherry

buds with thermo-therapy (38° C. for 6 weeks).

Control Measures

The sole method of controlling GRMV is to propagate and plant trees free

of the virus. Sources of propagating materials may be indexed on Kwanzan

flowering cherry, which appears superior to Mortmorency cherry as an indicator

for GRMV. Because GRMV is not seed transmitted, seedling rootstocks may be

safely used for propagation. The removal of infected trees may prevent spread

in sour cherry orchards.

Remarks

Green ring mottle is potentially an important disease of sour cherries because

the fruits of infected Montmorency trees are frequently unmarketable. Its effects

on fruit production and tree growth have not been studied adequately.

GRMV is common in several commercially important sweet cherry cultivars,

but the amount of economic injury that it causes, if any, is not known. Limited

data suggest that infected sweet cherry nursery trees are slightly smaller than

healthy ones (443). In peach, latent GRMV does not appear to reduce either

yields or growth of infected trees (318).

The prevalence of GRMV in some sweet cherry culivars is probably a result

of their having been topworked on diseased rootstocks (213, 467), but its widespread occurrence in other sweet cherry cultivars (see "Other Hosts") suggests

that the original cultivars sources may have been infected. Extensive indexing

at IR-2 Repository indicates that some peach cultivars are universally infected,

again suggesting that the original sources were infected.

The virtual restriction of GRMV to clones of North American origin suggests

that the virus is indigenous to North America perhaps to the West because the

virus is more common in western sweet cherry cultivars than those originating

in the East (213, 213, 467, 389).

An earlier suggestion that GRMV might be a strain of sour cherry yellows

virus (prune dwarf virus) (347) has not been supported by additional data.

Green ring mottle disease spreads in Montmorency sour cherry orchards inde-
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE ^99

pendently of the other viruses (21). Its rate of spread is generally much slower

than that of sour cherry yellows or Prioius ring spot, and the pattern of spread,

which tends to concentrate around a central locus differs from the spread patterns of the latter diseases. Moreover, GRMV has not been transmitted to any

of several herbaceous plants that are readily infected by PRSV or PDV. GRMV

passes across graft unions at a slower rate than PRSV or PDV {222).
PINK FRUIT

p. W. CHENEY, C. L. PARISH, and FOLKE JOHNSON

Pink fruit was reported first in Washington in 1934 (287) and was shown to

be caused by a transmissible virus (PFV) in 1940 (334). Orchard surveys

conducted in 1939 and 1942 revealed from 2 to 9 percent of the Montmorency

sour cherry trees in northwestern and central western Washington were infected

{166, 565). In terms of reduced sour cherry yield, pink fruit was considered

second in importance only to brown rot (Monilinia laxa Aderh. and Ruhl.)

(368). Pink fruit occurs in the sour cherry-growing areas of western Washington from the Canadian border to the Columbia River. A similar-appearing

disorder, reported in Idaho (47), may have been caused by the western Xdisease virus (E. C. Blodgett, personal communication).

Montmorency sour cherry is the only cultivar known to be naturally infected

by PFV. Inoculated trees of Early Richmond sour cherry and Ronald duke

cherry show typical pink fruit. Only questionable symptoms occur on Royal

and Bicentenaria duke cherry. Bing, Lambert, and Star sweet cherry are symptomless carriers. Italian Prune (Primus domestica), several peach cultivars, and

seedlings of P. emarginata and P. mahaleh are immune.

Diagnostic symptoms of pink fruit occur in the fruit (fig. 92), first appearing

about 2 weeks prior to harvest. Affected fruit are smaller than normal, pinkish

yellow to pinkish brown, and have brown, necrotic areas in the flesh. Afifected

fruit lack flavor and tend to drop prematurely. Normal and affected fruit may

occur on the same branch or even on the same spur of a tree. The ratio of

pink to normal fruit varies with the length of time elapsed since inoculation and

also the size and vigor of the tree when infected.

Leaves of affected trees may fold upward along the midvein, presenting the

appearance of drought. Diseased trees bloom later than normal, and tree growth

is suppressed.

Rootstocks have a marked effect on symptom expression. Although Montmorency trees on mahaleb stock may show symptoms the second year after

inoculation, these are meager, and the trees usually appear to recover. Conversely,

Montmorency on mazzard roots become more severely diseased until all the

fruit are affected. Montmorency on its own roots is more severely affected than

when on mazzard.

Transmission has been effected only by some form of grafting, using shoot

or root material. Symptoms appear from 15 to 27 months following inoculation.

Some diseased trees are still to be found scattered throughout the former fruitgrowing areas of western Washington. Most of these are in backyard orchards.

Replacement of diseased trees with virus-free Montmorency on mahaleb roots

could, in time, eliminate loss from pink fruit.

200
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 201

FIGURE 92.—Montmorency cherry fruit affected by pink fruit, showing small pinkish

yellow to pinkish brown color and necrotic areas in the flesh.
VIRUS GUMMOSIS OF MONTMORENCY

EARLE C. BLODGETT and MURIT D. AlCHELE

An undescribed virus was discovered (69) as a result of indexing mahaleb

seed source trees in the Pacific Northwest (1954-59) for sour cherry yellows

virus (SCYV) and Prunus ring spot virus (PRSV).

Trees of Montmorency on mahaleb rootstock were established at Puyallup and

Bellingham, Wash., to test for SCYV. The trees of Montmorency were budinoculated in the early fall with tissue from the seed source trees and observed

for symptoms the following summer. Most symptoms were typical, but Montmorency trees inoculated with tissue from seven mahaleb trees gave a new and

severe reaction. Previous indexing of these same trees on Shiro-fugen at Prosser,

Wash., and Corvallis, Oreg., had failed to detect PRSV.

The original seven mahaleb trees carrying virus gummosis virus (VGV)

showed no symptoms or apparent effect on their growth. Healthy Montmorency

trees bud-inoculated in the fall with infected mahaleb budwood showed symptoms the following growing season. Growth commenced normally in the spring.

When the new Montmorency shoots were several inches long (up to 12 inches),

the terminals died and curled downward (fig 93). New growth often took place

from buds below the dead tip, and this top killing usually was repeated one or

more times during the season. Some of the current year's shoots developed

necrotic areas even before the tips died. Gum pockets formed on the new shoots

and beads of masses of gum exuded. The same condition also occurred under

the bark of the scaffolds and trunk until, by the end of the season, the whole

tree became a mass of puffy blisters and gum. Affected trees are dwarfed, with

numerous, short, side branches and weak growth (fig. 94).

This type of gumming was first observed on Montmorency trees inoculated

in 1949 at Corvallis. The inoculum had been taken from a Napoleon sweet

cherry tree on mahaleb root. Natural spread of the disease was observed in a

block of 100 virus-free trees of Montmorency at The Dalles, Oreg., in 1952.

Five trees developed gumming and tip dieback symptoms in 1959.

VGV is not seed transmitted and does not incite symptoms on Bing and

Lambert cherry.

Montmorency trees propagated on mazzard rootstock with virus gummosisinfected budwood were affected less than those on mahaleb.

Although a great many mahaleb as well as other seed and scion source trees

have been indexed over the years in Oregon and Washington, only the original

seven trees infected by this virus have been discovered.

202
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE £03

FIGURE 93.—Current year's growth of Montmorency cherry afifected by virus gummosis,

showing typical dieback of the growing shoots.

FIGURE 94.—Right, three healthy Montmorency cherry trees; left, three Montmorency

cherry trees inoculated with buds from mahaleb seed trees afïected by virus gummosis

of Montmorency. AU trees are 5 years old.
VIRUS DISEASES OF SWEET CHERRY

ALBINO

H. R. CAMERON

Albino virus was discovered in the Rogue River Valley of southern Oregon

in 1937 (773). The virus moved rapidly within the valley and eliminated all

the commercial sweet cherry acreage. With the loss of the orchards, the virus

virtually disappeared and now is only found rarely. Most sweet cherry cultivars,

on either mazzard or mahaleb rootstocks, are severely affected. Lambert, Black

Tartarian, Macmar, and Montmorency sour cherry exhibit milder symptoms

and are not killed as quickly. Peach is not susceptible to albino virus.

Symptoms are usually quite striking, consisting of limb dieback and leaf

casting. The leaves are rolled inward and highly colored. Color varies from

orange to bright yellow to golden bronze through olive-brown. Leaves produced

in late summer come from terminal buds and are resetted and small. Young

green fruits remain small, become light colored, and fail to mature (fig. 95). A

FIGURE 95.—Normal Bing cherry, left; Bing cherry affected by albino, right, showing

small, light-colored fruit that failed to ripen.

204
HANDBOOK NO. 437, U.S. DEPARTMENT OF AGRICULTURE 205

heavy fruit drop may occur prior to harvest, but some small white fruit remain

attached well into the fall. Symptoms become more severe with time and result

in tree death in 1 to 4 years.

The virus is easily transmitted by budding or grafting, but a vector has not

been found. Inoculated sweet cherry trees died faster on mahaleb than on

mazzard rootstocks (763). Inoculated Montmorency sour cherry reacted more

severely on mazzard than on mahaleb rootstocks. Inoculated peach trees did

not transmit the virus when indexed on susceptible selections of sweet cherry.

Diseased tree removal was not effective during the period of rapid virus

spread. Recently, Lambert and Macmar have been planted in the Rogue River

Valley. The only commercial orchard is now 9 years old and has not shown any

symptoms of the albino disease. Inasmuch as this orchard has escaped infection,

it appears that either the virus is not present in other hosts or the vector is no

longer active. Provided the virus is not spread from occasional infected backyard

trees, it may be possible to reestablish plantings of sweet cherry in the Rogue

River Valley.
APPLE CHLOROTIC LEAF SPOT AND OTHER

FILAMENTOUS VIRUS INFECTIONS IN PRUNUS

A. JUERGEN HANSEN and R. M. GiLMER

Causal Viruses

Until the viruses of this rather heterogenous group have been classified more

precisely, they may be tentatively referred to as filamentous Prunus viruses.

Some isolates of this group have been designated as raspberry bushy dwarf virus

{105) or apple chlorotic leaf spot virus (CLSV) {25, 251). These viruses

should not be confused with the cherry chlototic leaf spot virus of some

European authors {25, 533), which is distinct.

History and Distribution

Filamentous viruses have been found repeatedly in Prunus during the last 10

years in the United Kingdom {105, 194, 195) as well as in Germany {29),

Poland {763), and Switzerland {90). Similar viruses were recovered from

sweet cherry trees in the United States in 1967 {251 and R. M. Gilmer, unpublished data) and in Canada in 1968 and 1969 {276 and A. J. Hansen, unpublished data). Although no field surveys have been made, these reports suggest

that filamentous viruses may be fairly common in commercial and ornamental

Prunus hosts {536).

Hosts

In Europe, filamentous viruses have been isolated from apricot, flowering

plum, peach, European plum; Pandy, and Black Spanish sour cherry; Volynska;

sweet cherry; and the species P. colina, P. fruticosa, and Krassa Severa duke

cherry {90, 106, 194, 195, 763). The North American isolates were obtained

from trees of the European sweet cherry cultivars Emperor Francis, Noir de

Chaournes {251)^ Frueheste der Mark, Pimento, and Yellow Spanish (R. M.

Gilmer, unpublished data) in a New York collection, and from cultivars Lambert

{276) and Stella (A. J. Hansen, unpublished data) in British Columbia. The

filamentous viruses were completely latent in the above seven infected sweet

cherry cultivars. One cultivar, Emperor Francis, had previously been indexed

on a range of woody stone fruit virus indicators and had failed to induce

symptoms in any of them.

Symptoms

In plum, symptoms much like those of plum pox (sarka) were observed in

England in a Wardwickshire Drooper tree from which CLSV was isolated

{195). In peach, infection with cherry CLSV resulted in the development of

narrow, slightly depressed meandering lines, darker green than the remainder

of the leaf lamina {195 and R. M. Gilmer, unpublished data). This dark-green,

sunken mottle was often restricted to one or two leaves of an infected seedling.

Similar symptoms occurred in inoculated apricot seedlings, but the mottle pattern

206
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE £07

was generally more ringlike (R. M. Gilmer, unpublished data). The Canadian

isolates did not induce any symptoms in either apricot or peach (A. J. Hansen,

unpublished data).

In France, a decline of apricot and Japanese plum is associated with scionrootstock incompatibility induced by CLSV (R. Bernhard and J. Dunez, unpublished data). CLSV also incites fruit deformities (pseudo plum pox) in

certain European and Japanese plum cultivars (R. Bernhard and J. Dunez,

unpublished data).

Among herbaceous plants, several members of the Chenopodiaceae are susceptible, and Chenopodium amaranticolor and C. quinoa are useful indicators

(fig. 96).

Transmission

Graft transmission from infected trees to susceptible woody hosts is readily

achieved, although complete invasion of the inoculated tree may take 12 months

or longer. The natural occurrence of filamentous viruses in a number of Prunus

cultivars suggests that transmission may occur in the field, but how transmission

is effected is not known. Numerous attempts to transmit the New York isolates

with dodder from woody or herbaceous hosts have been unsuccessful (R. M.

Gilmer, unpublished data). Attempts to detect the Canadian isolates in seeds

or seedlings of infected sweet cherry and C. quinoa gave similarly negative

results {216 and A. J. Hansen, unpublished data).

Characteristics of the Viruses

The characteristics of the filamentous viruses have been only partially determined: the thermal inactivation point (10 minutes) is between 42° and 50° C.

{251, 276), dilution end point is between 10"^ and 10"^ (-^76), longevity in

crude sap at 20° is several hours, and particle length as measured by electron

microscope is around 700 m/x.

Control Measures

The economic justification for control measures is doubtful because filamentous viruses are not associated with any particular Prunus disease, and because

their mode of field transmission is unknown. Their presence, however, might

synergistically increase injury from other viruses, and they may confuse indexing

results. Healthy scionwood could presumably be selected by indexing petals

of candidate material on C. quinoa.

Remarks

The discovery of filamentous viruses in stone fruits is relatively recent. It

is therefore impossible to even roughly estimate their prevalence in orchards or

their economic importance. These viruses were probably previously overlooked

simply because they do not induce symptoms on the commonly used woody

indicators, or because they infect the same herbaceous hosts as Prmius ring spot

and prune dwarf viruses.

The relationships of the cherry isolates to other filamentous fruit tree viruses
208 VIRUS DISEASES OF STONE FRUIT

are still being investigated. The New York cherry isolates correspond in most

characteristics to those of apple CLSV (Lister's type 1 apple virus) (231, 405,

406). The British Columbia isolates have been separated into two types on the

basis of host range, symptom expression in herbaceous hosts, and serological

relationships (A. J. Hansen, unpublished data).

FIGURE 96.—Necrotic lesions surrounded by green rings on a leaf of Chenopodium

quinoa inoculated with chlorotic leaf spot virus (CLSV) from a Lambert cherry tree.
BLACK CANKER

p. W. CHENEY, EARLE C. BLODGETT, and C L. PARISH

Black canker was first described in Oregon (774) and has been reported in

Washington and the Okanagan Valley, British Columbia (767). Sweet cherry

{Prunus aviurn) is the only known host. Napoleon is the most severely affected

cultivar, but severe symptoms have also been noted on Bing, Republican, and

Deacon.

The most distinctive symptoms of this disease are the rough black cankers

occurring on the scaffold limbs and branches of affected trees. Cankers start as

swollen areas on branches and twigs; and the bark splits lengthwise along these

swollen areas forming rough, thickened ulcerlike wounds (fig. 97). In some

FIGURE 97.—Rough, black cankers on limbs of sweet cherry tree affected by black canker.

209
210 VIRUS DISEASES OF STONE FRUIT

instances, cankers may completely girdle a twig or branch, causing dieback to

occur. Affected trees are generally debilitated. No fruit or leaf symptoms have

been observed.

Transmission has been effected by grafting shoot tissue from an affected

tree into a susceptible host. Symptoms occur 2 to 3 years following inoculation.

The nursery certification program, increased grower awareness of virus problems, and the apparent absence of vectors have combined to make a rarity of

this potentially economic important disease.
BLOSSOM ANOMALY OF CHERRY

C. L. PARISH, P. W. CHENEY, and E. W. ANTHON

This disease was noticed first in 1964 on a Bing sweet cherry tree {Prunus

avium) near Wenatchee, Wash. (137). Spurs from this tree were grafted to

healthy Bing trees. In one instance, 3 years elapsed between inoculation and

the appearance of symptoms; in another instance, symptoms appeared 1 year after

inoculation. In the first case, the trees were quite old and there was an appreciable distance between the inoculation site and the first flower bud. In the

second case, the trees were young and there was only 1 inch between the inoculation site and the first flower bud. As symptoms began to appear in the inoculated trees, varying amounts of green developed along the midribs of the

normally white petals. The amount of coloration in some blossoms ranged from

a narrow green streak, not much wider than the veins, to entire green petals (fig.

98). Some petals, as well as being entirely green, were leaflike in appearance.

Sometimes entire flower buds looked like leaf buds, except for the yellow

FIGURE 98.—Bing cherry blossoms affected by blossom anomaly of cherry, showing

green ateas in petals.

211
212 VIRUS DISEASES OF STONE FRUIT

anthers in the center of the bud. In some flowers, a few of the anthers differentiated into wide, petallike structures with green centers; in other flowers, the

entire stamen resembled a narrow petal. In a few instances, stigmalike and

stylelike structures arose from the top of anthers.

Fruits developing from the affected blossoms were more pointed than normal,

had roughened skin, and usually had a persistent style (fig. 99)- The disease

spreads very slowly in affected trees. Although the original test trees are old,

it has been 3 years since symptoms were first seen, and they have advanced only

about 5 feet from the inoculum sites. The disease cannot be considered

economically important at the present time.

The symptoms described above resemble those induced by aster yellows virus

in other plants. However, numerous attempts to transmit the causal agent of

blossom anomaly to aster by the six-spotted leafhopper have been negative.

FIGURE 99.—Fruits from a Bing cherry tree affected by blossom anomaly of cherry.

The cherry on the left is unfertilized; the five cherries in the middle are mote

pointed than normal, and at least part of the style has persisted on each. The fruit

on the right is a normal Bing fruit.
Causal Virus

This disease may be caused by the interaction of a virus with its host to cause

boron deficiency. The rosette symptoms have been transmitted by grafting (433 )

but have been corrected by apphcation of boron (436). A strain of cucumber

mosaic virus isolated from infected trees is the suspected etiological agent, but

conclusive evidence for this is still lacking.

History and Distribution

Similar symptoms in cherry were first observed in 1952, but did not reoccur

the following year. In 1962, trees with symptoms were observed near Salem

and the Mosier area of Oregon (J. A. Milbrath, N. D. Dobie, and H. R.

Cameron, unpublished data). In the following years, additional trees with

symptoms appeared in both areas.

Economic Hosts

The virus has not been isolated from woody hosts other than sweet cherry.

Mahaleb cherry (Prunus mahaleb) and peach (P. pérsica) have been infected by

tissue grafts but have shown symptoms only occasionally.

Other Hosts

A virus was transmitted by sap from rosetted cherry trees through National

Pickling cucumber to bean (Phaseolus vulgaris) and directly to bean from

peach infected by tissue grafts from cherry.

Symptoms

The most striking early symptom in cherry is the complete loss of crop on

the affected areas of the tree (fig. 100). The flowers open late and then

abscise prior to fruit set. Leaf symptoms are similar to those for boron deficiency. Leaves are elongated and narrow and curve in toward the midrib. This

may be accompanied by an interveinal chlorosis. In older infections, the leaves

originate from the terminal buds, giving a rosette of leaves at the end of bare

branches (fig. 101). The boron content of diseased tissue is usually lower than

that of normal tissue. Symptoms on bean consisted of epinasty similar to that

caused by cucumber mosaic virus (SS). No symptoms were reported on squash

(Cucúrbita pepo)^ tobacco (Nicotiana tabacum), petunia (Petunia hybrida),

Chenopodium amaranticolor, C. quinoa, Gomphrena globosa, Vinca rosea, or

zinnia (Zinnia elegans).

Transmission

Six graft-inoculated sweet cherries developed rosette symptoms within 3 years.

The two noninoculated check trees remained healthy. All trees were in the field.

213
214 VIRUS DISEASES OF STONE FRUIT

FIGURE 100.—Loss of fruit on sweet cherry branch affected by cherry boron rosette

(arrow) ; normal branch, below.

Transmission to herbaceous hosts has been irregular, and symptoms have not

been observed on trees inoculated from herbaceous hosts.

Control Measures

Because a deficiency of boron was associated with diseased tissue, spray and

soil applications of boron were tried. The vigor of the trees improved whenever

boron was applied. In some cases, two spray applications eliminated symptoms

during the following year. Application of boron has now become an acceptable

control for this disease.

Remarks

The data suggest an interaction in the tree between a virus and either the

movement or metabolism of boron.
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 215

FIGURE 101.—Rosettes of narrow leaves on sweet cherry tree affected by cherry boron

rosette (second year symptom).
CHERRY MOTTLE LEAF

p. W. CHENEY and C. L. PARISH

Causal Virus

Cherry mottle leaf virus (CMLV).

Synonyms

Severe mottle leaf (rugose type) ; mild mottle leaf (smooth type) (430,

766).

History and Distribution

Mottle leaf was first observed in Oregon in 1920 (764). The infectious

nature of the disease was established in 1935 (429, 331). Cherry mottle leaf

occurs generally in the sweet cherry-growing districts of Washington, Oregon,

Idaho, and British Columbia, and has been seen in California, Utah, and Montana (430). Cherry mottle leaf is most prevalent in foothill or canyon orchards

where wild bitter cherry (Prunus emarginata) is growing.

Economic Hosts

CMLV occurs naturally in sweet cherry and peach. Peach is symptomless

when infected by most strains of the virus. Transmission tests show the following cherry cultivars are severely affected by cherry mottle leaf: Bing, Heldefingen, Lamida, Larian, Sodus, Velvet, and Vic. Napoleon (Royal Ann) is

intermediately affected; Republican and Van are mildly affected.

Thirty-seven sweet cherry cultivars are symptomless or nearly symptomless.

Among these are Bada, Berryessa, Black Tartarian, Burbank, Chapman, Chinook,

Corum, Deacon, Ebony, Gil Peck, Jubilee, Lambert, Mona, Rainier, Sam,

Schmidt, Seneca, Spalding, Sparkle, Star, Stark Gold, Sue, Victor, and Windsor.

Sour cherry and duke cherry (Prunus avium x P. cerasus) are also practically

symptomless carriers of CMLV.

Other Hosts

Mottle leaf has been found naturally occurring in apricot and ornamental

flowering cherries (Prunus serrulata cv. Kwanzan (417) and Amanogawa and

P. yedoensis cv. Yoshino).

Transmission tests show that the following are essentially symptomless carriers: Burbank plum (P. saUcina), myrobalan plum, Drake and Nonpareil

almond, and seedlings of David peach, Amur cherry, mahaleb cherry, black

cherry, and Manchu cherry.

Apple and pear cultivars are resistant to the virus as are Italian Prune (P.

domestica) and seedlings of desert peach, Bessey cherry, and Klamath plum.

Symptoms

The most distinctive symptom of mottle leaf is the irregular chlorotic mottling

and distortion of the foliage, especially terminal leaves (fig. 102). High

216
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 217

FIGURE 102.—Mottled and deformed leaves of A, Napoleon and B, Bing cherry affected

by cherry mottle leaf. C, Shoot of Bing cherry showing severe leaf symptoms in the

new tip growth.
218 VIRUS DISEASES OF STONE FRUIT

temperatures may partially suppress symptoms on some leaves. The amount of

pucker, tatter, shot hole, and reduction in leaf size varies with the severity of

the virus strain as well as the cultivar of the host involved. There is no dieback

or leaf cast. Fruits of severely affected trees are small, late ripening, and lack

flavor, but are not misshapen. Diseased trees may produce a marketable crop for

many years. A lack of terminal growth and shortening of the internodes cause

CMLV-infected trees to appear rosetted.

Transmission

Transmission is readily obtained by budding or grafting any root or shoot

tissue from a diseased tree into a susceptible host. Under field conditions, leaf

symptoms were found to occur within 32 days after inoculation, whereas symptoms were noted in the greenhouse in 9 to 14 days (333). Graft transmission of

CMLV at 26° C. ranged from 0 percent at 66 hours to 100 percent at 106 hours.

Viruses with similar speed of transmission are cherry twisted leaf, apricot ring

pox, peach wart, and green ring mottle viruses (222), CMLV is not seed transmitted (219, 430).

A minute scale mite, Eriophyes inaequalis, which normally lives and feeds

on bitter cherry, was found to be an efficient vector of CMLV (L. S. Jones,

unpublished data). Single tree infections, widely separated from bitter cherry

trees or other diseased sweet cherry trees, indicate that mites can be carried long

distances in air currents or by some other means.

CMLV has not been mechanically transmitted or purified. It cannot be

eliminated from scion wood by hot-water dip at 50° C. for 20 minutes or

hot-air exposure at 37° for 21 days (P. R. Fridlund, personal communication).

Control Measures

In areas where there is a high incidence of cherry mottle leaf, diseased trees,

which are no longer producing profitable crops, should be removed and

replaced with noninfected trees of a tolerant cultivar. In districts where cherry

mottle leaf is uncommon and where susceptible cultivars (Bing and Napoleon)

are important, infected trees should be removed immediately to prevent them

from being a source of infection for the rest of the trees. Furthermore, tolerant

trees used as pollenizers should be indexed; if found to be carrying CMLV

they should be rogued.

Remarks

Where cherry mottle leaf is prevalent, it is of considerable economic importance. Fruits of infected Bing and Napoleon trees are reduced both in size and

number. The practice of replanting infected Bing orchards with tolerant cultivars

(primarily Lambert) to ofiiset this loss is only partially effective because the

price of Lambert cherries is usually lower than that of Bings.
CHERRY RASP LEAF

GEORGE NYLAND

Causal Virus

Cherry rasp leaf virus (CRLV).

Synonyms

The disease has been called leaf enation, ruffled leaf, and cockscomb.

History and Distribution

The disease was reported first from Colorado in 1935, and its virus nature

was established in 1942 (84). The disease is known to occur in most cherrygrowing districts in the West and British Columbia (31, 310, 442, 534).

Usually only a few trees are involved at a particular site. In Europe, leaf

enation is a prominent symptom of several cherry diseases (74, 167, 173, 380,

381, 480, 332, 391), and a single report from New Zealand describes a rasp

leaf disease of cherry (290). Arabis mosaic virus and raspberry ring spot virus,

alone or in combination with cherry leaf roll virus, are associated with most of

the leaf enation symptoms of the European diseases. Leaf enation in sour cherry

or sweet cherry in Europe and North America is also associated with infection

by certain strains of Prunus ring spot virus (27, 347, 349, 490, 493) and with

peach yellow bud mosaic virus (=tomato ring spot virus) (407, 437, 700).

CRLV is considered distinct from the other viruses that cause enations on cherry

leaves.

Economic Hosts

Rasp leaf has been reported primarily in sweet cherry cultivars and mazzard

seedlings but also occurs in Montmorency sour cherry (80). Sweet cherry on

mahaleb roots became infected and developed symptoms when buds from diseased Bing were placed in the mahaleb understocks (C. W. Nichols and George

Nyland, unpublished data). Mahaleb seedlings became infected when grown

in soil that had been obtained near infected orchard trees (700).

Other Hosts

CRLV has been transmitted mechanically to Chenopodium amaranticolor and

C. quinod and recently to Gomphrena globosa (490 and author's unpublished

data).

Symptoms

The most characteristic symptom of the disease is prominent enations on the

underside of the leaves (ñg. 103). The enations take the form of leafy outgrowths or raised protuberances between the lateral veins and along the midrib.

The leaves are more or less deformed ; many are extremely narrow, folded, and

distorted. The upper surfaces of the leaves have a rough, pebbly texture with

depressions corresponding to the enations on the lower surface. Some or all of

219
220 VIRUS DISEASES OF STONE FRUIT

FIGURE 103.—Napoleon sweet cherry leaves affected by cherry rasp leaf, showing

distortion and prominent enations on the lower surface.

the leaves on a shoot or branch may be affected. The virus is essentially systemic

in the tree or branch below the highest leaves with symptoms, but sometimes

affected spurs may be scattered among healthy ones. Newly infected trees in the

orchard usually develop symptoms first on leaves low in the tree. Spread within

the tree is slow unless the virus reaches a growing point. Then spread is more

rapid, seemingly by cell division in this case. Different isolates may move at

different rates, indicating variation in the virus. Many affected spurs and

branches in the lower portions of infected trees die, giving the tree an open,

bare appearance and reducing fruit production. Trees that are infected at an

early age grow poorly and produce few fruits. Sometimes young trees are killed

by the virus, especially if they are tissue-inoculated when they are 1 to 2 years

old. Mazzard seedlings infected by viruliferous Xiphenema americanum or by
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 221

implants of infected tissue of Chenopodium spp. have a high rate of mortality

(George Nyland and S. Lowe, unpublished data).

Symptoms in C. amaranticolor and C. quinoa consist of a very fine stipple

or dusty mottle that often shows only at the base of the leaf and persists for

only a few days before fading out. No local lesions or other symptoms are

produced on inoculated leaves; the best symptoms are in the partially expanded

terminal leaves. If infected plants are cut back, growth from lateral buds may

again show symptoms. C. quinoa usually shows stronger symptoms than C.

amaranticolor.

Transmission

CRLV is readily transmitted by tissue grafts, by sap mechanically to a very

limited host range, and by the nematode Xiphenema americanum. Cherry trees

inoculated by bud grafting {80), by placing infected pollen under the bark

(700), by approach grafting, or by placing tissue from infected Chenopodium

spp. under the bark (George Nyland and S. K. Lowe, unpublished data)

develop symptoms from 8 to 9 months to 2 or 3 years later. CRLV is retained

in soil and infects mahaleb and mazzard seedlings when they are planted in

infested soil in containers or in the orchard {700, 727). X. americanum was

among several plant parasitic nematodes detected in infested orchard soil (700).

Handpicked X. americanum acquired CRLV from mechanically inoculated

Chenopodium plants and transmitted it to healthy Chenopodium and to mazzard

seedlings. X. diversicaudatum in a parallel test did not transmit the virus (497).

Characteristics of the Virus

CRLV is a polyhedral, soil-borne, mechanically transmitted, nematodevectored virus of the type referred to by Cadman (104) as NEPO viruses. The

particle associated with infectivity is approximately 21 m/x in diameter, with

longevity of 10 days in expressed sap at room temperature, and a dilution end

point of 10-4 in Chenopodium quinoa sap. The isoelectric point is lower than

pH 4.5, and the thermal inactivation point in vitro is about 65° C. for 5 minutes.

The virus is fairly stable and is easily concentrated from sap clarified by

acidification and butyl alcohol. Yield of virus from Chenopodium spp. is low

(George Nyland and S. K. Lowe, unpublished data).

Control Measures

Removal of infected trees and trees immediately adjacent to infected trees

and deep-soil fumigation with a nematocide are suggested to eradicate the

disease in bearing orchards. Disease-free propagating stock should be used for

replants or for setting out new orchards.

Remarks

CRLV did not react with antiserum of raspberry ring spot, arabis mosaic,

or grapevine fanleaf viruses. Symptoms incited by CRLV in Chenopodium most

nearly resemble those described for arabis mosaic and fanleaf virus infection in

species of Chenopodium (George Nyland and S. K. Lowe, unpublished data)-.
CHERRY TWISTED LEAF

A. J. HANSEN and P. W. CHENEY

Causal Virus

Cherry twisted leaf virus (CTLV).

History and Distribution

Twisted leaf was reported in 1943 from the Okanagan Valley, British

Columbia (408), and Yakima County, Wash. (420). It is also known to

occur in Chelan County (420) and Stevens County, Wash. (-538). It has

appeared occasionally in Idaho (A. W. Helton, unpublished data) and at The

Dalles, Oreg. (J. A. Milbrath, unpublished data).

Economic Hosts

Sweet cherry is the only known economic host. Bing appears to be the most

severely affected cultivar. Other symptom-expressing cultivars are Lamida,

Long Stem Bing, and Rainier. Lambert and Napoleon are affected by a severe

form of twisted leaf (338). Van and Velvet react variably. Black Tartarian,

Deacon, Sam, Star, and Sue, as well as most other cultivars tested, can be

symptomless carriers of the virus (413, 416, 338).

Other Hosts

The only other host which has been found naturally infected is western

chokecherry (413). Apricot frequently shows ring pox or pit pox symptoms

when budded with CTLV-infected material. Almond, Burbank plum (Prunus

salicina), mahaleb cherry, sour cherry, and peach can be experimentally infected

but remain symptomless. Abundance plum (P. salicina), Italian Prune (P.

domestica), myrobalan plum, and bitter cherry are immune to CTLV (4/3,

338, and P. W. Cheney and C. L. Parish, unpublished data).

Symptoms

The most consistent symptom is an abrupt kink in the midrib or the petiole,

which causes the leaf to appear twisted (fig. 104). This is accompanied by an

even downward and slightly sideward curl (see smaller leaves in fig. 115, A,

p. 244) of the whole leaf. Leaves frequently develop unsymmetrically or stay

small. Parts of the midrib and of the lateral veins may become necrotic. In

addition, a severe stunt and shortening of the internodes causes the spurs to

appear bunchy (hg. 105). Both stunt and curling can be noticed from a distance. Once a tree has become infected, the disease spreads rapidly to most or all

branches, although scattered spurs may seem to be healthy. Symptoms appear

year after year, but their severity in field trees varies. In Washington (334),

symptoms of irregular fruit distortion accompanied by pedicel necrosis have

occasionally been observed in trees affected by cherry twisted leaf. The available

evidence indicates that this distortion is a characteristic induced by certain isolates

222
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 223

FIGURE 104.—Leaves from healthy (right) and cherrj' twisted leaf-affected {left) sweet

cherry, showing the typical kink in the midrib.

of the virus, and that it is more severe in older trees of medium vigor {556).

For diagnostic purposes, the leaf-twisting reaction of Bing is recognized as the

most reliable means of identification. Although the severity of the twisting in

Bing varies according to the strain, this cultivar has so far reacted with all isolates. Fruit distortion has been less diagnostic, as it varies more from strain to

strain. Moreover, fruit distortion can be caused by other unrelated viruses and

probably by physiological factors. Symptoms similar to twisted leaf may be induced by heavy infestation of black cherry aphid {Myzus cerasi Fab.). However,

these aphid-induced symptoms are characterized by absence of the petiole kink,

by the presence of live or dead aphids, and by an uneven distribution of affected

spurs in the tree.

Transmission

The mechanism of field transmission of CTLV has not been investigated in

detail. Twisted leaf occurs in the orchard at irregular intervals and in unpredictable, scattered patterns. In British Columbia {415, 416), the virus is present

in wild chokecherries even in places far removed from cherry orchards. This

points to the possibility that it is carried by an unknown vector from a native

host or a symptomless carrier into orchards.

CTLV can be transmitted easily from infected cherry to Bing by budding or

grafting. Symptoms will appear generally in the first and certainly in the second

year after inoculation. Seed transmission of CTLV is not known to occur.
224 VIRUS DISEASES OF STONE FRUIT

FIGURE 105.—^Branch from healthy, right, and cherry twisted Ieaf-a£Fected, left, sweet

cherry, showing severe bunching of leaves.

Characteristics of the Virus

CTLV has never been transmitted to herbaceous plants, has not been purified

directly from Prunus spp. tissue, and has not been detected with the electron

microscope. Attempts at heat treatment (20 min. at 50° C; 21 days at 38°)

have been unsuccessful (P. R. Fridlund, unpublished data). However, transmissibility and other indications point to a virus as the causal agent of cherry

twisted leaf.

Control Measures

At present, only preventive measures can be taken to keep twisted leaf under

control. Infected trees should be removed as soon as twisted leaf symptoms

appear. Native chokecherry should be eliminated from and around orchard

areas wherever feasible. Virus-indexed budwood should be used for all new

plantings including pollenizers.

Remarks

Twisted leaf occurs erratically in a very limited geographic area, and is

therefore of minor economic importance. It has been locally important in the

past where symptomless infected cultivars were budded into susceptible trees as

pollenizers (420).

Control depends entirely upon preventive measures, but these have apparently

been successful in the last 25 years, as no major outbreaks have occurred. How-
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 225

ever, as long as the source of field infections and the hypothetical vector are not

known, a potential threat of sudden epiphytotics remains.

Twisted leaf can be confused under field conditions with various other diseases. A fruit distortion similar to that caused by CTLV is induced by tomato

bushy stunt virus in Windsor cherry (16). This disease, which is sap transmissible and at present restricted to Ontario, differs from twisted leaf in the

absence of the leaf kink, in having a more severe leaf necrosis, and in having a

slower advance and less complete distribution of the virus in affected trees.

Fruit distortion can also be induced by xylem aberration, a disease occurring

occasionally in British Columbia. The short stem disease (8) differs from

twisted leaf mostly in that there is an extreme shortening of the peduncle. The

spur cherry disease (68) resembles cherry twisted leaf in that the foliage of

some cultivars (for example, Sam and Windsor) may be twisted in a similar

way. However, the extreme rosetting and the twig epinasty caused by spur

cherry disease differ from the symptoms of twisted leaf. Similarities and possible

relationships between cherry twisted leaf and apricot ring pox (216, 4l4, 413),

and between these two and the spur cherry disease have been discussed in the

section on apricot ring pox.
FRECKLE FRUIT

H. E. WILLIAMS and H. R. CAMERON

This disease of sweet cherry was first observed in 1952 in two Lambert trees

growing in an orchard at The Dalles, Oreg. (724). Symptoms were most conspicuous at harvest time. Most of the fruit on the affected trees was undersized,

immature, and spotted with necrotic brown flecks (fig. 106). Severely affected

fruits were deformed by irregular, shallow depressions; mildly affected fruits

were nearly smooth, with most of the brown necrotic area located near the stylar

end. No leaf symptoms were observed.

A virus was transmitted by bud-inoculation to Lambert and Bing sweet

cherry trees. Fruit symptoms developed in the inoculated trees but were less

severe in Lambert. The small affected fruits of Bing and Lambert matured

about 2 weeks late. Leaves on the inoculated Bing trees were distinctly mottled.

The fruit of inoculated Napoleon sweet cherry trees did not develop fruit

symptoms, but the leaves were mottled. Inoculated peach and apricot trees

did not develop fruit or leaf symptoms. No natural spread of freckle fruit has

been observed, and the disease is of no economic importance.

FIGURE 106.—Freckle fruit in Lambert cherry fruit, showing distortion, reduced size,

late ripening, and necrotic lesions, below; normal fruit, above.

226
FRUIT PITTING OF SWEET CHERRY

T. R. DAVIDSON and WAYNE R. ALLEN

Causal Virus

Tomato bushy stunt virus (TBSV).

Synonyms

Carnation Italian ring spot virus (CIRV), petunia asteroid mosaic virus

(PAMV), and pelargonium leaf curl virus (PLCV).

History and Distribution

Infected Windsor sweet cherry trees were first observed in 1962 (16). The

virus was isolated in 1963. The disease in sweet cherry is known to occur in

only two orchards near Stoney Creek, Ontario. The infected trees, all of the

Windsor cultivar 25 to 30 years old, were produced by the same nursery, now

defunct. The trees are on mahaleb rootstock, but the source of rootstock and

budwood is unknown.

Economic Hosts

Strains of TBSV have been found occurring naturally in the following

economically important plants: sweet cherry (16), tomato (618), grape (39),

pelargonium (313), petunia, muskmelon and privet (421), primula (462),

and apple (W. R. Allen, unpublished data).

Other Hosts

More than 60 other plants have been recorded as hosts of one or more strains

of TBSV (16, 315, 408, 420, 421). From a diagnostic point of view, the most

important are Nicotiana tabacum. Datura stramonium, Chenopodium amaranticolor, Petunia hybrida, Ocymum basilicum, Phaseolus vulgaris, and Antirrhinum

majus (16, 313, 421).

Symptoms

The leaves of sweet cherry trees infected with this virus tend to develop in

tight clusters. Necrosis of the midvein and some of the lateral veins causes a

sideways and downward twisting of the leaf that can be very extreme (fig.

107) Irregular necrotic areas in various parts of the leaves drop out, leaving

them with a wind-whipped appearance. The first leaves each year are most

severely affected, but symptoms are not confined to these. There is a very low

fruit set due to high flower abortion (fig. 108). Flowers that do not set often

have very short stems, occasionally twisted by necrosis. The fruit is misshapen

by sunken circular pits, and the flesh below these pits is often necrotic (fig. 109).

About 95 percent of the seeds in these fruits are aborted.

The twig wood is very brittle. Annual shoot growth is extremely short (fig.

108). Thus, from a distance, the trees appear rosetted.

227
228 VIRUS DISEASES OP STONE FRUIT

FIGURE 107.—Leaves from Windsor sweet cherry tree systemically infected with tomato

bushy smnt virus. Upper leaf surface shows severe twisting and veinal necrosis.

FIGURE 108.—Branch from a Windsor sweet cherry tree systemically infected with

tomato bushy stunt virus, showing leaf tufts, leaf twisting, shortened growth, and

poor fruit set.

Transmission

TBSV is easily isolated from infected sweet cherry trees by triturating young

leaves, petals, anthers, pollen, flesh from pitted areas of deformed fruits or

seeds in a mortar with carbamate-phosphate buffer pH 7.0 and then mechanically rubbing the mixture over carborundum-dusted leaves of herbaceous test

plants (16). Mechanical inoculation of Prunus mahaleb seedlings has resulted
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE £29

in infection of the inoculated leaf, but the virus has not become systemic. To

date, pollen transmission in sweet cherry has been unsuccessful. Also, attempts

at soil transmission using Olpidium have failed {16, 115, 644). Graft transmission from infected to healthy Windsor sweet cherry trees has been successful, but no natural means of spread is known.

Characteristics of the Virus

The TBSV particles from Prunus are more spherical than hexagonal and

average 30 mju in diameter. The sedimentation coefficient in sucrose-densitygradients was determined as 132s. Density-gradient-purified TBSV from Prunus

has a maximum thermal inactivation point (TIP) at 97° C. The TIP was

affected by the virus concentration and the purity of the preparation. The TIP

of the virus in raw extracted cucumber sap was 60°. TBSV from Prunus was

biologically and serologically active between pH 2.0 and 10.3. Antisera to

TBSV from Prunus cross-reacted with both TBSV and CIRV {15, 16).

Control Measures

This seems to be a very rare disease in sweet cherry. Conclusive evidence of

orchard spread is lacking. Therefore, removal of diseased trees will likely

eliminate the problem. If virus-indexed budwood and rootstocks are used for

propagation of new trees, there is little likelihood of this disease becoming

serious.

Remarks

This disease has been found in only two sweet cherry orchards and appears

to be confined to the cultivar Windsor. The virus is very readily isolated from

trees with symptoms as described, but indexing of symptomless trees, Windsor

or other cultivars, has failed to reveal any carriers of the virus. Because no

means of natural spread is known and conclusive evidence of orchard spread

FIGURE 109.—Pitted fruits from a Windsor sweet cherry tree infected with tomato

bushy stunt virus, right; two normal fruits on left.
230 VIRUS DISEASES OF STONE FRUIT

is lacking, this disease is of minor economic importance. However, the infected

trees produce Httle or no marketable fruit so the loss as related to these trees

is considerable. Therefore, the disease is potentially serious.

TBSV from Prunus is serologically related to TBSV and, to a lesser degree, to

CIRV {16). Other workers have shown that CIRV, PLCV, and PAMV are all

serologically related to TBSV and are therefore strains of this virus (3-? 6^ 421).

In Germany, PAMV has been isolated from grapes {59), and a similar strain

to TBSV from Prunus has been isolated from grapes in Canada (H. F. Dias,

unpublished data). More recently an isolate from apple has been found distantly

related to TBSV (W. R. Allen, unpublished data).

The symptoms caused by TBSV in sweet cherry are very similar to those

described for twisted leaf in western North America {408, 420), However,

those working with twisted leaf have been unable to isolate a causal virus on

herbaceous hosts.
LITTLE CHERRY

MAURICE F. WELSH and PHILIP W. CHENEY

Causal Virus

Little cherry virus (LCV).

Synonyms

K & S little cherry; sour cherry decline (Oregon).

History and Distribution

Little cherry disease was observed first in 1933, affecting sweet cherry trees

in one orchard near Nelson, British Columbia (207). During the ensuing 15

years, almost every cherry tree in the fruit-growing districts of the Kootenay

region of southeastern British Columbia became infected. There has been no

evidence of spread from this region to other fruit-growing districts of the Pacific

Northwest. Bud transmission was effected by Foster in 1941, and more extensively by Lott in 1944 (208).

Reeves, Cheney, and Milbrath (.562) demonstrated the common occurrence in

Kwanzan and Shiro-fugen (Primus serrulata) of a virus that induces small cherry

symptoms in sweet cherry. Subsequent investigations in Washington and British

Columbia (337, 361, 719) provided evidence that LCV and K & S virus are

indistinguishable in host range, symptoms on known hosts, rates of movement

in plant tissues, and ease of bud transmission. P. serrulata trees that had been

planted near the first infected British Columbia orchard, before the original

little cherry outbreak occurred, have been indexed and shown to be infected

(719).

Oriental flowering cherries, popular ornamentals in most countries where sweet

cherries are grown, were introduced from Japan to Europe in 1822 and to

North America about 1845 (361). Reports of the virus indexing of flowering

cherries growing in several countries suggest that LCV infects most trees of a

number of flowering cherry cultivars in several species wherever these

are grown.

Natural occurrence of little cherry disease has been reported in Utah plantings

of Burbank Black Giant (688). The virus that causes a decline of Montmorency

sour cherry orchards in Polk County, Oreg., when bud-transmitted to sweet

cherry cultivars, induces symptoms resembling those of little cherry disease

(439).

LCV is believed to occur commonly in sweet cherry in Japan (643). East

Mailing Research Station workers have reported widespread occurrence of LCV

in English orchards, and have detected its presence in sweet cherry cultivars

newly introduced to England from France, Italy, and Sw^eden (334, 333, 340).

Its detection has been reported in a number of cultivars in Switzerland (601),

and its presence in sour cherry is suspected in Poland (23). Transmission of

231
232 VIRUS DISEASES OF STONE FRUIT

LCV from sweet to sour cherry has been reported in Denmark (382). There

are unpublished reports of its occurrence in other European countries. In the

State of Victoria, AustraHa, LCV infects a number of cherry cultivars, but

spread is not apparent (P. R. Smith, personal communication).

Economic Hosts

All tested sweet cherry cultivars are susceptible, although they vary considerably in type and severity of reaction. In British Columbia, LCV was

bud-transmitted from sweet cherry to Montmorency sour cherry and returned

to sweet cherry, but there was no such passage of LCV through peach,

apricot, and prune (718, 722). In Washington, the virus was passed through

numerous duke and sour cherry cultivars but not through peach, apricot, prune,

plum, almond, and apple. All tested duke and sour cherry cultivars display

fruit symptoms.

Other Hosts

Some indexed bushes of wild bitter cherry, Pruniis emarginata var. mollis,

growing near diseased orchards in British Columbia proved to be infected with

LCV; other seedlings of this wild cherry were not systemically infected after bud

inoculation (722). In Washington, seedlings of P. mahaleh, P. emarginata,

and P. tomentosa were shown to be tolerant hosts, and P. pensylvanica displayed small fruit symptoms (author's unpublished data and P. R. Fridlund,

personal communication). The chokecherries P. virginiana, P. virginiana var.

demissa, and P. virginiana var. melanocarpa have not become infected when

bud-inoculated (J>60, 718).

Indexing at Wenatchee, Wash., of flowering cherry cultivars growing in the

United States and Canada (361), has provided positive tests for the following:

P. serrulata, 25 of 34 cultivars; P. sieboldii, 1 of 1; P. subhirtella, 2 of 6;

P. yedoensis, 1 of 3. Negative tests have been given by one cultivar each of

P. sargenta, P. incisa, and P. nipponica. Similar indexing in England (114,

333 and A. F. Posnette, personal communication) has detected presence of

LCV in 17 cultivars of P. serrulata; two cultivars each of P. subhirtella, P.

yedoensis; and one each of P. jontanesiana, P. avium cv. Flore-pleno, P. inctsa;

but not in two tested cultivars of P. serrulata and P. subhirtella and one each of

P. cerasus var. rhexii cv. Flore-pleno and P. lannesiana. The virus has been

detected by indexing in 13 flowering cherry cultivars in Japan (643).

Symptoms

Symptoms have been seen in sweet, sour, and duke cherries. Those on the

fruit are the most apparent and economically important, but foliage symptoms

are displayed by many cultivars; tree vigor is usually impaired when trees have

been infected for a few years.

Fruit symptoms on Lambert, the cultivar most extensively planted in the

region of disease occurrence in British Columbia, are fairly consistently displayed and can usually be diagnosed with reasonable assurance. The fruits

develop normally through the early part of the season but never fully ripen.
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 233

At picking time, the cherries are one-half to two-thirds normal size, dull red,

angular, and pointed, usually with three flat sides tapering toward the distal

end (fig. 110). In the season following infection, the fruits are usually light

to medium pink and even smaller than in subsequent years. In all seasons,

they may hang on the trees for weeks without ripening fully.

On most other cherry cultivars, the symptoms resemble those on Lambert,

but are less severe and more variable. On Bing, the fruits are severely affected

in the season after infection, but in subsequent years they may vary from small

and medium red to large and black and from irregular to normal in shape.

On cultivars with firm, broad-shouldered fruits, such as Van, the color and

shape are altered little, but the size and sweetness are reduced. On most white

cherries, such as Napoleon, the symptoms are characteristically milder than on

black-fruited cultivars. Montmorency fruits usually vary from normal size and

color to small and light-colored with little change in shape.

Fruit symptoms vary considerably in severity for all cultivars from season

to season, from district to district, and from orchard to orchard. Zinc deficiency

has been shown to accentuate their severity in many Kootenay orchards (720).

Limbs of affected trees that are severely shaded bear normal fruits, and fruits

on nonfoliated portions of branches are usually normal {716).

For all tested cultivars, the symptoms are comparable whether trees are

grown on mazzard or mahaleb rootstocks (.560, 718).

Foliage symptoms are displayed by many cultivars. On diseased Lambert

FIGURE 110.—Lambert cherry fruit affected by little cherry, left and right, showing

smaller size, duller color, and angular and pointed shape, compared with normal

Lambert fruit, center.
234 VIRUS DISEASES OF STONE FRUIT

trees, the fruit crop is readily visible at picking season—less hidden in the leaf

canopy than on normal trees. Careful examination indicates that most leaves

have slight marginal upcurl. On a number of other cultivars, this foliage upcurling is more apparent and is accompanied by marked reddening or bronzing

of the leaf surfaces. The coloration may appear during summer months when

there is an interval of cool nights and sunny days. It is usually most apparent

in September and October.

Often the coloration is apparent first on the under surface of the uprolled

margins of the leaves, but characteristically it develops most strongly in the

interveinal areas of the upper surface of the leaves; the tissues bordering the

midrib and main veins retain their normal color (fig. 111). Usually symptoms

appear first on the basal leaves of the current season's growth.

Foliage reddening is mild to moderate in Bing. Cultivars that are recorded

as displaying strong coloration and that therefore have had frequent use as

indicators for LCV include Sam, Deacon, Mazzard F12/1, Star, and Van (534,

560, 721).

Observations in orchards and test plots suggest that trees infected with LCV

suffer gradual loss of vigor. Cultivars that display severe foliage symptoms

decline most rapidly. In a LCV tolerance breeding program in British Columbia, several of the seedlings which were selected for expanded trials because

they produced desirable fruit in the several seasons following inoculation, have

FIGURE 111.—Star cherry leaves affected by little cherry, showing red coloration in

the areas between the main veins and the retention of green along the midrib and

larger veins. Leaf on right is normal.
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 235

displayed severe foliage upcurling. Subsequently, the foliage has become sparse,

vigor has declined, and fruit size has diminished.

Transmission

The remarkably rapid natural spread of LCV in British Columbia between

1933 and 1950 (208) suggested transmission by an agent that was abundant

and efficient. Natural spread has been recorded in experimental plantings of

sweet cherry in Washington (361) and Oregon (438). Surveys indicate that

natural spread has occurred in commercial plantings in England (333, 340).

In transmission tests at Crestón, British Columbia (717), 18 orchard trees

and seven trees under screen displayed little cherry symptoms after caging of

Macrosteles fasdfrons (Stal.) on the foliage. Similar caging of Scaphytopius

octitus (Say) and Vsammotetùx lïvïdellus (Zett.) gave symptoms in one tree

for each species. Proportions of successful transmissions were low for all three

species. All tests were performed after 1950 when the rate of natural spread

is believed to have dropped to a low level (723), so there is justification for

doubting whether any of the three leafhopper species is the vector responsible

for the original rapid spread of LCV in the Kootenay region. Transmission

was not effected by similar tests with 21 other leafhopper species in 11 tribes

of seven subfamilies; with nine species of insects in other families and with

six species of mites.

There is considerable evidence that infected flowering cherries can be maintained adjacent to sweet cherries for long periods without natural spread of

LCV to sweet cherry (3G1, 688), although once the virus is transmitted to

sweet cherry by budding there is spread to other sweet cherries. It seems possible that all spread from flowering cherry to sweet cherry can be attributed to

natural root grafting or to vector transmission from suckers that frequently

arise from mazzard rootstocks on which flowering cherry trees are grown.

Bud transmission is usually 100 percent successful when buds are taken from

any part of a tree that has been infected for 2 years or longer. Characteristically,

fruit and foliage symptoms appear on inoculated limbs within 1 year of bud

inoculation, and throughout the tree within 2 years. However, LCV transmission requires a relatively long period of graft union contact and falls

into Fridlund's Rate 1 group (222). This suggests that LCV may be

phloem-limited in tree tissues.

Establishment of doddor (Cuscuta subinclusa Dur. & Hilg) on LCV-infected

flowering cherry and on Vinca rosea has induced symptoms on the latter that

include stunting, diminution of flower size, chlorosis, and slight proliferation

(R. M. Gilmer, personal communication).

There have been no reports of success in juice transmission of LCV.

Control Measures

In British Columbia, two approaches have been made to control of little

cherry: prevention of its establishment in parts of the province where it does not
236 VIRUS DISEASES OF STONE FRUIT

occur, and development of resistant varieties to allow reestablishment of a

cherry industry in the Kootenay region.

Under the British Columbia Plant Protection Act (1954), a Little Cherry

Control Area was established, embracing the province's principal disease-free

cherry-growing districts. Preventive measures included the prohibition of all

movement of fruit trees and fresh fruits from the Kootenay region to the

Control Area and enforced removal of affected cherry trees that might be

found in surveys of the Control Area. Subsequently, these measures were

complemented by compulsory eradication of all ornamental flowering cherry

trees within the Control Area and prohibition of their further planting. So far,

the disease has not become established within the Control Area.

Among hundreds of sweet cherry cultivars tested by various workers, all

have become infected when bud-inoculated with LCV. In British Columbia,

a tolerance breeding program has been attempted. Thousands of seedlings of

the more tolerant commercial cultivars have been inoculated and grown within

the region of disease occurrence. Several have shown promise during the first

three seasons of fruiting. A sweet cherry of Lambert type, found within the

Kootenay region, does not appear to become infected by natural spread, although

it becomes severely affected when bud-inoculated.

LCV has been inactivated in buds of several flowering cherry and sweet

cherry cultivars by low-intensity, relatively low temperature, long exposure heat

therapy (37.5° C. for 3 to 4 weeks (499); 37° for 21 days (P. R. Fridlund,

personal communication) ; or 35° for 14, 21, and 25 days (A. F. Posnette and

R. Cropley, personal communication). Several cultivars of flowering cherry,

thus rendered free from LCV, have been made available to nurserymen. LCV

has not been inactivated in sweet cherry by dipping budsticks for 20 minutes

in hot water at 50° (P. R. Fridlund, personal communication).

Remarks

In England, (A. F. Posnette and R. Cropley, personal communication),

most isolates from sweet cherry plantings give milder symptoms on standard

indicators than those induced by isolates from flowering cherry. Symptoms of

widely differing severity have been obtained during indexing at Wenatchee,

Wash., of flowering cherry collections from various parts of United States and

Canada and in the indexing of sweet and sour cherry in Oregon (722). This

has been interpreted as evidence of strain differences among LCV isolates.

X-disease virus in sweet cherry has been reported as 'little cherry" in a

number of publications. The only obvious similarity between the two viruses

is in the symptoms that they induce in sweet cherry growing on mazzard rootstocks. The many differences that have been noted (360, 718) include symptoms induced in sweet cherry on mahaleb rootstocks, ease of bud transmission,

interval between inoculation and appearance of symptoms, differences in foliage
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 237

symptoms on sweet cherry, ability of X-disease virus to infect chokecherry,

P. mahaleh, and peach, (none of which become infected with LCV), demonstrated occurrence of LCV in P. ejnavginata and its varieties (not hosts of

X-disease virus), and vector relationships to the extent that they are known.
CUCUMBER MOSAIC VIRUS INFECTION IN PRUNUS

J. H. TREMAINE

Cucumber mosaic virus (CMV) and Prunus necrotic ring spot virus

(PRSV) were transmitted together to cucumber seedlings by mechanical inoculation with leaves from a Montmorency sour cherry tree showing green ring

mottle symptoms and with leaves from a Black Tartarian sweet cherry tree showing tatter leaf symptoms (715, 736). After several transfers in cucumber plants,

the viruses were separated by sap transmission to tobacco seedlings, which

separated CMV and showed primary necrotic etching, systemic chlorotic rings,

and vein-banding patterns (fig. 112). Sap inoculation of cucumber seedlings

with extracts of infected tobacco leaves induced chlorotic and necrotic spots on

the inoculated leaves and a systemic mosiac pattern (fig. 113). The cucumber

seedlings sometimes appeared to recover. The thermal inactivation point of

CMV from Prunus was between 65° and 70° C. and the dilution end point between 10-2 and lO"'*. The isolate of CMV from sour cherry was purified from

infected cucumber plants and had a sedimentation coefficient of 100 s (667).

The CMV isolates from both sour cherry and sweet cherry reacted with

antiserum of cucumber mosaic virus strain Y (667.)

The isolation of CMV from Prunus on herbaceous hosts was not always

successful. However, its frequent isolation from peach (P. pérsica L.) seedlings

bud-inoculated from the two original sources and failure of isolation from other

trees is good evidence that CMV was not a contaminant. The symptoms induced

by CMV alone in Prunus hosts are not known. Peach and sour cherry seedlings

infected with PRSV and CMV together did not show symptoms differing from

similar plants infected with PRSV only. CMV is probably not involved in

the production of the green ring mottle or tatter leaf symptoms observed in

FIGURE 112.—Primary necrotic flecking and systemic chlorotic ring- and vein-banding

patterns in tobacco infected with cucumber mosaic virus ÍCMV) from Prunus.

238
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE £39

FIGURE 113.—Cucumber inoculated with cucumber mosaic virus (CMV) from Prunus,

showing necrotic and chlorotic spots on inoculated leaves and typical mosaic in

systemically infected leaves.

the original sources, because CMV was not isolated from other trees showing

these symptoms.

CMV from Prunus was transmitted from cucumber to tobacco and back to

cucumber by the aphids Aphis gossypii and Myzus persicae. However, natural

spread from infected peach seedlings to adjoining peach and sour cherry trees

was not observed in tests over a 10-year period.
ROUGH BARK OF SWEET CHERRY

CARL W. NICHOLS

Rough bark of sweet cherry {Primus aviufn) has been reported only in Cahtornia near the community of Valyermo in Los Angeles County and only on the

Lambert cultivar (484). The symptoms on sweet cherry resemble certain symptoms produced by the necrctic rusty mottle (380, 632) and black canker (774)

viruses. They consist of severely roughened bark on the trunk and scaffold

branches from which masses of gum exude (fig. 114, A). They differ from

the rough bark and gumming symptoms that occur on the trunks and scaffold

branches of Burbank cherry trees (fig. 114, C) wherever this cultivar is grown

in California. The symptoms on Burbank are more severe, are always associated

with enlarged nodes on branches 7 years old or older, and have not been shown

to be caused by a graft-transmissible entity. Apparently, this latter disorder is

the rough bark disease of cherry reported in California by Thomas (647, 648).

Leaf symptoms typical of those produced by the Prunus ring spot virus (132)

are the only ones that have been observed on the infected Lambert cherry trees.

Rough bark and gumming symptoms identical to those seen on Lambert cherry

trees in the Valyermo area were produced by bud inoculation on Lambert and on

trees of a mazzard seedling clone that resembled Black Tartarian (fig. 115, B

and D) but not on Napoleon and Bing. Trees inoculated in the fall produced

the first bark symptoms the second summer after inoculation. These symptoms

were discrete, raised bark blisters a few centimeters across, which were similar

to those of cherry bark blister (necrotic rusty mottle) in California (632).

These blisters appeared to coalesce and rupture, forming rough areas from

which masses of gum exuded. The rough areas with exuding gum continued

to develop until, in the third summer after inoculation, they covered large

portions of the trunk and scaffold branches of the inoculated trees. During

the first and subsequent dormant seasons after bark symptoms appeared, the

nonroughened bark on the trunks of the inoculated trees had a dark, shiny

appearance in comparison with the uninoculated checks (ñg. 115, D).

Typical Prunus ring spot leaf symptoms (132) were produced by inoculation

from the Valyermo source on Guame peach; Bing, Lambert, and Napoleon

sweet cherry; and the mazzard seedling clone. A positive ring spot reaction,

gumming and bark necrosis (46)2)^ was produced on Shiro-fugen flowering

cherry. This reaction suggests that either there was more than one virus present

in the infected Valyermo trees or the rough bark virus is related to Prunus

ring spot virus.

240
HANDBOOK NO. 437, U. S. DEPARTMENT OP AGRICULTURE £41

FIGURE 114.—A, Lambert sweet cherry tree near Valyermo, Calif., with rough bark

and gumming (arrous) symptoms of cherry rough bark; B, mazzard seedling clone

with rough bark on trunk during third summer after inoculation with cherry rough

bark virus; D, same tree as in B showing gumming (arrows) and dark shiny

appearance of trunk during third dormant season after inoculation. C, Burbank sweet

cherry tree with nontransmissible big node and canker symptoms similar to those

caused by rough bark virus.
RUSTY MOTTLE GROUP

BRYCE N. WADLEY and GEORGE NYLAND

Causal Viruses

Rusty mottle virus (CRMV), mild rusty mottle virus (MRMV), necrotic

rusty mottle virus (NRMV), and Lambert mottle virus (LMV) incite the

diseases included in the rusty mottle group. Rusty mottle has also been called

severe rusty mottle to distinguish it from mild rusty mottle {112^. CRMV

and MRMV are considered to be closely related, based on certain similarities in

the diseases they cause in cherry. Both rusty mottle and mild rusty mottle

originally were included in the description of rusty mottle (^569^. NRMV

and LMV are considered to be closely related, based on certain similarities

in the diseases they cause. Because some characteristics are common to all

four diseases, they are included here in a rusty mottle group under two names —

rusty mottle and necrotic rusty mottle. Cherry bark blister is a synonym for

necrotic rusty mottle.

History and Distribution

Rusty mottle was reported by Reeves in Washington in 1940 as a new virosis

of cherry that had been repeatedly transmitted during the previous 5 years by

grafting (3^2). In 1947, Zeller and Milbrath (JIO) distinguished mild rusty

mottle from the Washington disease complex. In 1945, a rusty mottle disease was

described in Utah, which is now recognized as necrotic rusty mottle (574, ^76,

382). Later, Reeves and Richards (369) described differences in the types of

rusty mottle found in Utah and Washington, but reached no conclusions as to

their relationship. Lambert mottle, which appears to be related to necrotic rusty

mottle, was reported from British Columbia in 1945 (409) and Montana in

1951 (10- Cherry blister bark, now recognized as necrotic rusty mottle, was

described in 1949 in California (632).

The various diseases of the rusty mottle gfoup are distributed in sweet cherrygrowing areas in Washington, Oregon, Idaho, Montana, Utah, California,

and British Columbia. The rusty mottle disease as described in Washington

and designated subsequently as severe rusty mottle (772) is not known to occur

in California or Utah. Necrotic rusty mottle occurs where cherries are grown

in Western United States and was reported in Great Britain (339).

Host Range

All sweet cherry cultivars tested, mazzard and mahaleb seedlings, Manchu

cherry, peach, apricot, damson plum, and sour cherry are susceptible to the rusty

mottle viruses, although symptoms may not be evident in some.

Necrotic rusty mottle is most severe in Lambert, Seneca, Sam, Hudson, and

Bing, and moderate in Napoleon, Black Republican, Van, Windsor, Lyons,

Macmar, Chinook, and Rainier (-580, 682, 68 5). Cultivars in which symptoms

242
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 243

may be very mild or masked are Black Tartarian, Burbank, Orb, Schmidt, Napa

Long Stem Bing, Deacon, Cardofer Frühe, and Dicke Braune Blankenburger.

In Great Britain, Frogmore, Noble, Lambert, and Bing are damaged {359).

LMV caused symptoms only in Lambert, Seneca, and Starking Gold Giant

cherries of 10 cultivars tested {463) and could not be recovered from inoculated

trees of Shiro-fugen flowering cherry, Montmorency sour cherry, chokecherry,

Italian Prune, apricot, plum, P. emarginata var. mollis, and four cultivars of

apple and one of pear {418, 463, 683).

Rusty mottle and mild rusty mottle were equally severe on the sweet and sour

cherry cultivars tested and also infected peach, apricot, damson plum, some

flowering cherry cultivars, and P. mahaleb, P. virgimana, P. tomentosa, and P.

serótina {7, 684. 770).

Symptoms

Necrotic rusty mottle.—Symptoms in sweet cherry vary considerably with the

cultivar, strain of the virus, and the weather during the early growing season.

Symptoms appear earlier and are more severe during a cold, late spring. The

first leaf symptoms appear 3 to 6 weeks after full bloom. With Lambert mottle,

the buds on upper portions of the shoot fail to open or die soon after opening

{411). Angular necrotic spots form in the leaves. The necrotic areas may be

limited to discrete spots, or they may involve large areas of the leaves {ñg. 115).

Leaves that are more than 50 percent necrotic usually are cast, whereas those

that remain develop the characteristic senescent yellow mottle with green islands

or bands 2 to 3 weeks before harvest {380). The leaf symptoms at this stage

are very similar to those of rusty mottle or mild rusty mottle. Other leaves with

scattered angular necrotic spots may develop shot hole as the necrotic areas fall

out, but the leaves remain on the trees. Leaf symptoms usually are inconspicuous

during the summer and early fall in areas with continuous high temperatures.

Autumnal senescence of the leaves occurs somewhat earlier in diseased than

in healthy trees. Striking leaf patterns of prominent green rings and lines

on a background of yellow, brown, or brilliant red are produced following

the onset of cool fall temperatures (fig. 116).

As the disease develops in the tree, part of the buds and leaf spurs may be

killed, resulting in bare, rangy branches with terminal tufts of foliage {ñg. 117).

In more advanced stages of the disease, the older branches of the tree are killed

and water sprouts develop from the lower portion.

Bark symptoms consist of shallow, necrotic areas, discrete shallow gum blisters,

or deep gum pockets that originate in the wood. Both the virus isolate and the

host cultivar influence the type and degree of bark symptoms. Bark blisters and

deep gum pockets are common in Bing, but general bark necrosis is common in

Lambert.

The brown, angular, necrotic spots, rusty chlorotic areas, shot holes of the

leaves, and the blisters, gum pockets, and general necrosis of the bark constitute

the most important diagnostic symptoms of the disease {380, 684). Infected
244 VIRUS DISEASES OF STONE FRUIT

FIGURE 115.—Top, Leaves from Bing cherry, below row, inoculated with necrotic rusty

mottle virus; small Bing cherry leaves, above row, have twisted leaf symptoms. B, Leaves

and fruit of Napoleon cherry affected by Lambert mottle.
HANDBOOK NO. 437, U.S. DEPARTMENT OP AGRICULTURE £45

FIGURE 116.—Senescent leaves in late fall from Lambert cherry tree with necrotic

rusty mottle, showing characteristic rings and line patterns.

trees are killed more quickly in areas with severe winters than in areas with

relatively mild ones. Lambert, Sam, Seneca, and Hudson often fail to survive

the second season after infection in Utah.

Rusty mottle and mild rusty mottle.—The first foliage symptoms in cherry

appear 4 to 5 weeks after full bloom (532). The small basal leaves are the first

to show chlorotic mottling. The chlorotic areas remain light green, and the

remainder of the leaf rapidly develops late-season coloring of bright yellow,

brown, or red (fig. 118). The afîected leaves soon abscise. Thereafter, variable

chlorotic mottling of most of the foliage takes place (555). Symptoms of mild

rusty mottle do not change much after initial leaf fall and appearance of mottling

except for some bronzing of the leaves through the summer (fig. 119) (772).

With rusty mottle, many of the older leaves rapidly develop autumnal colors

and subsequently drop, resulting in the loss of 30 to 70 percent of the leaves by

the time fruits are mature (552). Fruits are smaller, have insipid flavor, and

ripen late. Infected trees decline, and the main limbs die back. Trees afîected

by mild rusty mottle decline more slowly than those affected by rusty mottle

(770). Foliage symptoms occur in peach trees inoculated with buds from

infected cherry trees and are not unlike those produced in cherry (444, 552).

Montmorency sour cherry trees in the field from which MRMV was recovered

in Oregon (444, 772) and trees in Oregon and California which were inoculated with MRMV from sweet cherry had leaves that were smaller than normal,
246 VIRUS DISEASES OF STONE FRUIT

FIGURE 117.—A, Fourteen-year-old Lambert cherry tree showing bare, rangy limbs and

tufted terminals characteristic of advanced stage of necrotic rusty mottle; B, right,

young Lambert tree inoculated with buds from tree in A and showing retarded

leafing and blossoming compared with uninoculated tree, leff.

showed mild mottling and rustiness, and, later, necrotic areas. Some affected

leaves were cast.

No distinctive symptoms have been observed in apricot, Italian Prune, damson

plum, or chokecherry. Occasionally, Kwanzan and Naden flowering cherry

showed slight leaf symptoms {417, 772).

Transmission

The rusty mottle group viruses are easily transmitted through tissue grafts to

susceptible host plants. They have not been transmitted mechanically in expressed juice. The incubation period is usually less than 1 year but may be

as much as 3 years. Sometimes, only part of a tree will show symptoms the

first season after infection, but by the second season the virus will be distributed

throughout the tree. Trees inoculated in August will develop symptoms the

following spring. Trees inoculated as the buds are breaking dormancy often

develop symptoms within 30 days (6, 555, 682, 770). Natural spread of rusty
HANDBOOK NO. 437, U. S. DEPARTMENT OP AGRICULTURE 247

mottle disease is slow in sweet cherry orchards and often occurs only to nearby

trees. Most of the disease in orchards results from propagation of infected trees

by nurseries. Mild or symptomless cultivars often play an important part in

perpetuation and spread (9, 411, 685).

Characteristics of the Viruses

NRMV was inactivated in Lambert cherry budsticks treated in a hot-water bath

at 50° C. for 10 or 13 minutes or at 52° for 5 minutes (487), but MRMV

was not inactivated by hot air in 4 weeks at 38° (George Hyland's unpublished

data). The virus nature of this group of diseases is assumed, but the easy cure

by heat of necrotic rusty mottle is similar to some diseases of suspected mycoplasma nature. The viruses have not been purified, so nothing is known of their

physical or chemical properties.

Control Measures

Planting of virus-free nursery trees should give economic control of this

disease. Diseased trees should be removed as they are discovered to prevent

natural spread. Several cultivars commonly used to pollinate major cultivars of

sweet cherries may be symptomless hosts and have transmitted NRMV when

infected buds were grafted to sensitive varieties {682). Symptomless cultivars

should be indexed before budwood is taken for propagation.

FIGURE 118.—Bing cherry leaves affected by mild rusty mottle, showing chlorotic lings

and mottle.
248 VIRUS DISEASES OF STONE FRUIT

FIGURE 119.—A, Normal leaf of Bing cherry; B, comparable leaves afïeaed by rusty

mottle, showing various patterns that develop on leaves that are cast prior to harvest;

C, branch from a Bing cherry tree affected by rusty mottle, 1 week before harvest,

showing that the fruits are not malformed but that the leaf cast has been heavy.
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 249

Remarks

Evidence that necrotic rusty mottle is quite different from mild rusty mottle

is provided by the difference in heat stability of the viruses. NRMV was inactivated by relatively short hot-water treatments, but MRMV was not inactivated

when infected cherry trees were heat-treated for 4 weeks in air at 38° C. Evidence that NRMV and MRMV may be related is provided by similarity of

symptoms in cherry and because mild rusty mottle interferes with or partially

protects against necrotic rusty mottle (682, and authors' unpublished data).
SHORT STEM

C. L. PARISH and PHILIP W. CHENEY

Causal Virus

Short Stern virus (SSV).

History and Distribution

Short stem was first discovered at Flathead Lake, Mont., in 1958 (4, 5, 8, 10).

It was later found at Hood River, Oreg., in 1962, although it was not identified

as such until 1964.

Economic Hosts

All sweet cherry cultivars tested.

Other Hosts

The virus when introduced by bud inoculation affected sweet cherry.

Abundance plum (Prunus salicina), and seedlings of P. maackn and P. davidiana which exhibited symptoms resembling those of twisted leaf. Drake

almond, Riland and Tilton apricot, Elberta and J. H. Hale peach, and seedlings

of P. besseyt, P. capulí, P peiisylvanica, and P. serótina were symptomless carriers of SSV.

Indexing of the following plants inoculated with SSV failed to reveal the

presence of the virus : Golden Delicious apple, Malus platycarpa, Russian apple

seedling (R12740-7A), Prunus andersonii, P. vhginiana, P. tomentosa, Chilcott

and Fiebing plums (P. americana), Italian Prune and Tragedy prune (P.

domestica), Burbank plum (P. salicina), Shiro plum (hybrid), and Bartlett

pear.

Symptoms

Symptoms of the short stem disease occur on leaves, fruit, and fruit stems.

Constriction of the veins or midrib causes part, or all, of the leaf to tip or roll

downward, resembling aphid injury. The twisting and rolling of the petiole or

blade first appears in April or May on the spur leaves. Later, some leaves on

the current season growth may become affected. This malformation is permanent,

and affected leaves are retained by the tree until the time of normal abscission.

Fruit symptoms usually occur as shock symptoms on a small percentage of

cherries on newly infected trees. Rough misshapen fruits can usually be observed the first and second year following infection. In some instances, color

break may also occur on the misshapen cherries, resulting in dappled, bumpy

fruits. As the name of the disease indicates, shortened fruit stems are the most

characteristic symptom (fig. 120). The shortened stems usually do not occur to

an appreciable extent until the second year following infection; this symptom

develops more slowly throughout the tree. The fruit stems vary from nearly

normal length to as short as one-quarter inch in length. At this stage, the shock

250
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 251

FIGURE 120.—A branch from a short stem-infected Lambert cherry tree showing twisted

leaves and both long and short fruit stems on the same branch.

symptoms of bumpy, dappled fruit no longer occur; the only symptoms are

twisted leaves and short fruit stems.

Transmission

The virus can be transmitted easily by tissue grafts. It spreads naturally

in the field, but the vector is not known.

Control Measures

It is strongly recommended that infected trees be removed so they will not

serve as sources of inoculum. Virus-free propagating materials should be used

for replanting.

Remarks

Symptoms incited by SSV resemble those incited by tomato bushy stunt virus

in sweet cherry in Ontario (16). However, attempts to isolate tomato bushy

stunt virus from short stem infected trees have been negative (authors'

unpublished data).
SPUR CHERRY

EARLE C. BLODGETT and MURIT D. AlCHELE

Causal Virus

Spur cherry virus (SCV).

Synonyms

Plath Bing; spur Bing.

History and Distribution

An 8-year-old Bing cherry tree {Prunus avium), thought to be a mutant,

was discovered in an orchard near Yakima, Wash., in 1962. The tree was

producing a good crop of what appeared to be normal Bing fruits on a compact

or spur-type growth. Indexing on Bing showed that this type growth was caused

by a previously undescribed virus {ßS^.

Natural occurrence has been limited to the original tree. Nursery stock has

been propagated by several nurserymen and sold as dwarf Bing cherry trees and

budwood has been distributed for experimental purposes to other areas and

States.

Economic Hosts

Of 41 cherry cultivars inoculated with SCV, 18 showed reduction in growth.

The responses were cultivar specific and variable {156, 269). Inoculated Tilton

and Riland apricot were affected (136).

Other Hosts

J. H. Hale peach, Kwanzan flowering cherry, Mazzard F12/1, seedlings of

P. capulí, P. maackïî, P. serótina, and P. tomentosa, when artificially infected,

are symptomless carriers of SCV. Similarly infected mazzard and mahaleb

seedlings are known to be carriers. The virus could not be recovered by indexing inoculated plants of Shiro plum, Italian Prune, Bartlett pear, and Russian

apple (R/12740-7A). Inoculated Elberta peach did not show symptoms, and

the trees have not yet been reindexed.

Symptoms

Effects on sweet cherry trees vary from none on some cultivars to severe leaf

epinasty and bark necrosis of current season's growth on others. Some cultivars

are dwarfed in varying degrees because of reduced internodal space (hg. 121),

and a few show a spiral growth. Tips of stunted shoots are thicker, rougher,

and more brittle than normal. As a group, sour cherry cultivars are less affected

by the virus than sweet cherries and, in some cases, appear to be stimulated

{6S, 156 and P. W. Cheney, M. D. Aichele, C. L. Parish, and E. C. Blodgett,

unpublished data). Apparently there are no fruit symptoms on cherries. Cultivars observed in fruit include Badacsoner, Bing, Deacon, Early Richmond,

English Morello, Montmorency, Napoleon, Schmidt, Sue, and Van (P. W.

252
HANDBOOK NO. 437, U. S. DEPARTMENT OP AGRICULTURE 253

FIGURE 121.—Efifect of the spur cherry virus. On the left are 10 Van nursery trees simultaneously budded and inoculated the year before. On the right are 10 Van nursery

trees similarly propagated, but not inoculated. All trees are on mazzard root.

Cheney and C. L. Parish, personal communication). Tilton and Riland apricot,

when bud-inoculated with SCV, show typical apricot ring pox symptoms.

Transmission

Transmission is easily accomplished through budding or grafting. Virus

movement within a sweet cherry tree (e.g., Bing) appears to be rapid because

trees single-bud inoculated in the fall will exhibit good symptoms early the next

season. There is no evidence of natural spread in orchards, although spread

through natural root grafts of closely spaced cherry trees has occurred.

Control Measures

Use certified nursery stock for propagation. Stock propagated from SCVinfected mother trees is not eligible for certification.

Remarks

Propagation in the nursery from budwood from infected Bing cherry trees

results in poor bud stands and irregular and variable growth (6S). A few nearnormal appearing shoots from the original diseased tree grow as normal Bing

trees in the nursery row, but most nursery budlings grown from affected shoots

appear to make dwarfed trees (E. C. Blodgett and M. D. Aichele, unpublished

data). The virus appears to affect susceptible sweet cherry cultivars more

severely when the trees are propagated on Prunus avium rootstocks than on P.

mahaleb (P. W. Cheney, M. D. Aichele, C. L. Parish, and E. C. Blodgett,

unpublished data).
SWEET CHERRY ROUGH FRUIT

BRYCE N. WADLEY

Cherry rough fruit was discovered in I960 in plots at the Howell Field

Station, Utah State University, North Ogden. Symptoms were observed in Van

(Prunus avium) and in other sweet cherries with labels indicating Iranian

origin {683, 687). Budwood was apparently brought into the station by students

from Iran in 1957. Because of lack of suitable rootstocks for propagation,

some of the buds were grafted to Van and others were placed in mahaleb trees.

The virus nature of the disease was determined during 1960-64. All affected

and inoculated trees were destroyed in 1965. No evidence of natural spread

was obtained.

All sweet cherry cultivars tested are hosts of cherry rough fruit virus (CRFV).

These include Van, Bing, Lambert, Napoleon, and Valera, and 32 sweet cherry

selections from Iran. Peach, apricot, Italian Prune (P. domestica), and Montmorency sour cherry were inoculated but developed no symptoms. No attempt

was made to recover the virus from these plants.

The most characteristic symptoms are the roughened and crinkled surface of

affected fruit at maturity (fig. 122). Fruit symptoms on dark-fruited cultivars

# ^ O #0^

A O O O 9 49

;9 €9 O 9 019

FIGURE 122.—Three fruits at right edge are normal Van sweet cherries; the others are

fruits of Iranian cherry selections and Van afifected by cherry rough fruit, showing

roughening and crinkling.

254
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 255

initiate as small, irregular-sized red spots. As the fruits mature, these spots

intensify in color and become bright red before color develops in the surrounding

tissue. The flesh beneath the spots appears to stop growing and matures earlier

than the surrounding tissue. This leads to depressions and an uneven, roughened

surface. As the fruits mature, the colored spots become obscured but the

crinkled surface remains. No diagnostic leaf symptoms have been observed,

although leaves on an infected Van tree were smaller and paler green, and

terminal growth was less than that on an adjacent healthy Van tree. Fruit

symptoms vary from year to year but are generally more severe on large fruit than

on small. Symptoms are milder on light-colored fruit cultivars; they do not

develop red spots but do produce some rough fruit.

Transmission was readily achieved in bud or tissue grafts to sweet cherry.

However, no symptoms developed until the second or third year after inoculation.

Then, only fruits growing near the inoculum buds developed rough fruit symptoms. The virus moved slowly through the inoculated trees, and, after 5 years,

fruits on many branches were still healthy. The virus moved somewhat faster

in Van than in Bing or Lambert.

Infected trees should be removed and destroyed. Van is suggested as the index

host for this virus. This virus disease was inadvertently introduced into the

United States in budwood from a foreign source and illustrates how easily such

diseases can be brought in if the budwood is allowed to bypass plant quarantine

inspection.
TOBACCO MOSAIC VIRUS INFECTION IN PRUNUS

R. M. GILMER

Tobacco mosaic virus (TMV) was initially isolated in 1967 in New York

from sour and sweet cherry trees (231). TMV has since been recovered from

mahaleb rootstocks that originated in Washington and Oregon, a fact suggesting

that the virus may be widely distributed in stone fruits.

TMV has been isolated from trees of sour cherry, sweet cherry, and from

seedlings of mahaleb cherry. Other stone fruits are probably infected, although

TMV was not isolated from any of eight peach cultivars or from peach seedlings

in limited indexing.

TMV was isolated from apple (231, 373), pear (263), and grape (237).

Isolates from sweet cherry infect a large number of herbaceous plants, including

Chenopodium quinoa, a useful host for recovering the virus from stone fruits.

Havana 423 tobacco, a local lesion host, \^ useful for confirming virus identity.

TMV is evidently a parasite but not a pathogen in stone fruits because none

of the trees from which TMV was isolated have shown any symptoms attributable

to TMV infection. The foliage of infected mahaleb seedlings was normal in

appearance and the seedlings grew vigorously. A Montmorency sour cherry tree

in the Geneva virus-indexed foundation planting contained TMV, but the tree

appeared completely normal in all respects. Several infected sweet cherry trees

of different cultivars were also without symptoms.

All of the isolates of TMV recovered from the stone fruits closely resemble

isolates obtained from apple, pear, and grapes. All are "y^^^ow" strains, similar

to the tomato or Dahlemense isolates. The thermal inactivation point is between

90° to 95° C, and dilution end point in expressed C. quinoa sap is 10'^ or

greater. Electron micrographs depict straight rods about 300 m/x in length.

It is doubtful that the occurrence of TMV infections in cherries is of any

economic significance. Infected trees are without symptoms, and the present,

very limited data suggest that the concentration of TMV in infected cherries is

quite low (231). In direct isolations from cherry foliage, inoculum usually

induced only 1 to 3 local lesions per plant in the sensitive indicator C. quinoa,

and attempts to recover TMV from leaves of known infected trees often failed.

The virus was transmitted more readily from petals than from leaves (231).

How TMV is transmitted in the stone fruits is not known. Recovery of TMV

from yearling mahaleb seedlings suggests that TMV may be transmitted through

seeds of stone fruits as it is in apple, pear (263), and grapes (237).

256
XYLEM ABERRATION

A. JUERGEN HANSEN

Xylem aberration is a little-understood disease syndrome of sweet cherry,

sour cherry, and apricot. It has been reported only from the Okanagan Valley,

British Columbia (412, 419). Field symptoms consist of stunting and severe

distortion of terminal shoots, irregular weaving growth of sideshoots, distortion

of leaves similar to that encountered in the twisted leaf disease, irregular fruit

distortion, development of cankers on shoots and branches, and extensive gumming throughout the framework. After bud transmission from infected field

trees, the same range of symptoms was encountered in indicator trees. In

addition, a severe necrotic streaking and pitting in the wood of the trunk and

major branches was observed (fig. 123). All symptoms were most severe on

sweet cherry, notably Sam, and occurred in a milder form in Montmorency sour

cherry. In Wenatchee (Wenatchee Moorpak) apricot, leaf twisting was not

observed, but pitting was similar to that in sweet cherry.

Field spread of the syndrome has not been observed, although affected trees

were found in scattered locations. However, natural spread has occurred over

short distances in experimental plots. In experimental work, inoculated trees

have not always developed the full range of symptoms; especially the wood

pitting has been absent in several cases where other symptoms were present.

The nature of the xylem aberration syndrome has not been definitely established. Transmissibility, natural spread, and the type of symptom induced are

the only indications that a virus may be involved. The disease differs in several

aspects from Prunus stem pitting {206, 396, 470) observed in the East and

should be considered a separate disease unless future research shows that a

relationship exists.

257
258 VIRUS DISEASES OF STONE FRUIT

FIGURE 123.—Xylem aberration. Severe pitting in trunk section of a cherry tree

(bark removed).
NONTRANSMISSIBLE DISORDERS THAT

RESEMBLE VIRUS DISEASES

ALMOND CORKY SPOT

H. K. WAGNON, H. E. WILLIAMS, and J. A. TRAYLOR

An excessive necrotic leaf spotting disorder of Nonpareil almond trees was

first noted in 1936 in a young orchard of mixed almond cultivars in Butte

County, Calif. From 1936 to 1938, C. F. Kinman conducted virus transmission

studies on the disorder, and from 1940 to 1944, G. L. Stout, L. C. Cochran,

and E. E. Wilson carried out additional studies. During 1957-63, the problem

of virus transmission was further investigated, particularly in regard to diseasefree almond nursery stock and to verify previous tests (634, 701).

The cause of almond corky spot has not been determined but is known to be

associated with occasional almond seedling rootstocks. Early work provided

evidence that virus might be involved because symptoms developed on healthy

Nonpareil scions grafted to affected orchard trees; however, graft-inoculation

tests on almond seedlings (634, 701) and on healthy Nonpareil trees failed to

demonstrate a graft-transmissible agent and also failed to show the disorder

to be bud-perpetuated. The disorder occurs often on Nonpareil but occasionally

on Jordanolo. Corky spot develops only on cultivars budded to seedling almond

rootstocks, particularly those grown from bitter almond (P. amygdalus) seed.

The outstanding symptom is the development of extensive necrotic spotting

of the leaves, the spotting being predominantly near the leaf margins (hg. 124).

The necrotic spots begin to appear as early as April and increase in size and

number as the season advances. By late summer, all or parts of the necrotic

areas may fall away, thus creating a perforated leaf with irregular margins.

The roots of a limited number of trees that were examined had bark that

was thicker than normal and somewhat spongy in texture. Stem pitting symptoms have not been observed on these affected roots.

The disorder should not be confused with oedema, which is characterized by

similar symptoms developing under certain environmental conditions. Oedema

is somewhat rare in almond and is not restricted to the Nonpareil cultivar.

Usually, when oedema occurs, it affects many trees in a planting and does not

occur consistently each year on the same tree as does corky spot.

259
260 VIRUS DISEASES OF STONE FRUIT

FIGURE 124.—Four Nonpareil almond leaves showing necrotic spotting symptoms of

corky spot, compared with normal leaf on the left.
APRICOT GUMBOIL

GEORGE NYLAND

Gumboil is a nontransmissible disorder of apricot in California (652) known

to occur in Contra Costa, San Benito, Santa Clara, San Joaquin, and Stanislaus

Counties. Scattered aiïected trees occur in orchards of Royal and Tilton.

The disease is most striking in trees at least 10 years old. Affected trees

are smaller and less fully branched than unaffected trees. There is some

dieback of small shoots, and annual terminal growth is less than normal.

The most conspicuous symptom is the extremely rough, cracked bark of the

trunk and older branches (fig. 125). The roughness becomes less pronounced

toward the younger portions of the tree, where it gives way to more or less

discrete swellings in the wood and bark. Surface bark removed from these

areas reveals masses of brown gum in pockets of necrotic tissue (fig. 126).

In older branches, the pockets extend from the inner wood to the surface of

FIGURE 125.—^Apricot gumboil. A 15-year-old tree of Royal apricot on Myrobalan 29C,

showing rough bark and overgrowth at the union.

261
262 VIRUS DISEASES OF STONE FRUIT

the bark (fig. 127). On 3- to 6-year-old shoots, only discrete blisters, or

gumboils, can be seen. Gumboils are difficult to find in wood younger than

3 years.

On myrobalan roots, affected trees are markedly overgrown at the union

FIGURE 126.—Apricot gumboil. Scaffold limb of a 15-year-old tree of Royal apricot

(tangential face) showing pockets of gum and necrotic tissue.
HANDBOOK NO. 437, U. S. DEPARTMENT OP AGRICULTURE £63

(fig. 125). Such trees exhibit excessive development of root suckers. The

understocks are much smaller than those of normal trees of the same age.

Affected trees are usually the first in the orchard to show signs of water stress

between irrigations.

Fruits are fewer on affected trees than on healthy trees, but otherwise appear

normal for the variety. Typically, they mature a few days earlier than fruits

on unaffected trees.

FIGURE 127.—Apricot gumboil. Scaffold limb of Royal apricot (cross section) showing

gum-filled necrotic lesions extending radially from 4th-year wood.
264 VIRUS DISEASES OF STONE FRUIT

Distribution of diseased trees in the orchard suggested that propagation was

the means by which the disease was spread. Most affected trees of the same age

showed the same degree of symptom expression. A tree was occasionally found

with symptoms more severe or advanced on one side or in one or two main

branches than in the others. No partially affected trees were found. Affected

trees occurred singly or in scattered groups of two or more. In one case, it was

possible to trace the origin of affected trees to a specific orchard containing

diseased trees.

The disorder is perpetuated by buds or scions from affected trees placed on

Myrobalan 29C, myrobalan seedlings, or apricot seedlings, but not when peach

seedling rootstock is used. Healthy scions of Royal and Tilton grafted on an

apricot tree with good symptoms of gumboil did not develop symptoms in

5 years. When buds from trees with symptoms of gumboil were placed in

healthy trees of Royal and Tilton, no transmission occurred during the following

10 years (6:52 and author's unpublished data). All attempts to transmit the

disorder in tests reported earlier failed.

There are at least three types of rough bark disorders of apricot, none of

which has been transmitted ; gumboil is the type most often encountered.

Gumboil and other rough bark disorders of apricot can be avoided by using

healthy trees as sources for propagation.
CHLOROTIC FLECK OF MYROBALAN PLUM

R. M. GiLMER

History and Distribution

The name, "chlorotic fleck," suggested by Brase and Parker (97), appears

preferable to the term "asteroid spot" applied by Hildebrand {307), who

originally described the disorder. Asteroid spot had been previously used as

the name for a virus disease of peach (162) not related to the present disorder.

Chlorotic fleck was initially observed about 1941 in New York. Hildebrand

{507) reported an incidence as high as 90 percent in myrobalan nursery stock.

The disorder is common every year in New York nurseries, but its prevalence

fluctuates considerably.

Schuch {605) observed a similar or identical leaf flecking of Brompton plum

{Vrunus domestica) in Germany in 1937. Although chlorotic fleck has not

been reported specifically from other areas, it is undoubtedly more widespread

than the limited published observations indicate.

Economic Hosts

Myrobalan plum and Brompton plum are the only reported hosts. A

closely related disorder, yellow spot of peach, occurs in California (746) and

has been observed on peach seedlings in New York and Pennsylvania (R. M.

Gilmer, unpublished data).

Symptoms

In New York, symptoms of chlorotic fleck are evident from late June until

October but are more prevalent in late August and September. Chlorotic fleck

appears only on fully expanded, mature leaves, and the symptoms persist for

the remainder of the growing season after they have developed.

Chlorotic fleck is most prevalent on 1- or 2-year-old myrobalan seedlings

and is much less common on large myrobalan trees. When symptoms occur

on large trees, they are commonly restricted to the foliage of water sprouts or

suckers arising at the base of the trees.

Circular chlorotic spots or flecks, ranging in size from mere pinpoints to

spots 1 to 2 mm. in diameter, develop on mature leaves. Although spots may

occur anywhere on the leaf lamina, they are often concentrated along the midrib

or lateral veins (fig. 128). Margins of the smaller flecks are often diffuse,

but in the larger spots, the margins are usually sharply defined. Such spots

may show indications of one or more concentric rings.

The number of chlorotic flecks on a single leaf may vary from one to many;

if flecking is abundant, the leaf lamina is often distorted and twisted. Severely

affected terminals are rosetted with many leaves reduced in size, and the entire

myrobalan seedling may be severely stunted.

Symptoms may also develop in the young bark of affected shoots. Spots on

265
266 VIRUS DISEASES OF STONE FRUIT

FIGURE 128.—Symptoms of chlorotic fleck on leaves of myrobalan plum infested with the

eriophyid mite, Aculus fockuei.

young bark are generally oval rather than circular, generally larger than foliage

flecks, and are often reddish.

Chlorotic fleck of myrobalan plum is a toxicogenic injury resulting from

feeding by an eriophyid mite, Aculus fockuei (Nal. & Trt.). Schuch {60})

associated the same mite with leaf flecking of Brompton plum in Germany. A

related disorder, yellow spot of peach (p. 292), is induced by a closely related

mite, A. cornutus (Banks), in California {746), and what is presumably the

same mite has been found on peach seedlings with yellow spots in New York.

Mites feeding on mature foliage did not induce chlorotic fleck, but symptoms

appeared 13 to 33 days after the mites fed on immature leaves {258). Wilson

and Codiran {746) similarly found that yellow spot of peach occurred only

after A. cornutus had fed on immature foliage and that about 12 days elapsed

A related disorder, yellow spot of peach (p. 292), is induced by a closely related

from the injection of a toxin by the mites.

The possibility that chlorotic fleck is a virus disease with A. fockuei as its

vector appears to be conclusively excluded by the failure to transmit the disorder

by bud inoculation or propagation from afi^ected seedlings (2.58).
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 267

Control Measures

Chlorotic fleck was completely eliminated in nursery plants by three applications of a miticide at 2-week intervals from late June through early August

(238).

Remarks

Hildebrand (307) reported that the occurrence of chlorotic fleck in myrobalan rootstocks resulted in poor budtake of Italian Prune buds and subnormal

growth of Italian Prune budlings. Brase and Parker (97) also found that

Italian Prune, Stanley, and Abundance plum budlings were less vigorous when

propagated on myrobalan seedlings with severe chlorotic fleck. Since the disorder is easily controlled, increases in grade of nursery stock may repay the

costs of application of a miticide.
CONSTRICTION DISEASE OF STANLEY PRUNE

K. G. PARKER and R. M. GILMER

Synonyms

Decline of Stanley prune.

History and Distribution

Brase (96) discovered a constriction of the rootstock immediately below

the union with the scion in declining trees of Stanley prune {Prunus domestica)

m New York. The affected Stanley trees were propagated on myrobalan seedling

rootstocks and appeared in orchards planted after 1943 but not in those planted

before this date. Brase (personal communication) considered that the presence

of constriction in plantings made after 1943 was possibly associated with the

change from European to domestic sources for myrobalan rootstocks caused

by World War II.

Constriction is common in Stanley prune orchards in New York. Few or

many trees of an orchard may be affected—occasionally, so many that the entire

planting is removed. As far as the authors are aware, constriction is not a

serious problem in other areas because Stanley prune is not widely grown

elsewhere.

Economic Hosts

Stanley prune is the only cultivar of commercial importance affected with

constriction but identical symptoms have been observed in selections of several

breeding lines of prunes developed at the New York State Agricultural Experiment Station. Very similar disorders have been reported in apricot or Japanese

plum propagated on myrobalan rootstocks. (See "Remarks.")

Symptoms

Constriction may develop at any time after a Stanley tree is propagated until

at least the 10th year of growth in the orchard. Incipient constriction may

occasionally be visible in 1-year-old nursery trees, but more commonly the

disorder is not evident until 1 to 5 years after the tree is planted in the orchard.

Since the scion-rootstock union is commonly planted below ground, the early

stages of constriction are generally overlooked until it has progressed to the

point that tree growth is affected. Many affected trees grow vigorously for

2 to 5 years before foliage symptoms are observed.

The initial symptoms are weak growth of terminals and yellowing and upward

rolling of the foliage. Kirkpatrick et al. {373) reported loss of chlorophyll

from the interveinal areas of the leaves. These areas gradually change from

green to yellow to yellow-orange and ultimately become bright red. The areas

immediately contiguous to the veins remain green for some time but finally

also become orange or red. At this stage, the leaf margins are necrotic, and

areas of necrosis may develop in the lamina.

268
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE £69

Affected trees are weakly anchored in the soil. When the scion-rootstock union

is examined, a pronounced overgrowth of the scion is evident (""inverted

shoulder") and the rootstock is markedly reduced in diameter (fig. 129).

The overgrown scion tissues are cheeselike in consistency. Numerous, abnormally large lenticels appear in the scion bark immediately above the union.

Below the union, the bark of the rootstock is necrotic in large areas or completely

dead (fig. 130).

FIGURE 129.—Overgrowth of the scion and constriction of the myrobalan rootstock in

Stanley prune tree right. A normal Stanley tree of the same age at left.
270 VIRUS DISEASES OF STONE FRUIT

Cross sections at the union area reveal considerable disorganization of the

phloem and xylem of both scion and rootstock.

Affected trees usually die within 1 to 2 years after the foliage symptoms,

which result from constriction, become evident. Less commonly, affected trees

collapse completely within a short time, particularly under conditions of severe

moisture and temperature stress.

Control Measures

Brase and Parker (97) found that Italian Prune trees propagated on myrobalan seedlings did not develop constriction even though Stanley trees propagated on seedlings of the same lot became constricted. Brase (personal

communication) therefore suggested the use of Italian Prune as an intermediate

stem piece between the Stanley scion and myrobalan rootstock. During the past

8 years, Stanley trees with such interpieces have not developed constriction.

Brase (unpublished data) also tested selections of myrobalan as prospective

seed source trees. The seedling progenies from these selections are currently

being tested as rootstocks for Stanley. Some of them appear promising for direct

propagation with Stanley.

FIGURE 130.—Left, Three Stanley prune trees with constriction, showing varying degrees

of necrosis of the myrobalan rootstocks after temoval of bark; right, normal Stanley

prune tree of the same age with bark removed.
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 271

Remarks

Parker and Brase (unpublished data) compared the occurrence of constriction

in five individual selections of Stanley scionwood propagated on myrobalan

seedlings from six seed source trees. The presence and severity of constriction

were consistently associated with the source of rootstocks and were not influenced by scion source. Constriction commonly developed in trees propagated

on seedlings of a myrobalan tree infected with Prunus ring spot virus (PRSV) ;

however, constriction also developed in several trees propagated on seedlings

of a second myrobalan tree not infected with PRSV.

Brase and Parker {97) suggested that the later development of constriction

in Stanley trees was perhaps related to the occurrence of a chlorotic spotting in

the leaves of some myrobalan seedlings. Hildebrand {507) had previously

suggested that this leaf spotting might be of genetic origin. Later studies by

Gilmer and McEwen {258) demonstrated that this chlorotic leaf spot in

myrobalan resulted from feeding by an eriophyid mite.

Progenies of certain breeding lines of plums, particularly those derived from

either of the two parents of Stanley (Agen x Grand Duke) also developed

constriction when propagated on myrobalan seedlings. Of selections of four

breeding lines in which Grand Duke was a parent, 30 to 50 trees propagated

on myrobalan in I96I had died of constriction by I968 (J. P. Watson,

unpublished data). Occasionally, constriction also developed in selections of

breeding lines derived from Imperial Epineuse and Golden Transparent Gage

(j. P. Watson, unpublished data).

Day (185) noted a disorder much like constriction in Kelsey plum (P.

saJicina) and Sergeant plum (P. domestica) on seedling myrobalan rootstocks

and in French Prune and Sergeant trees on clonal myrobalan rootstocks. A

similar disorder was reported in apricot propagated on myrobalan seedlings

(543). Whether these difficulties are identical with constriction or not,

myrobalan seedlings from different seed source trees obviously vary considerably in their compatibility with certain plum cultivars.

Although a virus causation has not been completely excluded, there is

no direct evidence that constriction is caused by a virus. The absence of

constriction in Stanley trees separated from the myrobalan rootstock by an

intermediate stem piece of Italian Prune suggests that a virus is not involved.

Clearly, the incidence of constriction is higher in certain lots of myrobalan

rootstocks, and constriction develops only when such rootstocks are propagated

with certain prune cultivars. These observations suggest that constriction is a

type of scion-rootstock incompatibility affected by the genetic composition of

both scion and rootstock. Yet this explanation is difficult to reconcile with the

fact that in many instances constriction develops only after the tree is several

years old. It is possible that initial mild stages of constriction weaken the trees

just enough to predispose them to low temperature injury at the union and

that this further injury leads to the further development of constriction {373).
HIGH TEMPERATURE MOTTLE OF

MONTMORENCY CHERRY

PAUL R. FEIDLUND

Leaves on rapidly growing shoots of apparently virus-free Montmorenq^

sometimes expand with mild to severe mosaic patterns of light and dark green.

The symptoms resemble those of a virus-induced mosaic or a chimaera (fig.

131). The patterns may continue to appear in the succeeding leaves that are

formed on the shoot. However, because a shoot usually ceases to elongate when

these mosaic symptoms appear, the symptoms are primarily limited to a few of

the tip leaves. The mosaic persists after the leaves enlarge, but symptoms never

appear in older, expanded leaves.

The upper surface of an affected leaf appears to have a pebbled texture with

raised dark and sunken light-green areas, but this is probably an optical illusion.

Additionally, the lighter areas appear to border on the veins, but this is not

always true.

The exact cause of this nontransmissible abnormality is unknown, but it is

primarily a greenhouse problem associated with high temperatures, particularly

at night. At Prosser, Wash., greenhouse-grown Montmorencys frequently

produce this symptom if constant temperatures are maintained at 26° C. or

higher, but symptoms rarely occur at lower constant temperatures. Symptoms

FIGURE 131.—Right, Two leaves of Montmorency cherry showing mottle induced by

high temperature, compared with normal leaf, left.

272
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 273

occur more frequently late in the spring than during the winter, but this may

result from a seasonal rise in greenhouse temperatures. When the conditions

for symptom production in Montmorency appear ideal, a few plants of other

species may also produce abnormal tip leaves. For instance, oriental flowering

cherry, P. serrulata, may have distorted tip leaves with abnormal veins, and

apricot may form tip leaves similar to those affected by 2, 4-D. However, the

abnormality is invariably more frequent in Montmorency than in the other

species.

Field grown Montmorency at Prosser rarely are affected. A late-summer

mildew infection of the tip leaves can be confused with this abnormality.
ITALIAN PRUNE LEAF SPOT

A. W. HELTON

Synonyms

Italian Prune leaf spot sometimes is called shot hole (296, 303), and it may

be referred to by a number of descriptive terms indicative of any of the several

associated symptoms (294, 297).

History and Distribution

Symptoms of leaf spot generally are found wherever the Italian Prune (Prunus

domestica) cultivar is grown (294, 297). These symptoms often are severe

and have caused increasing concern among prune growers since the condition

was first reported in Idaho in the 1930's (49, 34). Leaf spot occurs in serious

proportions in the prune-growing districts of Oregon, Washington, Idaho, and

Utah (377). Nursery improvement programs have reduced the severity of the

problem in parts of the West, but no known clone of standard Italian Prune is

entirely free of the condition in all orchard environments.

Economic Hosts

Italian Prune is a common host, but conditions with similar appearance have

been observed on Stanley prune (294) and Beaty plum (610).

Symptoms

First growth in the spring generally is normal, with symptoms developing

early in the summer. The necrotic spots, from which the name of the disorder

is derived, may vary from very small ( 1 to 2 mm. ) to large blotches of dead

tissue (fig. 132) that sometimes coalesce and engulf most of the leaf. Trees

affected with leaf spot often express several symptoms which may be classed

together as the leaf spot complex (292, 297). The characteristic brown spots

may not always be present, but where they occur they frequently develop concentric lines in the browned tissues. Such spots sometimes drop out, leaving

a shot hole condition that can be confused with infections of Coryneum blight

(303) or Prunus ring spot virus (PRSV) (294). The most common of the

symptoms that may accompany the brown spots is a chlorotic mottle (59, 577)

reminiscent of virus or powdery mildew infection or of prune leaf casting mottle

(255). The mottling symptom often is more prevalent than the brown spotting

symptom, and it generally precedes or accompanies the brown spotting. The

mottling may be very indistinct or very striking, most often consisting of lightgreen to rusty areas scattered over the surfaces of affected leaves.

The various symptoms of leaf spot grade into each other and may disappear

and reappear in affected branches (297). This is true also of the genetic abnormality in prune trees known as crinkle (64, 298). Such behavior does not

typify the classical concept of a genetic disorder. Severity of the various symp274
HANDBOOK NO. 437, U. S. DEPARTMENT OP AGRICULTURE 275

FIGURE 132.—Italian Prune leaves showing variations of the brown leaf spotting symptoms most characteristic of leaf spot. Note the accompanying chlorotic spotting where

the necroses are less advanced.

toms seems to be governed primarily by environmental conditions {60), and, in

extreme cases, extensive defoliation results (49).

The presence of leaf spot can lead to depressed yields (.584), severe fruit

drop (49, 584), and production of shriveled, sunburned, gum-spotted fruits

{49, 584).

Nursery trees with leaf .spot generally produce dwarfed and unsatisfactory

orchard trees. Growth of less affected trees may be near normal. Bloom and

fruit set seem to be affected only in the most severe cases. Trees propagated on

peach rootstocks seem to be more adversely affected than those on myrobalan

plum roots.

Control Measures

Removal of affected trees is advisable when extreme symptoms develop or

when symptoms are detected in newly planted trees. Propagating wood should

be taken only from selected clones with a minimum leaf spot history. Even with

the best clones now in use, occasional leaf spot trees have been observed in the

propagations.

Remarks

Italian Prune leaf spot symptoms have not been reproduced in unaffected

trees by exhaustive tests employing standard grafting techniques (49, 297, 577).

However, the symptoms can be perpetuated to varying degrees in growth from
276 VIRUS DISEASES OF STONE FRUIT

carrier buds that have been grafted to other trees. Therefore, leaf spot is a

bud-perpetuated condition, and hence a genetic disorder, despite the fact that

perpetuated symptoms often are unstable and may disappear after 4 years or

more (297). Although the symptoms are similar, infection with PRSV does

not cause leaf spot, but leaf spot is common in PRSV-infected trees (296).
ITALIAN PRUNE SPARSE LEAF

EARLE C. BLODGETT

This abnormality of standard Italian Prune is characterized by lack of foliage

(37). Trees affected with sparse leaf are large, round-headed, tend to be

umbrella shaped, and develop an open type of growth. When the trees are

young, growth is probably nearly normal. In the orchard, affected trees can be

identified easily when in leaf by their lack of foliage and in the dormant stage

by their shape. There may be an abnormal delay of about 10 days in time of

blooming (62) and of leafing out.

Affected trees bear very sparingly. The prunes are perhaps larger than normal,

but they seem to be normal in color, shape, and texture.

The foliage on affected trees is extremely sparse in comparison with that on

normal trees. The sparseness seems to be due principally to lack of small-twig

growth on which leaf and fruit buds are normally borne. Apparently the lower

and inner small branches either do not form or die soon after they are formed.

The leaf surface of affected trees is little more than an estimated 50 percent

of that on normal trees. The foliage is confined largely to twig terminals on the

periphery of the tree. The early leaves in particular are deformed somewhat

similar to sweet cherry leaves affected with crinkle leaf. They are smaller than

normal and have irregular margins and diffuse mottling.

Although transmission tests were not completed, the disorder is regarded

as a genetic abnormality that can develop as a mutation. Budwood for propagation should be taken from normal bearing trees.

277
NONINFECTIOUS BUD FAILURE IN ALMOND

DALE E. KESTER

Synonyms

Shatter-bud; crazy-top; muletail.

History and Distribution

This disorder was first described by Wilson and Stout (742) in 1944, but

trees affected by noninfectious bud failure were observed in CaHfornia almond

orchards many years prior to that time. The disorder first occurred in Nonpareil

and Peerless and for many years was not considered a serious problem. It

began to cause serious concern when Jordanolo, a variety introduced in 1937,

began to be affected in high percentages in commercial orchards (743). The

disorder has become so severe in Jordanolo that this cultivar is no longer

planted. In 1953, it was discovered in Jubilee. Since about 1950, the incidence

of affected trees of Nonpareil, the leading commercial cultivar, has increased

significantly, particularly in newly established areas in the San Joaquin Valley of

California. Since then, the disorder has appeared in such otlier cultivars as

Harpareil and Merced.

Trees affected by the disorder are found throughout the almond-growing

districts of California. It is particularly prevalent in the upper end of the

Sacramento Valley and the southern part of the San Joaquin Valley. Affected

trees have been reported from Turkey, Israel, and Tunisia (H. K. Wagnon, P.

Spiegel-Roy, and E. E. Wilson, personal communication)

Economic Hosts

Almond cultivars affected include Nonpareil, Peerless, Jordanolo, Harpareil,

Jubilee, and Merced. The last four cultivars are offspring of Nonpareil. In

addition, numerous unnamed seedlings and selections, have been affected, particularly when Nonpareil or Jordanolo is one of the parents. The disorder has

been reported in Marcona, a cultivar rarely grown in California (689).

Symptoms

The disorder is manifested through two principal symptoms or characteristics :

(1) failure of vegetative buds to grow out in the spring (bud failure) and

(2) cracked or roughened areas on shoots (rough bark). The level of expression can vary continuously from slight, where only a few buds are affected, to

severe, where practically all buds are dead and extensive rough bark areas occur.

Bud failure results from the fact that vegetative buds become necrotic some

time during late summer or fall (390, 597). These seemingly dormant buds

fail to grow out in the spring and abscise and drop about 6 weeks later. Consequently, bud failure characteristics are best determined in the spring within

6 to 8 weeks after growth begins. If examined later than that, identification

may be obscured by new growth and the inability to distinguish between bud

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HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE £79

failure and other factors causing lack of set. Not all of the buds will fail on

the branch, and those that remain viable will grow into normal-appearing shoots

during that same summer. These few shoots are usually vigorous and grow at

right angles to the branch. Growing points on these shoots are normal during

the early part of the growing season but lose their viability sometime during the

summer or fall, although this fact is not apparent until they fail to grow the

following spring. Repeated annual cycles of this bud failure result in a recognizable atypical growth pattern (fig. 133).

Sometimes bud failure is limited to the center part of the shoot, with normal

growth at the end to give the so-called muletail look. If failure occurs in buds at

the end of the shoot, dieback results. Foliage is sparse.

Flower buds on affected branches are usually normal unless the tree is very

severely affected. Very often the flowers on moderately affected branches will

bloom late—1 to 2 weeks after those on nonaffected branches. Fruit set is not

affected.

Cracked bark results from necrosis of a portion of bark cortex (-597).

Affected areas may vary from small lesions one-half inch or less in length at the

node to areas extending a foot or more along a branch. The beginning of such

cracked bark areas can often be observed on new shoots by late summer or

early winter. The rough bark areas become more pronounced and are particularly characteristic of branches 2 to 3 years old or more. The wood beneath the

rough areas is often discolored. The rough bark bands do not necessarily develop

every year on a given tree but may occur in 2 to 3 year cycles.

Control Measures

Control of noninfectious bud failure in a commercial planting is achieved

either by replacing the entire tree or by topworking. Scions can be taken either

from a different cultivar known to be free of the disorder or from the same

cultivar but from a nonaffected source. Which procedure is best to follow is

a horticultural decision. A tree that is not seriously aflfected might well be

left until production falls to an uneconomic level.

Prevention of the disorder depends either on developing or identifying clonal

lines not affected by the disorder or by developing propagation sources for budwood with no or low potential for the disorder. Unfortunately, no reliable

method exists to carry out these objectives.

The following guidelines may be helpful in reducing the probability of

propagating trees with bud failure.

1. Select budwood source trees that are at least 5 to 6 years old or older.

Since symptoms are most apt to appear during the early life of a tree, this

precaution may increase the chances of avoiding potential affected sources.

2. Examine the trees carefully for bud failure or rough-bark symptoms. If

some trees of a given orchard are affected, it is likely that others, though outwardly normal, will carry the potentiality. Consequently, it would be better to

avoid a source where some trees are affected.
280 VIRUS DISEASES OF STONE FRUIT
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 281

3. Maintain the identity of trees propagated from specific budwood sources.

If a program of followup inspection of orchards propagated from specific sources

is practiced, it should be possible in time to identify sources that have less bud

failure potentiality than others.

Remarks

Graft trmismission tests.—Tests for graft transmission from Nonpareil, Peerless and Jordanolo have been negative although the disorder is readily budperpetuated {741). Affected Nonpareil trees have been topworked with scions

from normal trees. The growing scions have then remained normal for observation periods up to 20 years. Topworking has become an accepted practice to

control the problem, although it is difficult to obtain completely nonaffected

scionwood of some varieties. Bud failure in other cultivars later found to be

aifected (Merced, Harpareil, and Jubilee) has not been tested specifically, but

the disorder appears to be the same as that in Nonpareil, Peerless, and

Jordanolo. Heat treatments do not overcome bud failure (George Nyland,

unpublished data).

This disorder has some similarity to almond virus bud failure in which set is

reduced, fruit are misshapen, and foliage is upright, greener, and persists later

into fall than with noninfectious bud failure.

Seed transmission.—Noninfectious bud failure is a genetic abnormality

readily transmitted by seed (740). Transmission from parent to offspring

appears to account for the origin of the disorder in current almond cultivars.

Two aspects of the bud failure problem exist. One is the distribution of

aflPected trees within specific clones with vegetative propagation. The other is

the identification of susceptible clones arising as selections from families of

seedling trees.

The distribution of bud failure trees in aifected clones tends to follow a

random pattern, although some observations suggest a directional aspect. It is

not possible at present to identify an affected tree before the external symptoms

actually appear. Bud failure is bud-perpetuated but can also develop in trees

propagated from source trees that were outwardly normal (744). The bud

failure phenotype can develop at any age. There is likely to be a gradual increase

in the number of afifected trees within an orchard, although the increase is more

likely to be greatest while the trees are relatively young. The percentage of

affected trees that develops in any one orchard can range from a few percent to

75 percent or more. There is usually a continuous gradation in severity from

none to slightly afiPected to severely aflPected, not only in different trees but also

FIGURE 133.—A, Nonpareil almond afïected by noninfectious bud failure, showing, in

center, one vigorously growing branch less afïected than the others; B, Nonpareil almond

tree showing, at right, unaffected branches that developed from a healthy graft placed

on understock 7 years previously and, at left, the branches that developed from the

affected understock.
282 VIRUS DISEASES OF STONE FRUIT

within the same tree. If a mildly affected tree is pruned severely, the new growth

will be normal at first but eventually will develop bud failure, often more

severely than before.

Wilson (744) has described progressive increase in percentage of affected

trees with consecutive vegetative propagations from a single source beginning

with the original seedling tree. The vegetative generations have been designated

as S (original seedling tree), S + 1 (first scion generation), S + 2 (second

scion generation), and so on. The differences in phenotypic levels of expression

within a clone are gametically transmitted (366). An association between

incidence of bud failure, high summer temperatures, and rapid shoot growth

has been noted, but a cause and effect relationship has not been established

experimentally.

The inheritance of bud failure from normal and affected parental trees has

been investigated (363, 366). The pattern of inheritance found involves the

production of families of seedling individuals, each of which exhibits all the

potential instabilities described in the previous paragraph but differ in the level

of bud failure potentiality that each inherits. In crosses involving affected and

nonaffected Nonpareil and Peerless, there was a continuous gradation from those

individuals that developed extremely severe symptoms when 1 or 2 years old

to those that developed symptoms only after many years and after the trees had

been propagated into advanced scion generations. The age when the bud failure

phenotype develops within a family of seedlings is directly related to the bud

failure severity in the two parents. Bud failure is transmitted through both

male and female gametes. Families derived from crosses where both parents

were affected showed early and pronounced development of bud failure;

families from crosses where only one parent was affected were less precocious

in bud failure development; and families from crosses where neither were

affected produced some bud failure individuals but only after much delay and

after trees had been propagated into advanced scion generations. The development of individuals of this latter group that are normal but with bud failure

potential appears to account for the existence of bud failure susceptible varieties

from breeding programs.
NONINFECTIOUS PLUM CRINKLE LEAF

T. S. PINE

Noninfectious plum crinkle leaf is a severe leaf distortion of Japanese plum,

analogous in many ways to prune crinkle leaf and sweet cherry crinkle leaf, that

occurs occasionally in southern California and Washington {525). Single

branches or an entire tree may be affected. The disorder is found most often in

the Santa Rosa cultivar and its derivatives.

Affected portions of trees are conspicuously dwarfed. The leaves are one-third

to one-half normal size and distorted in a variety of patterns: strap-shaped,

pronounced lobes along the margins, or severely indented margins (fig. 134).

Some leaves show a pale-yellow pattern along the margins or a mottle extending

over the whole blade. Affected leaves are thickened and tend to become brittle

early in the growing season. Leaf midveins are enlarged, and the entire leaf

venation is formed irregularly. Leaves produced early in the growing season are

FIGURE 134.—Leaves from a Santa Rosa plum tree affected by noninfectious plum

crinkle leaf and showing various leaf distortions.

283
234 VIRUS DISEASES OF STONE FRUIT

always deformed; later leaves may be nearly normal. A few blossoms may appear

on affected branches, but they are imperfectly formed. Affected trees and

branches are almost entirely unfruitful. Many leaf and fruit buds abort, so that

affected trees appear sparse and stringy. Although this disorder is readily budperpetuated, all attempts to transmit it through tissue grafts have failed.

Plum crinkle leaf apparently results from a genetic instability. The disorder

is of economic importance only when affected budwood is introduced into

nursery operations. Although symptoms of plum crinkle leaf resemble closely

those of prune crinkle leaf and sweet cherry crinkle leaf, the leaves of affected

plum trees are more severely distorted than those of prune or sweet cherry.
NONINFECTIOUS PLUM SHOT HOLE

T. S. PINE and MAURICE F. WELSH

Noninfectious plum shot hole occurs occasionally in commercial plums in the

West and commonly in some hardy plum hybrids in the Great Plains States and

the Canadian Prairie Provinces. The disorder was described first on Beaty

plum, a hybrid of Prunus angustifoliayiP. munsoniana {610). Because this

condition occurs frequently in native P. munsoniana, it was thought that the

trouble might be the result of a genetic weakness in P. munsoniana and that

this weakness was carried in plums arising as seedlings and hybrids of this

species (611). However, the appearance of plum shot hole in varieties and

hybrids not related to P. munsoniana indicates the disorder is not species-limited.

Spring growth of affected P. salicina trees is normal. As the season progresses,

the older leaves at the base of the shoots develop translucent flecks that enlarge

rapidly. The centers of these spots turn brown or purple-brown, and in most

cases the dark-colored areas separate from the rest of the leaf at a definite line of

cleavage and drop out (fig. 135). The resulting shot hole condition develops

progressively toward the shoot apex, and by midsummer the foliage is riddled

with holes. The spots and holes in most leaves range in size from pinpoints to

1 to 2 mm. in diameter, their size usually being inversely proportional to their

number in the affected leaf. The spots are generally circular but may become

irregularly shaped as several spots coalesce. Affected trees vary individually in

FIGURE 135.—Noninfectious plum shot hole in leaves of Beaty plum, showing dark

necrotic spots leading to shot hole.

285
286 VIRUS DISEASES OF STONE FRUIT

symptom expression, some being severely and others only mildly damaged. In

some trees, the spots are small and the centers do not fall out; in other trees,

the spots are large and the centers fall out as they are formed. The general

vigor of affected trees is not reduced. The disorder is known to be seed borne.

Although noninfectious plum shot hole has never been transmitted from affected

to healthy trees by bud grafts, it is readily perpetuated in growth from the

inserted buds.

Throughout the Great Plains States and the Canadian Prairie Provinces

similar symptoms are common on western sand cherry x plum hybrids, such as

Sapa and Opata (fig. 136). Yellow blotching occurs on the leaf lamina on

one or both sides of the midrib, usually accompanied by leaf puckering. The

yellow tissue becomes necrotic and is shed. Frequently all leaves on long portions of shoots are reduced to midribs only.

Other hardy "prairie" plums such as Grenville, Radisson, and Tecumseh

frequently suffer similar leaf tattering. However, the loss of leaf lamina is not

preceded by yellowing or necrosis, but by the appearance of lines of fine shot

holes that radiate from the point of pedicel attachment to the upper leaf margins. Mild symptoms of this type are occasionally apparent on Italian Prune

FiGtJRE 136.—Noninfectious plum shot hole in leaves of Sapa plum, showing various

stages of yellow blotching, puckering, necrosis and shedding of necrotic tissue.
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 287

(P. domestica) and other plum cultivars. These syndromes have persisted in

plum clones subjected to heat therapy.

Noninfectious plum shot hole apparently is a genetic abnormality. It is not

economically important but can be confused with infectious diseases having

similar symptoms. It has many characteristics in common with Italian Prune

leaf spot. It differs from plum rusty blotch in symptomatology and by being

a midseason rather than an early season disease.
PEACH FALSE WART

C. G. WEIGLE

Peach false wart (578) is seen occasionally in the West on fruits of several

cultivars of peach. It bears this name because it shows some resemblance

to the symptoms on fruit caused by peach wart virus. As with peach wart,

there are no observable symptoms except on fruit. But false wart differs from

virus-caused wart in several ways.

False wart differs in the number of fruits it affects on a tree. Only one to five

affected fruits, rarely 10 to 15, are found on an orchard tree. The warty fruits

are not confined to one branch or spur, and trees with affected fruits are randomly scattered in the orchard. The warts are characteristically different from

those found on virus-infected fruit. The erumpent growths are usually large

and somewhat variable in shape. They may be found any place on the sides of

fruits, but generally not at the stylar end. Generally, there is only one wart

on a fruit. The center of the wart often has bony tissue, which compares in

hardness with the seedcoat. The bony tissue in some warts extends, like a

needle, up to three-eighths of an inch into the flesh. Gumming is not characteristic (fig. 137). Moreover, the condition does not persist in the tree from year

to year. Buds from trees with affected fruits failed to produce the condition

FIGURE 137.—False wart on peach fruits. Two fruits at left show "crease wart."

288
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 289

when grafted to healthy trees, and warts did not appear in the growth from

the inserted buds.

While the cause of peach false wart has not been determined, it is generally

accepted to be the result of feeding punctures made by one or more species of

hemipterous insects. False wart may be the same as "beady wart" mentioned

by Blodgett (31) but differs from "crease wart," which Blodgett considers to

be a varietal reaction. False wart is not economically important. It is described

here since it presents a diagnostic problem in the ñeld because of its similarity

to virus-caused peach wart.
PEACH VARIEGATION

A. W. HELTON

Peach variegation was reported first in 1940 from Idaho (48). Since that

time, the condition has been recognized on several peach varieties in Idaho, and

it probably occurs in most peach-growing districts. The disorder sometimes is

referred to as a chimaera (53, 63). Symptoms generally appear on a single

branch of affected trees. Whole trees seldom are affected even when buds in

the axils of symptom-bearing leaves are used to produce new trees.

Naturally occurring symptoms have been observed in J. H. Hale, Elberta,

Redhaven, and peach cultivars and seedlings of unknown identity. Similar

symptoms have been found in Idaho in sweet cherry and sweet cherry seedlings,

mahaleb cherry, myrobalan plum, Italian Prune, apple, and strawberry (Fragaria

pesca) (293).

Peach leaves affected by variegation produce streaky blotches, characterized

by three distinct, sharply delimited shades (fig. 138)—normal green, light

green, and cream to white. Growth of affected twigs generally is reduced, and

a yellowish discoloration of the bark tissues sometimes is associated with the

FIGURE 138.—Leaves of J. H. Hale peach showing typical symptoms of

noninfectious variegation.

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HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 291

foliar symptoms. Trees only partially affected need not be removed, but wood

from them should not be used for propagation.

Peach variegation symptoms may be confused with those of peach calico, but

the latter is not characterized by the three distinct shades of color. Variegation is

not transmissible. It is bud-perpetuated, but the perpetuated symptoms may not

be of the same intensity as those of the original tree. This is true for the other

affected species as well as peach. Observed variation in symptoms on a tree from

one year to another suggests that environmental conditions influence symptom

intensity. Peach variegation is of minor economic importance.
PEACH YELLOW SPOT

NORTON S. WILSON and T. S. PINE

Peach yellow spot is a nontransmissible disorder caused by the peach silver

mite, Aculus comutus (Banks). This is the eriophyid mite that also causes

widespread silvering of peach foliage just before leaf drop in the autumn. The

disease is characterized by yellow spotting, vein-associated leaf chlorosis,

longitudinal leaf rolling, and stem spotting (746). The leaf discoloration,

which closely resembles the symptoms of several mosaic-type virus diseases, is

caused by a toxin injected by the mite during feeding. The toxin may move short

distances within the leaf, either by diffusion among the parenchyma cells or

along vascular bundles, but cannot be considered generally systemic.

Affected peach seedlings develop light-yellow chlorotic spots and vein

feathering in the young leaves approximately 10 days after the mite feeding

(fig. 139). In severe cases, the spots may coalesce to produce a vivid leaf

mottle. Leaves of some cultivars (e.g., Salberta) develop spots with red

borders that become necrotic and drop out, producing a shot hole effect. Spots

also appear in current-season growth, being obscure and pale yellow at first but

increasing in size to become slightly raised and darker. Affected leaves of some

cultivars (e.g., J. H. Hale) often show puckering and longitudinal rolling.

h- '*•»•»'

FIGURE 139.—Damage caused by the mite Aculus comutus in Lovell peach leaves:

chlorotic spotting on left; heavy vein feathering on right.

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HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE £93

Symptoms develop only in leaves that are rapidly growing and unfolding and

not in fully mature leaves. Production of vein feathering seems to be correlated with infestations of very young leaves in which the toxin is introduced

directly into the vascular bundles. Affected trees are not permanently damaged.

Populations of A. cornutus fluctuate greatly, and traces of earlier infestations

can be difficult to detect by the time yellow spot symptoms are evident.

Symptoms similar to those described above, and associated with infestations

of A. cornutus, were seen on both peach and apricot in British Columbia (Maurice F. Welsh, unpublished data). Leaf patterns in apricot usually were larger

than those in peach, and the leaves were most severely affected. Plum rootstocks

(P. cerasifera), growing in the same planting, also developed a strong mottle in

the tip leaves.
PLUM RUSTY BLOTCH

T. S. PINE

History and Distribution

Plum rusty blotch was reported first in I960 (524) as occurring in Santa Rosa

and Late Santa Rosa plums (Prunus salicina) in California, but the disorder

had been seen in several parts of the State prior to that time. It is now known

to occur in all the plum-growing areas of California (519). Similar disorders

have been reported in Israel (67) and Argentina (678).

Economic Hosts

The only known stone fruit trees affected by this disorder are Japanese plums

and hybrid plums closely allied to P. salicina. Symptoms of the disorder have

been seen in Elephant Heart, Gaviota, Howard Miracle, Kelsey, Laroda, Late

Santa Rosa, Nubiana, Redroy, Santa Rosa, Shiro, and Star Rosa growing in

California orchards. The disorder has been induced experimentally in

Abundance and Beauty plums. Affected trees have been found growing on

their own roots and on apricot, plum (Marianna and myrobalan), and peach

rootstocks.

Symptoms

In new spring growth of affected trees, chlorosis develops at the base of the

leaf blade and progresses toward the apex along one or both margins (fig. 140).

This chlorosis tends to be continuous at first but may eventually take the form of

chlorotic blotches. Within a few weeks, the blotches become reddish-brown, and

many small red spots appear in the discolored areas. These spots may increase

to about one-eighth inch in diameter or remain the size of a pinpoint. Eventually

they all become necrotic and drop out, leaving the blotchy portions of the leaves

irregularly shot holed. The rusty blotch and necrosis may cover the whole leaf

blade when leaves are severely attacked. Affected leaves are reduced to one-third

to one-half the size of healthy leaves and tend to become misshapen as the growing season progresses. Young or old leaves on a branch may show the onset of

symptoms first, but by midsummer all the leaves on an affected branch usually

show some damage.

Symptoms in orchard trees generally are observed first on a single branch.

Because the leaves are discolored and reduced in size, these branches appear

stringy and are readily noticed. Affected branches produce few blossoms and

almost no fruit. However, leaf symptoms and reduced fruit production may not

occur simultaneously.

Control Measures

Plum rusty blotch was not eliminated from buds of affected trees by heat

treatment for 7 weeks at 38° C. (George Nyland, unpublished data). Removal

of affected branches does not prevent the appearance of symptoms in other

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\

FIGURE 140.—Leaves of Santa Rosa plum affected by plum rusty blotch showing

typical reddish-brown blotches.

portions of a tree. Damage from this disorder is reduced by selecting budwood

for propagation from source trees that have a history of producing healthy

foliage and consistently high yields of fruit.

Remarks

Plum rusty blotch originally was described as a transmissible disorder

resembling a virus disease (524). Healthy-appearing experimental trees had

developed clinical symptoms of rusty blotch 4 years after being inoculated with

buds from affected trees, and the appearance of the disorder in nearby untreated

trees was assumed to result from the natural spread of a virus by an unknown

vector. Although these experiments were repeated several times, the continued

appearance of rusty blotch in untreated trees and the widespread occurrence of

genetic disorders in plums generally suggested that more evidence was needed

before this disorder could properly be called a virus disease. Nontransmissible
296 VIRUS DISEASES OF STONE FRUIT

leaf shot holing, although quite different in symptomatology from rusty blotch,

occurs in many plums and plum hybrids (770) and makes definite characterization of plum disorders a difficult procedure.

In recent investigations, healthy-appearing Beauty plum trees, which have

not been found naturally affected in orchards, developed symptoms of rusty

blotch the second year after they were approach-grafted to affected Santa Rosa

trees. Abundance plum, in which rusty blotch has not been seen in commercial

plantings, developed symptoms the first year after they were bud-grafted or

approach-grafted to affected Santa Rosa. Although untreated trees of these two

varieties remained normal-appearing, it is not known at the present time if the

symptoms were induced by a virus, by another graft-transmissible pathogen, or

if the association of affected tissues merely hastened the appearance of a genetic

change.

The appearance of plum rusty blotch in the cool, humid coastal valleys of

California as well as in the hot, inland valleys seems to indicate that climatic

conditions are not a factor in its development. Good cultural practices do not

diminish the severity of symptoms or reduce its incidence in affected orchards.

Development of foliar symptoms and reduction in fruit set are more evident

in Santa Rosa than in other plum cultivars, probably because Santa Rosa and

its related cultivars are grown more extensively in California. Although other

cultivars may develop severe symptoms, the disorder is found in proportionately

fewer orchard trees and is of less economic importance. Plum line pattern and

noninfectious plum shot hole sometimes occur in trees with rusty blotch, but

this coexistence does not interfere with the development of the symptoms of

each disease.
PRUNE CRINKLE LEAF

EARLE C. BLODGETT

The Italian Prune, like Bing and Black Tartarian sweet cherry, is subject to

genetic abnormalities. Crinkle leaf symptoms are similar and common in both

prune and cherry, although there is no apparent connection.

Prune crinkle leaf is known in both regular and early sports of Italian Prune

cultivars and is widespread in the Northwest. It has been noted on the prune

cultivars Emily, Merton, and Hungarian.

Leaves on crinkle leaf affected trees show a wide range of leaf deformities,

the most common of which are uneven margins and distorted blades (fig. 141).

Affected leaves generally are smaller and lighter in color than normal leaves

and often show chlorotic areas near the restricted portion of the blade. The

mottled or marbled appearance is dull and quite distinct from the even green

of normal leaves. In older trees, prune crinkle leaf symptoms may occur only

on one spur or one branch, or on larger portions of the tree. These frequent

occurrences on formerly healthy branches probably represent genetic instability.

The symptoms and characteristics are quite similar to those described for sweet

FIGURE 141.—Six Italian Prune leaves affected by prune crinkle leaf, showing irregular

margins, distortion, and chlorotic areas; normal leaf in center.

297
298 VIRUS DISEASES OF STONE FRUIT

cherry crinkle leaf, which occurs most commonly on the Bing and Black Tartarian sweet cherry. Trees with prune crinkle leaf usually are dwarfed; the

growth is spindly, and the fruit may ripen earlier than normal. In general,

crinkle leaf-affected trees tend to be unfruitful. Fair crops may set, but most

of the fruit falls before maturity. The fruit stems on affected trees are noticeably

shorter than those on normal trees. There are cases, however, in which trees with

prune crinkle leaf are extremely vigorous but unproductive. A similar condition is often found in sweet cherry trees affected with crinkle leaf. Examples

are known in which normal branches developed on crinkle leaf-affected prune

trees.

Trees affected by crinkle leaf usually are dwarfed and have a denser foliage

than those with sparse leaf, another genetic abnormality of prune. Transmission

tests consisted of topworking crinkle leaf trees with scions of healthy prune.

No transmission was obtained after 3 to 4 years in two separate tests (64).

Limited trials indicated that a small percentage of seedlings grown from Italian

Prune seeds, collected from a commercial cannery, developed symptoms of

crinkle leaf.

In nursery stock grown 15 to 20 years ago in Washington, crinkle leaf was

very common. Under the present certification program, the disease is virtually

unknown in the nurseries. The frequency of crinkle leaf mutations is very low

in prune as compared with crinkle leaf in Bing cherry.
PRUNE LEAF CASTING MOTTLE

K. G. PARKER and R. M. GILMER

Synonyms

Prune mottle; prune leaf mottle.

History and Distribution

In the original description of prune leaf spot, Blodgett (49) reported a mottle

was often present in leaves with leaf spot. In some years, only mottle symptoms

developed on certain trees, and the leaf spot symptoms were absent. In this and

a later report (:53), he presented evidence that prune leaf spot was budperpetuated but not transmissible. He suggested that leaf mottle might be a

preliminary phase of leaf spot, but considered the evidence inadequate to determine whether leaf mottle was bud-perpetuated (-53).

Prune leaf mottle is apparently common in the West, because the complex

of leaf spot and mottle was observed in Oregon, Washington, and Utah (72).

The senior author observed that leaf mottle symptoms similar to those occurring

in New York were common in prune orchards in Washington in 1951.

Leaf mottle symptoms were observed in Italian Prune trees in the East for

many years prior to an initial report in 1952 (HO). The disorder was fully

described as leaf casting mottle in 1957 (233).

Economic Hosts

In New York and other Eastern States, leaf casting mottle is common and

widely distributed on Italian Prune. Identical symptoms have been observed on

several other prunes, including Albion, Tragedy, Grand Duke, and Hungarian

(233). The disorder has never been observed on Stanley prune.

Symptoms

The foliage of affected Italian Prune trees is initially normal. In midsummer,

chlorotic spots appear on many leaves; these spots finally become brownish

yellow and translucent, with indefinite margins (233). Somewhat later, the

leaf lamina between the spots becomes yellow with a green halo surrounding

individual spots (ñg. 142). Many individual spots become necrotic in their

centers, and severely affected leaves soon drop.

Richards et al. (386) suggested that prune leaf mottle and prune leaf spot

were distinct. They described prune leaf mottle appearing in mature leaves as

small, diffuse, light-green or chlorotic areas irregularly scattered over the leaf

lamina with chlorotic areas coalesced in places to form a mosaic pattern. During the summer, gray or purple-brown necrotic centers often developed in the

chlorotic areas. Affected leaves often dropped prematurely but sometimes persisted with a muddy or gray appearance and irregular marginal chlorosis.

Both reports (233, 386) indicate that symptoms are more severe with increasing defoliation at high temperatures. Environmental conditions are ob299
300 VIRUS DISEASES OF STONE FRUIT

\^

FIGURE 142.—Prune leaf casting mottle in Italian Prune leaves: Chlorotic spots, upper,

and green halos around spots on yellow leaf lamina, lower.

viously significant in severity of symptoms. Minor variances in symptoms

observed in Utah and New York very likely result from differences in the

environment of the two areas.

Control Measures

As indicated in the following section, leaf casting mottle is bud-perpetuated.

The sole practicable control is to propagate trees from scion sources free of the
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 301

disorder. Scionwood source trees should be examined carefully for foliage

symptoms, particularly at midseason and after extended periods of high

temperatures. In trees with very mild symptoms, foliage may appear quite

normal in many years, and symptoms may not become evident until the trees

have reached considerable size.

Richards et al. (386) suggested that Italian Prune may have an inherent

weakness because most trees of the variety are affected by leaf mottle or leaf spot.

It would, perhaps, be advisable not to use varieties affected with such disorders as parents in breeding programs.

Remarks

In New York, trees were propagated on peach rootstocks from four sources

of Italian Prune scions: symptomless; mild leaf casting mottle; severe leaf

casting mottle; and leaf crinkle (also bud-perpetuated). The resulting Italian

Prune trees were cross-budded in all possible combinations, and growth of the

original scion and of the inserted buds was observed for 4 years. During this

period, the identities of each of the original scions and of growth from the

inserted buds were not affected, i.e., symptomless scions were free of symptoms;

those from the severe mottle source evidenced severe mottle symptoms. No

evidence of possible virus transmission from scion to scion was observed.

Symptoms very similar to leaf casting mottle developed in the greenhouse on

seedlings derived from crosses in which Italian Prune, Tragedy, or Grand Duke

were parents (233 ). Characteristic leaf casting mottle symptoms later developed

in many of these seedlings when grown in the field. These observations suggest

that leaf casting mottle is a genetic abnormality.

Helton (297) presented data indicating that symptoms were often absent in

trees that had previously developed symptoms of leaf mottle, leaf spot, or other

disorders. Such variations perhaps again result from environment or other

conditioning factors.

Cain and Boynton (110) reported yield reductions in trees with leaf casting

mottle, with the amount of fruit reduction positively correlated with severity of

foliage symptoms. Set of fruits was reduced on affected trees, and a large

number of fruits dropped prematurely. Because leaf casting mottle is extremely

common in Italian Prune trees in New York, it undoubtedly causes a

considerable reduction in yields.
PUSTULAR CANKER OF TRAGEDY

PRUNE

T. S. PINE

Pustular canker was described from California in 1941 as a disease limited

to Tragedy prune (^Prunus domestica) and possibly caused by a virus (<52i).

It has not been reported from other States. Small, diamond-shaped pustules

break through the bark of affected trees, usually in the young growth

of the upper branches (fig. 143). The pustules develop into hard, roughened

cankers that may remain small or become much elongated along the axis of the

branch. Cankers have appeared in yearling trees in nurseries, but some trees

have not shown the abnormality until they were 5 to 10 years old. Growth

of cankered trees is somewhat stunted, twig necrosis is present occasionally, and

fruit production is progressively reduced. Repeated attempts to transmit this

disorder from affected Tragedy trees to healthy trees of other P. domestica

cultivars or to other Prunus spp. have all failed. However, pustular canker is

easily bud-perpetuated (.527).

FIGURE 143.—Small pusmlat cankers on branch of Tragedy prune.

302
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 303

Pustular canker is less evident in orchards that receive maximum attention

under good climatic conditions but increases in severity during exceptionally

warm weather or when cultural practices are relaxed. Although high summer

temperatures may favor the development of this disease, affected trees have

been found in both the cooler coastal valleys and the warmer interior valleys of

California. As a cultivar-limited genetic abnormality, pustular canker is not

a threat to the culture of other prune cultivars. "Little diamond canker," a

common name for this disorder, is no longer used because of possible confusion

with prune diamond canker, a disease known to be caused by a virus.
STANDARD PRUNE CONSTRICTING MOSAIC

H. KEITH WAGNON

Standard prune constricting mosaic is known only in California and occurs

only on Standard prune {Prunus domestica) {655, 691, 701). The disorder

is of minor economic importance because Standard now is being grown on a very

limited scale in California. Originally considered to be caused by a virus, on the

basis of inoculation tests on Standard prune and peach {655), subsequent

observations and tests indicated that the disorder is a. genetic abnormality peculiar

to the Standard prune {691, 701).

Symptoms consist of few-to-many chlorotic spots, %6 t^o Vè i"^ •" diameter,

in the leaf blade. A distinctive leaf-constricting feature of the disorder is the

result of the concentration and coalescing of the spots in a band across the

top half of the leaf (fig. 144). Often the chlorotic areas become necrotic and

FIGURE 144.—Leaves of Standard prune afifected by constricting mosaic and showing

chlorotic spots and leaf constriction near chlorotic areas, compared with normal leaf,

lower left.

304
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 305

fall out, leaving only the midvein. The symptoms are more conspicuous in

warm weather and are more severe in growing nursery stocks than in orchardplanted trees. Trees growing in the cooler coastal valleys of California may

have few or no symptomatic leaves. Progeny trees produced from symptomless

trees have the potentiality of developing symptoms of the disorder when grown

under hot summer temperatures.
SWEET CHERRY CRINKLE LEAF, DEEP SUTURE,

AND VARIEGATION

EARLE C. BLODGETT and GEORGE NYLANI)

Synonyms

Crinkle leaf has been called curly leaf, wild trees, male trees, red bud, maple

leaf, and unproductive cherry. Synonyms for deep suture are long leaf and

rough leaf. Variegation is also called white crinkle.

Nature of the Disorders

The disorders of crinkle leaf, deep suture, and variegation are genetic.

Crinkle leaf and deep suture frequently occur in the same tree. Variegation

is most often seen in seedlings and foreign cultivars (18, 89, 333). Repeated

experiments by many workers have shown that these disorders are readily perpetuated in buds and scions. Trees propagated from buds from diseased shoots

are nearly always diseased. Trees propagated from healthy-appearing trees or

from healthy portions of partially affected trees may or may not show symptoms.

A single recessive controlling gene is postulated for which certain cultivars

prone to crinkle such as Bing and Black Tartarian and to variegation such as

Hedelfingen are heterozygous. Symptoms appear in a heterozygous tree when,

presumably, a further mutation of the particular gene occurs (364).

History and Distribution

Crinkle leaf was first described by Kinman (368) in 1930 under the name

of unproductive cherry. It has been the subject of many investigations and

countless observations (166, 364, 369, 333, 364, 378). Deep suture was first

described by Reeves (333) in 1941. Distribution of both disorders coincides

with the culture of susceptible cultivars, and few if any orchards of these

cultivars are free of the diseases. Variegation has been reported from several

European countries and from New Zealand (18, 89, 333). Repeated attempts

by many workers to transmit the disorders have always failed.

Economic Hosts

Crinkle leaf and deep suture have been observed principally on Bing and

Black Tartarian sweet cherry. Crinkle leaf has been noted on Black Republican,

Chinook, Eagle, Burbank, Dr. Flynn, Ox Heart (of America), Shelton, Waterloo Heart, and Moreau. Because these cultivars (except Black Republican) are

planted sparingly, crinkle is uncommon except on Bing and Black Tartarian.

Neither crinkle nor deep suture occur on Lambert or Napoleon. A similar

disease is known on plum and prune but there appears to be no specific relation.

In most cases, a low percentage of the three disorders is seed-transmitted (334),

but in some cases, the percentage is high (18, 364, 378). Variegation is

reported on Hedelfingen from Canada (364) and has been seen on other cultivars imported from Europe to the West and Canada. In New Zealand, St.

306
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 307

Margarets cultivar is most commonly affected, and the disorder has been seen

on six other cultivars (18).

A small percentage of mazzard seedlings may show deep suture symptoms.

Symptoms

Crinkle leaf.—Trees of Bing and Black Tartarian severely affected by crinkle

leaf appear wilted and have foliage that resembles that of maple trees. Leaves

on affected trees are variously misshapen and mottled f figs. 145 and 146, C and

D). Margins are often indented and abnormally serrated through failure of

blade tissue to develop. Some leaves are oddly and severely distorted with deep

sinuses and lobes and accentuated tips and bases. If removed from the tree,

they would hardly be recognized as cherry leaves. The inhibited areas are

usually lighter green and have a silvery upper surface and many more veins per

unit area than the remainder of the leaf, which is darker green than normal.

The light-green areas are present when the leaf first appears in the spring.

Uneven expansion appears to be associated with a mixture of tissues some of

which have more chlorophyll than others. Leaves developed later in the growing season, especially on sucker shoots, are often less affected than those produced in the spring. The total leaf surface of a moderately affected tree is

approximately three-fourths that of a normal tree; yet affected trees are not

noticeably reduced in growth.

Trees affected with crinkle leaf are unfruitful, not because of failure to blossom but because many blossoms are smaller than normal and are visibly

defective. The peduncles are short, and most pistils are short and slender and

have a tendency to discolor early (fig. 146, A and B). Some of the discolored

pistils are brown before the flowers open, others become brown soon afterward,

and few develop into fruits. Such fruits are small, pointed, and often have a

raised suture (fig. 146, C); they are attached with their long axis at an angle

to the stem. Flowers near the base of the preceding season's growth often fail

to open fully. The swollen buds on such growth become reddish, and some

of them remain in place for a number of weeks.

In many instances, a tree may appear entirely normal, but, upon close examination, small branches, twigs, or even a few leaves, can be found affected. Trees

commonly have both normal-appearing branches and branches affected with

crinkle leaf. In some instances, an entire tree is badly affected.

Sweet cherry deep suture.—Cherry trees affected with deep suture have

variable percentages of malformed leaves (fig. 147) and fruits, and different

trees display different degrees of malformation. Sometimes entire trees are

severely affected, but at other times scattered branches through a tree or only

certain lateral ones exhibit symptoms. A severely affected tree viewed from a

distance often has a drooping appearance like one suffering from drought.

Nursery trees affected with deep suture are often dwarfed. When such trees

are transplanted, they grow very slowly, and the foliage is sparse and malformed.
308 VIRUS DISEASES OF STONE FRUIT

FIGURE 145.—Sweet cherry leaves affected by crinkle leaf: A, Bing; B, Black Tartarian;

C, normal Black Tartarian leaf.
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 309

FIGURE 146.—A, Exposed pistils of blossom clusters from Black Tartarian cherry tree

affected by crinkle leaf; B, comparable pistils from an unaffected Black Tartarian tree.

C, Fruit and leaves from a Burbank cherry tree affected by sweet cherry crinkle leaf;

D, comparable fruit and leaves from an unaffected Burbank tree.

Some trees show very little leaf malformation other than a thicker, more

leathery texture and a slight rugosity, whereas the leaves of others are reduced

to narrow ribbons, many of which may be only a midrib in parts and not over

1 inch wide on other parts. The mildly affected trees may show the characteristic deep suture type of leaves in the spring, but the leaves produced in summer

may be nearly normal in shape. This makes detection in the nursery more

difficult.
310 VIRUS DISEASES OF STONE FRUIT

FIGURE 147.—A, Leaves from a Bing cherry tree affected by sweet cherry deep suture;

B, comparable unaffected leaf from a Bing tree.

Some leaves are actually longer than normal, and their lateral veins are shorter

on one side or both sides of the midvein, whereas other leaves merely appear

to be longer because of their relative narrowness. The surface of the leaf may

be very rough, but not puckered. The periphery of some leaves may be irregular

or the leaf may be perforated. The leaf margins usually have fewer serrations

than normal and sometimes serrations are lacking in portions of leaves. A

faint interveinal chlorosis may be present on some leaves during the late spring,

but it is less evident later in the season. Pronounced chlorotic areas like those

found on trees affected with crinkle leaf do not occur. Affected leaves often tend

to develop a bright sheen on the surface and are darker green than normal. Late

spring frosts sometimes cause certain leaf malformations to develop on normal

leaves. Some of these may easily be confused with the leaf symptoms of deep

suture.
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 3X1

Affected fruits have a pronounced depression on the suture side and are

normally rounded at the end (fig. 148). Fruits with deep suture are most often

borne relatively near leaves that exhibit symptoms.

Vigorous, healthy nursery trees of Bing may have some lower leaves with

distortions that resemble the symptoms of crinkle or deep suture, and these make

nursery inspection difficult. Only by experience can adequate differentiation be

made in the nursery.

Symptoms of crinkle leaf and deep suture may occur together on parts of the

same branches and fruit symptoms may not always correlate perfectly with leaf

symptoms. It is well recognized, too, that severity of symptoms in affected trees

may vary year to year.

FIGURE 148.—Bing fruits affected by sweet cherry deep suture, showing pronounced

depression in the suture.
312 VIRUS DISEASES OF STONE FRUIT

Variegation.—^Trees with this disorder produce leaves which lack chlorophyll

in certain areas. Chlorosis may be seen as creamy or white spotting, flecking, or

streaking, or sometimes the chlorotic areas gwQ a marbled appearance. Symptoms

may be restricted to a few flecks or may involve most of the leaf surface and are

best seen in mature leaves. Variegated areas may occur on any part of the leaf

but often occur near the margins. Leaves are sometimes distorted, and, when

symptoms are severe, they roll upward at the margin (78). Portions of trees or

entire trees may show symptoms. Seedlings with severe variegation may die soon

after germination {564). Severely affected trees are smaller than normal, lack

vigor, and bear undersized fruit {18, 89).

Control Measures

Both crinkle leaf and deep suture are regarded as mutations and not as virus

diseases because they have not been transmitted and do not spread. Hence,

an affected tree is not a menace to healthy trees. Repeated experiments by many

workers have shown that both crinkle leaf and deep suture are readily perpetuated in scions or buds. Tests conducted by the senior writer showed that crinkle

leaf may occur in nursery stock even if apparently healthy budwood is used from

a partially affected tree.

It is therefore desirable to inspect mother trees carefully and avoid as sources

of budwood those with even a trace of these disorders.

In the orchard, young trees showing crinkle leaf or deep suture symptoms

should be removed and replaced or they should be grafted over with healthy

scions. Older trees normally are kept until they are no longer economical.

Topworking afl^ected trees to varieties that are not susceptible has been suggested and is sometimes practiced. The cutting out of affected branches in

young trees is recommended if only a few are affected. Crinkle branches should

not become main scaffold branches. Healthy nursery stock produced under an

adequate certification program is the best control known, but it will not guarantee complete freedom from crinkle or deep suture.

Climate or perhaps other environmental factors greatly influence the incidence

of crinkle leaf and deep suture. An experiment was made to observe the effect of

geographic location on crinkle leaf and deep suture (J. A. Milbrath and George

Nyland, unpublished data). In 1959, alternate buds from current season budsticks of Bing clone 260 were placed into mahaleb seedlings in nurseries at

Corvallis, Oreg., and Davis, Calif. At each location, 60 trees were transplanted

as yearlings into test orchards and observed for symptoms of crinkle leaf and

deep suture. During 8 years, only one shoot with typical symptoms of crinkle

was seen in the trees at Corvallis, but many shoots and spurs with symptoms

were seen in the trees at Davis, beginning the second year after planting. Of the

57 trees remaining at Davis the eighth year after planting, 23 showed crinkle

leaf and 25 showed deep suture in at least one spur or shoot. In general, the

symptoms were very mild. Only 12 had neither crinkle nor deep suture. The
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 3^3

trees affected by deep suture averaged two strikes per tree, and those affected

by crinkle averaged three strikes per tree at Davis.

Pruning had a marked effect on the number of strikes per tree of both crinkle

leaf and deep suture. In the experiment described above, the trees were pruned

in three ways: (1) cut heavy, as for budwood, in late August or early September;

(2) dormant pruned just prior to budbreak for 2 or 3 years to make a manylimbed, vase-shaped tree; and (3) no pruning, except when planted, and later

only to remove serious cross-branches. Terminals were not cut back.

The least strikes per tree, averaging all trees, were in treatment 1 ; the most, in

treatment 2 (32 times greater than treatment 1 for crinkle and three times

greater for deep suture). Treatment 3 had 11 times more strikes of crinkle

than treatment 1 and four times more strikes of deep suture. These results

possibly can be explained on the basis of the total number of buds allowed to

produce spurs or shoots in each treatment.

The results are encouraging for the future of cherry mother blocks because

trees cut heavily, as for budwood, had the least crinkle and deep suture.

Remarks

Both crinkle leaf and deep suture are very important cherry diseases.

Crinkle can reduce the crop by 50 percent or more, and deep suture can cause

total rejection of fruit at the packing house if lots are badly affected. Annual

losses from these disorders are probably greater than from the virus diseases.

Certain lots of Bing fruit from trees affected by crinkle leaf are known to have

been marketed as Lambert because of the delay in ripening and the shape of

affected fruit.

Repeated attempts to prove that crinkle leaf and deep suture are caused by

virus have not been successful. It is difficult to understand why some Bing

trees will remain healthy and others from the same source growing in the

same general areas will "break down" partially or completely after several years.

This may be a case of mutation triggered by certain environmental conditions.
DIAGNOSIS OF STONE FRUIT VIRUS

DISEASES AND CERTAIN DISORDERS THAT

RESEMBLE VIRUS DISEASES

Virus disease symptoms can be simulated by mineral deficiencies or excesses,

damage by herbicides, air pollutant injury, or the efifects of low temperatures.

To make suitable evaluations of causal factors, the following sections on nutritional disorders, herbicide injuries, and air pollution injuries have been included

in the Handbook.

Symptoms that may be induced by nutritional imbalances as well as by viruses

include foliar chlorosis (for example, by iron or manganese deficiency or by

peach yellows, sour cherry yellows) ; leaf spotting and shotholing (for example,

by arsenic toxicity, nitrogen deficiency, or by Prunus ring spot) ; little leaf and

rosette (for example, by zinc deficiency or by peach rosette) ; bark cankering,

splitting, and gumming (for example by boron deficiency, boron toxicity,

manganese toxicity or by necrotic rusty mottle, prune diamond canker, Prunus

stem pitting).

Foliage and fruit symptoms induced by 2,4-D and 2,4,5-T herbicide injury

on most Prunus s^táts (for example leaf and shoot distortion of apricot and

plum, soft and red sutures on peach fruits) often have been mistaken for symptoms of virus diseases. The foliage yellowing, spotting, and cupping symptoms

induced by other herbicides may also be mistaken for virus disease symptoms.

There are several useful criteria that can be used as aids in selecting the

most probable causal factor for a given disease or disorder. Distinctive patterns

(for example, rings, patterned mosaics, vein-associated flecking) are more frequently characteristic of virus infection than of nutritional disorders. Knowledge

of the history of disease development in the orchard and observation of the

pattern of occurrence are useful. Thus, if the symptoms have increased in severity

gradually through several seasons in most trees of a planting, a nutritional

disorder must be strongly suspected; whereas, if one or more trees in a planting

develop well-defined symptoms while other trees of the cultivar display no

symptoms, there is more likelihood that a virus is responsible. Moreover,

although some viruses induce shock symptoms in one season only, virus diseases

are most likely to aflfect the same trees in successive seasons, with or without

spread to additional trees.

Assessment of such patterns of disease occurrence, with review of nutritional

practices in the orchard, cataloging of herbicide applications in the vicinity,

assessment of the likelihood of pollutant injury, and consideration of cold

temperature experiences that may have been significant, should be a prelude to

designation of any unfamiliar syndrome as a virus disease. Success in transmit314
HANDBOOK NO. 437, U. S. DEPARTMENT OP AGRICULTURE 315

ting the disease by budding or grafting from affected trees to healthy trees of

the same cultivar is usually accepted as confirmation that the disease is virusinduced.
NUTRITIONAL DISORDERS THAT

RESEMBLE VIRUS DISORDERS

C G. WOODBRIDGE^

In 1946, Shear et al. {607) discussed nutrient element balance as a fundamental concept in plant nutrition and pointed out how seldom balance was

attained. Not only is the intensity of nutrition important but also the balance

between the elements. It is now accepted that optimum nutrient intensity and

balance for a given plant vary with the species, cultivar, age, rootstock, and fruit

load of the plant. The environment—season, light (quality and intensity),

temperature (soil and atmospheric), diurnal fluctuations, and moisture—is also

a variable factor affecting optimum nutrient levels. An incipient deficiency

may cause a reduction of growth and in crop load in all plants, yet no symptom

of the deficiency can be observed. Characteristic symptoms of deficiency are

present when nutrient element balance is greatly disturbed.

Nutrient deficiencies in stone fruits are found in all areas. The most commonly needed element is nitrogen, and symptoms of nitrogen deficiency have

been well characterized. We feel that the philosophy of nitrogen fertilization has

become one of growth regulation rather than deficiency correction. Toxicity

symptoms are not so well characterized, but in Washington they are being

caused by the overzealous use of high-nitrogen fertilizers close to the trunks of

young trees. Phosphorus deficiencies are not common in stone fruits. Potassium

is deficient in many areas, and its need in stone fruits has received considerable

attention. The results of study of the minor elements, both deficiencies

and toxicities, have been fascinating because of the vast range of symptoms

that may be observed and because of dramatic responses that the application of

a small amount of a deficient element can effect {135, 138, 624, 704). Many

deficiencies cause similar twig dieback symptoms. Gumming can be associated

with many abnormal conditions. Because of their similarity, leaf patterns, due to

mineral deficiencies or excesses, frequently can be identified only after extreme

care (for example, the interveinal chlorotic patterns in peach caused by zinc or

manganese deficiencies).

Insufficient chilling of trees in parts of an orchard may cause symptoms that

may be confused with mineral deficiencies. In this category, a slow breaking

of dormancy may be thought to be a boron or a zinc deficiency.

The relationship between the diseases and mineral nutrition has not been

well understood nor particularly well classified. Some work has been done

on the relationship of virus disease and nutrition. Christensen and Walker

{141) in Utah have reported an interaction between virus infection and nutrient

*The names of contributing authors are given in their respective sections.

316
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 317

status of both sweet and sour cherries and between X-disease of peach and

nutrition. Affected tissues contained more nitrogen and phosphorus than did

noninfected trees. Wilks and Stewart (J20) showed that the quaHty of the

fruits on Lambert {Prunus avium) trees infected with little cherry virus may be

adversely affected by zinc deficiency in the absence of recognized zinc deficiency

symptoms.

Nutrient toxicities have been associated with abnormal leaf, twig, bud, and

fruit development. Sometimes, the symptoms have been produced first in sand

culture and later recognized in the field. Some of the toxicities have been due to

high-nutrient levels in the soil or in irrigation water or in both. Arsenic

toxicity resulted from the use of heavy applications of arsenic-containing sprays

in the 1930*5.

Symptoms alone cannot be used to distinguish an actual mineral deficiency

from an induced mineral deficiency. For example, iron deficiency symptoms

may be induced by high levels of aluminum. Also, multiple deficiencies may

occur together. In these instances, diagnosis can be difficult. Positive identification of a deficiency or of an excess cannot always be made from isolated

leaves. It is usually best to see the whole tree. Frequently, one also needs to

use the results of tissue and soil analysis.

In the diagnosis of virus diseases and nutritional disorders, practical experience

is very valuable. In the following sections, deficiency and excess nutritional

problems that resemble virus diseases have been described. For more information, the reader is directed to the following publications: "Diagnostic Criteria

for Plants and Soil" (i3:5), "Fruit Nutrition" (i38), "Hunger Signs in Crops"

(624), and "Diagnosis of Mineral Deficiencies in Plants by Visual Symptoms"

(704).

Nitrogen Deficiency (E. L. Proebsting, O. W, Davidson, and

E, L, Proebsting, Jr.)

On a given soil in California, peach frequently shows symptoms first, but

almond and Japanese plum show them a little later. European plum may not

show any marked symptoms except reduced growth (544, 343). In the East,

also, peach shows more marked symptoms of nitrogen deficiency than other

stone fruits, but symptoms may be shown by all Vrunus species. Chemical

analysis of suitably selected leaf samples provides a useful measure of nitrogen

status.

The pale green to yellow leaves of all plants grown in a soil low in available

nitrogen is a well-recognized symptom of nitrogen deficiency (42). When the

supply of nitrogen in the soil is limited, trees gradually redistribute a large

portion of their nitrogen from old to new tissues. As a result, the mature and

nearly mature leaves turn from dark green to yellowish green (fig. 151). The

yellow in these leaves gradually increases, and the petioles and veins become

tinged with red. By this time, linear growth of the twigs has been checked, and

the leaf size is reduced. Moreover, the twigs and leaves are relatively hard. In
318 VIRUS DISEASES OF STONE FRUIT

1 to 3 weeks, red or red-brown spots appear between the large veins of the leaf

blades if the deficiency is acute. In advanced stages of nitrogen deficiency, many

of the reddish spots develop into necrotic areas. Gradual abscission of the leaves

from the base of the current-season growth toward the tip follows.

Terminal-shoot growth is frequently short and thickened, and the fruit buds

are numerous. The percentage of flowers setting fruit is greatly reduced. In case

of severe nitrogen shortage, the shoots also are short and slender, and the number of fruit buds is less than on normal trees. Potassium-deficient trees also

frequently have small, light-green leaves similar to those on nitrogen-deficient

trees. In the case of potassium deficiency, however, the terminal shoots are more

slender and the internodes are long. The red spotting of leaves of severely

afiiected trees is characteristic of deficiency of nitrogen. Lack of this essential

element in the soil is the only deficiency that results in reddish discoloration

of the leaf.

Fruits growing on trees low in nitrogen ripen earlier and are more highly

colored than fruits on trees high in nitrogen (12, 178, 346, 602, 623). Freestone peach fruits that are nitrogen deficient tend to taste more astringent and be

more fibrous than fruits grown on trees that are high in nitrogen {346). Cheeks

of nitrogen-deficient fruits may not fill out properly, and the flesh tends to cling

to the pit.

Excess nitrogen delays fruit maturity and results in poorer skin color on fruit

of a given firmness. Too much vigor can result in shading out lower interior

fruiting wood. On young trees, nitrogen toxicity may result if large amounts of

nitrogen fertilizer are applied directly at the trunk. Symptoms may include rolling of leaf margins toward the upper side of the midrib and necrosis that tends

to be marginal. Chemical analysis will show very high levels in affected leaves.

Nitrogen deficiency is easily corrected by application to the soil of inorganic

sources of nitrogen such as ammonium sulfate, sodium nitrate, ammonium

nitrate, or organic material containing soluble nitrogen {344, 624).

Phosphorus Deficiency (W. E. Ballinger)

Phosphorus deficiency has been reported and described largely for peach

{177).

When peach trees are grown in sand culture, the first symptom of phosphorus

deficiency is the development of dark, dull-green to purplish-green foliage (fig.

149). The leaves show no puckering or crinkling along the midrib, and the

blade is leathery, flat, and narrower than normal for the cultivar. When the

phosphorus shortage is severe, the veins on the underside of the leaf and the

petiole may be purplish. In orchards in North Carolina, leaves of trees deficient

in phosphorus were dark green and, in late summer, became bronzed with a

reddening of veins and petioles. Abscisson of basal leaves of shoots was premature. Fruit from trees low in phosphorus are small, flat cheeked, cracked,

astringent, low in soluble solids, bitter, early ripening, and have a bluish-red

overcolor and overall poor quality.
FIGURE 149.—Elberta peach leaves showing symptoms of mineral deficiency when trees were grown in sand cultures with indicated element

withheld: A, phosphorus; B, manganese; C, nitrogen; D, iron; E, magnesium; P, calcium; G, potassium. H, Comparable leaf from tree

grown on a complete nuttient.

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320 VIRUS DISEASES OF STONE FRUIT

Where phosphorus deficiency symptoms have been observed under field conditions, the trouble has been corrected by applications of phosphate fertilizer.

Fertilizers containing phosphorus should be applied to ensure production of

good cover crops in orchards.

Potassium Deficiency (O. C. Compton)

Potassium deficiency has been reported and described for almond, apricot,

peach, plums (Prunus domestica and P. sal/ana), and sour cherry. No reports

describing potassium deficiency of sweet cherry growing under field conditions

have been found. Chandler (134) observed "... sweet cherry trees can obtain

enough potassium from soils in which apple trees and some varieties of Domestica (European) plum trees will be injured seriously by potassium deficiency."

Our observations in Oregon confirm these by Chandler. The symptoms have

been described recently by Fritzsche et al. (224) for sweet cherry trees grown

in nutrient solutions.

Lack of available soil moisture and heavy cropping accentuate the symptoms

although young nonbearing trees often show severe deficiency. Removal of topsoil by erosion or grading operations often creates areas of acute deficiency.

In California (398, 400), leaves of afiPected almond trees are light green and

show tipburn early in the season. Marginal scorch often occurs near the leaf

tip, and leaves assume a boat-shaped appearance on vigorous shoots. More

severe deficiency results in sparse foliage, decreased growth, terminal dieback,

and lowered yields. Deficiency symptoms develop in leaves containing 0.7 percent potassium or less dry weight. Reports from California (398, 400) indicate

that potassium-deficient apricot trees have leaves that are pale green, tend to roll

or cup upward, and are sparse. Shoot growth is reduced. Marginal scorch and

dieback occur when the deficiency is severe. Size of fruit and yields are reduced.

The deficiency develops when leaf potassium is at 2.0 percent or less, a level

considerably higher than for other stone fruits.

Potassium deficiency symptoms in peach are characterized by upward rolling,

pale leaves in midsummer or thereafter, which increases in severity from basal

to terminal leaves (138, 398, 400, 401) (ñg. 150). With acute deficiency,

older leaves become crinkled at the midrib, and marginal and submarginal

necrosis develops, producing irregular margins and a shot hole effect (fig. 151).

Slender shoots, reduced set of fruit buds, and small fruits that ripen prematurely

accompany these leaf symptoms. These symptoms are not usually evident at

leaf potassium levels above 0.75 percent, although the critical level is 1.0 percent

potassium in midsummer leaves (401),

Symptoms of the deficiency on the French (Agen) prune cultivar (398, 400)

show first as small, light-green leaves. Marginal necrosis or leaf scorch soon

develops, especially with a heavy crop. Severe deficiency results in small, abnormally colored fruits and shoot dieback. Leaves of Italian Prune in New York

(94) show midsummer loss of green color starting at the margins. Chlorosis
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 321

FIGURE 150.—Two-year-old peach trees: A, Adequately supplied with nitrogen and

potassium; B, adequately supplied with nitrogen but deficient in potassium, showing

narrow leaves with a tendency for the margins to roll upward.

FIGURE 151.—Peach leaves showing severe upward rolling and marginal necrosis

characteristic of potassium deficiency, left, compared with normal leaf, right.
322 VIRUS DISEASES OF STONE FRUIT

develops, and older shoot leaves roll toward the upper surface. Increasing deficiency produces marginal necrosis. Symptoms of moderate to severe deficiency

on the Italian Prune in Oregon (fig. 152) vary from slightly mottled, lightyellow leaves that roll upward in August to leaves showing marked chlorosis

with a slight to moderate marginal necrosis at harvest (fig. 152). Fruits are

reduced in size. Deficiency symptoms usually develop on all varieties at or

below 1.0 percent potassium in midsummer.

Leaf rolling combined with a light-green color on the older leaves are early

symptoms of the deficiency in sour cherry (224, 239). In advanced stages the

leaf margins on the lower surface first become bronze, and then scorched.

Small leaves and fruits, shortened slender growth, and greatly reduced yields

are characteristic of severely affected trees. The symptoms develop at or below

0.75 percent potassium in midsummer leaves.

Potassium deficiency was corrected easily in prune, peach, or cherry orchards

growing in coarse- to fine-textured soils of the Coastal Plains, the North

Atlantic, and the north central regions. Application of 1 to 6 pounds per tree

of potassium chloride, depending on tree age, produced satisfactory recovery

(138). Mulches of straw, hay, or manure also increased leaf potassium, often by

several times.

In areas of low to nonexistent summer rains, such as the tree fruit areas of

the Pacific Coast States, improvement usually requires heavy applications of

potassium fertihzers. In Cahfornia (398, 400, 401), at least 25 pounds of

potassiufp sulfate per tree is necessary, except on certain acid or sandy soils

where half this amount produced satisfactory results. Italian Prune trees in

Oregon required 12.5 to 15 pounds per tree of potassium chloride to produce

recovery. Smaller amounts applied annually were ineffective. The larger

amounts were effective for several years. Deep placement of potassium chloride

increased the response in California (400). The high fixation of potassium in

the residual acid soils of the Willamette Valley has been bypassed effectively by

use of potassium nitrate foliage sprays applied 6 to 8 weeks after bloom.

Calcium Deficiency (Norman F. Childers)

Peach is the only stone fruit species known to suffer from calcium deficiency

in orchards (284).

When peach trees are grown in a nutrient solution lacking calcium, the first

symptom of the deficiency is usually decreased terminal growth; the older leaves

may be of normal size, but the young leaves are usually smaller than normal

(fig. 149). The leaves are dark green, and no chlorosis is evident. Later, a

large chlorotic, then necrotic, area develops in the center of some of the younger

leaves, particularly on the lateral spurs and shoots (fig. 153). It is a large,

characteristic spot involving tissue on either side of the midrib. The older

leaves later show marginal chlorosis and breakdown. Finally the leaves drop

at the shoot tip; then the ends of the shoots may die back. Under controlled

nutrient conditions, calcium deficiency is shown first in peach foliage, where
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 323

potassium and magnesium are relatively high. In the field, calcium deficiency

has greatly curtailed root extension of peach.

Magnesium Deficiency (W. E. Ballinger)

Magnesium deficiency on this continent has been noted only on peach. When

peach trees are grown in a magnesium-deficient nutrient solution, the older

green leaves may develop light-gray or fawn-colored spots in the area between

FIGURE 152.—Italian Prune branch showing fall leaf symptoms of potassium deficiency

in Oregon: chlorotic blotches and slight to moderate marginal necrosis.
324 VIRUS DISEASES OF STONE FRUIT
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 325

the veins (ñg. 149). In severe cases, the spots may enlarge and take in the

edges of the leaves (fig. 154). In early stages, leaves may show a chlorosis

somewhat Hke the early stages of iron chlorosis. The leaves of severely affected

trees shed from the base toward the tip, and only a few of the youngest leaves

may remain near the growing tip. As the green fades out between the veins,

the leaf tissue takes on a papery, gray appearance, and the dead spots may

enlarge and envelop the outer margin of the leaves. Under controlled nutrient

tests in sand culture, magnesium deficiency appears first where calcium or potassium is relatively high in relation to magnesium. Two types of magnesium

deficiency symptoms on leaves in orchards in North Carolina Sandhills may

develop: (1) marginal and interveinal necrosis (described above) which

develops quickly, followed by leaf drop and (2) marginal chlorosis (fig. 155,

F) (427). Symptoms are more prevalent on trees bearing large crops of fruit

than on trees with small or no crop loads (138).

For long term correction on sandy soils, apply magnesium sulfate up to 2.5

pounds per tree per year. Use dolomitic limestone to correct acid soil conditions.

Spraying the leaves with a solution of magnesium sulfate (epsom salts) may

give a quicker response. Avoid applications of excessive amounts of potassium

fertilizers or low-magnesium limes.

Manganese Deficiency (Omund Lilleland and K. Uriu)

Manganese deficiency has been found on almond, apricot, sweet cherry, sour

cherry, peach, European plum, and Japanese plum.

A distinct pattern has been observed on the leaves of all stone fruit species

in which manganese deficiency has been noted. The midrib and main veins with

adjacent bands of tissue of varying width remain green, whereas the interveinal

and peripheral areas of the leaf edges may be chlorotic (fig. 149; fig. 155).

Generally chlorosis does not occur until the young leaves have attained full size,

and it becomes more pronounced on the older leaves as the season progresses.

Only in very severe cases is there a dwarfing of shoot growth and the development of a spot necrosis into a shothole condition of the leaf (fig. 156). Nontypical symptoms may occur when both zinc and manganese or iron and

manganese are deficient and the correction of the zinc or the iron may reveal the

more typical manganese symptoms. Multiple deficiencies of manganese, zinc,

iron, and even other elements may infrequently occur, in which cases symptomatology alone is inadequate to diagnose the trouble.

There appears to be an excellent correlation between the results of leaf

analyses and the manganese status of fruit trees. Studies with many kinds of

FIGURE 153.—A, Peach leaves showing symptoms of calcium deficiency. B, French

prune twigs and leaves showing injury due to boron excess. C, Apricot leaves and

D, peach leaves showing injury due to sodium excess. E, Peach leaves and F, peach

branches showing arsenic injury.
326 VIRUS DISEASES OF STONE FRUIT

fruit trees in many places have shown a fairly constant critical value of 15 to

20 ppm manganese on a dry-leaf basis in midsummer. There are fewer data

on toxicity or excess manganese than there are on manganese deficiency, but the

value for excess is probably close to 1,000 ppm in the leaf.

Manganese deficiency is easily corrected by foliage sprays in early spring.

An earlier recommendation of 5 pounds of manganese sulfate has been reduced

FIGURE 154.—Leaves from a peach tree grown in a magnesium-deficient nutrient solution:

A, Severe symptoms; B and C, mild symptoms.
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 327

to the present 2 pounds of manganese sulfate in 100 gallons of water for

California orchards. MnEDTA at V2 to 1 pound per 100 gallons of water has

also given good correction. If annual spraying is inconvenient over a number

of seasons, a correction may be obtained in alkaline soil by an application of

sulfur.

Iron Chlorosis (Walter J. Kochan)

A number of factors influence the amount of iron required to prevent

chlorosis, so a precise sufiiciency level cannot be given. However, the susceptibility of stone fruits to lime-induced iron chlorosis from most susceptible to least

susceptible has been assigned as follows: peach, sweet cherry, plum, apricot,

and almond.

Foliar symptoms of iron chlorosis are a reduction in chlorophyll content and

a paling of the green of the leaves (fig. 157). As the disturbance becomes more

acute, the areas between the veins become yellow; if not corrected, the deficiency

may cause the entire leaf to become white, progressing to dead leaf margins (fig.

149). Severely chlorotic leaves are smaller than nonchlorotic leaves. With very

severe deficiencies, the small branches will die, beginning at the tips. The young

leaves that emerge are chlorotic; if iron is made available, they will become

green. Mature, green leaves do not become chlorotic. Although chlorosis is not

specific for any element, this complex of symptoms is such that the deficiency

may be identified. Diagnostic techniques (388) used in conjunction with the

foliar symptoms aid in confirming the deficiency.

Many methods have been recommended to cure lime-induced iron chlorosis.

All, apparently, have some merit, but none is without drawbacks. Dilute sprays

of iron sulfate early in the season may correct the deficiency but must be

repeated to include developing shoots. Injecting iron salts into bored holes

in the trunk or large limbs was probably the most successful treatment before

synthetic iron chelates were introduced but were time consuming and destructive

of tissue. An iron chelate was first used successfully in culture solution (331) ;

its agricultural potential was demonstrated in citrus (627) and exhaustively

studied (703); and its beneficial effects on peach on a calcareous soil were

demonstrated (379). The principal function of the chelating complex seems

to be that of preventing the formation of insoluble iron salts in the soil.

Zinc Deficiency (David R. Walker, R. L. Smith, and W. H.

Chandler)

Chandler (133) listed sweet cherry as the most susceptible of the stone fruits

to zinc deficiency. Other stone fruits afiiected, in order of susceptibility, seem to

be Japanese plum, European plum, peach, apricot, almond, and sour cherry.

The deficiency is often referred to as "little leaf." Leaf symptoms, more than

any other symptoms, have been emphasized in describing the deficiency syndrome

(ñg. 158). Leaves that develop in early spring at the apex of a long shoot may

be much smaller than normal (about 1 inch long and I/4 inch or less wide).

Shortened internode growth results in leaves crowded very closely into tufts at
328 VIRUS DISEASES OF STONE FRUIT
HANDBOOK NO. 437, U. S. DEPARTMENT OP AGRICULTURE 329

N^-

FIGURE 156.—Shothole in peach leaves associated with a severe manganese deficiency.

the terminal end, resulting in the disease sometimes being called rosette (fig.

159).

In the early stages, irregular splashes of yellow or chlorotic areas occur

between the veins. These isolated chlorotic areas gradually coalesce until continuous bands of yellow extend from near the midrib to the outer edge where

they form a continuous chlorotic leaf margin (663). Most of the leaves have

wider green areas along the veins and around the yellow areas than manganesedeficient leaves have, and the yellow tends to be paler and less golden. Leaves

at the end of some summer shoots may be creamy yellow, with very little

green even along the veins. Red or purple blotches sometimes occur on these

chlorotic areas. Tissue in these spots may dry up and drop out, producing a

shot hole effect. In some varieties of plums, stippled foliage occurs due to small

chlorotic areas scattered over the leaf. Wavy leaf margins and crinkling of

midribs occurs especially on the tip leaves. In apricot leaves, the margins curve

upward forming a cup-shaped effect. Premature leaf fall may also occur. Short

FIGURE 155.—A, Peach leaves showing a gradient of manganese deficiency symptoms;

B, Montmorency cherry leaf showing manganese deficiency symptoms; C, Montmorency

cherry leaf from a manganese-deficient branch; and D, a comparable leaf from a

branch cured by injection of manganese sulfate; E, prune leaves showing symptoms

of iron deficiency, left, compared with normal leaves, right; F, peach leaves showing

symptoms of magnesium deficiency.
330 VIRUS DISEASES OF STONE FRUIT

FIGURE 157.—Leaves of French (Agen) prune showing characteristic pattern in reduction

of chlorophyll due to lack of available iron; normal leaf, lower left.

twigs, undeveloped buds, small leaves, and early leaf fall result in bare limbs

and dieback, which is common on affected trees. Weak wood which fails to

harden and, in extreme cases, death of the tree occurs as a result of this

deficiency (fig. 160).

Zinc-deficient trees often produce small yields of undersized or misshapen fruit.

Fruit in the top of the tree and especially toward the end of the branches, tend

to be progressively much smaller than normal. Deficient peach and Japanese

plum trees produce more flattened fruit than normal. Mature peaches from zincdeficient trees break down sooner after harvest than those of normal trees.

Apricot fruits are less flattened than normal, more nearly round, and greatly

reduced in size to that of medium-sized cherries. Flat, pointed peaches have

been observed on zinc-deficient trees.

The leaf and fruit symptoms may appear on just one or a few branches with

the rest of the tree appearing healthy. The symptoms sometimes resemble

X-disease (663). Distinguishing features are that X-disease does not cause a

reduction in leaf size, the leaves may turn downward, and they may drop off

prematurely.

Many soils have a great capacity to render zinc unavailable to trees. In some

of the Pacific Slope soils this fixing capacity is so great that 1,000 to 1,500

pounds of zinc sulfate applied to an acre of soil may not supply the necessary

ounce or two of zinc to an acre of trees. In Florida, however, soil applications
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 33I

of one-half pound to 5 pounds per tree of ZnS04 were effective in eliminating

zinc deficiency symptoms (189).

Dormant sprays of ZnS04 applied as a separate spray just before the buds

start to swell, at the rate of 10 to 50 pounds per 100 gallons, has been the

main control measure for peach, almond and Japanese plum. The amount

required depends on the severity of the symptoms. Apricot does not respond

as well as peach to dormant spraying, and therefore stronger solutions must

be used.

Foliar sprays of ZnS04 have been used successfully. Up to 8 pounds per 100

gallons without lime has been used without injury reported. Hydrated lime,

calcium caseinate, and calcium hydroxide have been used with ZnS04 to reduce

plant injury. A solution of 10 pounds ZnS04, 5 pounds hydrated lime, and

100 gallons of water applied any time during the growing season but preferably

in the early spring has been used successfully (87). Spraying three to four

consecutive seasons may be necessary and every other year thereafter to control

severe deficiencies. Foliar sprays have been applied at the rate of 12 to 25

pounds ZnS04 and half as much hydrated lime in 100 gallons of water. Foliar

injury is more likely to occur under humid conditions. Foliar applications

of 5 pounds of ZnS04 plus 2.5 pounds of calcium hydroxide per 100 gallons

was more effective in controlling the deficiency than soil applications of 500

pounds ZnS04 per acre or 25 pounds ZnS04 per 100 gallons as a dormant

spray (426).

Synthetic chelated zinc materials (NaoZn-EDTA or NaZnH-EDTA) applied

to the soil (1 pound per peach tree in June) was reported as being more effective

than dormant ZnS04 sprays applied at the rate of 12 pounds per 100 gallons

(426). Natural chelated zinc has been effective as a foliar spray at the rate of

5 pounds per 100 gallons. This material must be applied early in the spring

while the fruit is small in order to avoid a fruit residue problem.

Although trunk injections of ZnS04 and zinc-coated nails driven into the

trunk have been recommended as control measures, they are not being used

much at present. Considerable labor is involved and some tree injury has

occurred from these practices.

Copper Deficiency (K, Uriu mid Carl J, Hansen)

In this country, copper deficiency has been observed on plum (Prunus

donnestica and P. sdiana) and almond. In South Africa, the deficiency has

been observed on plum (?. sdichia), apricot, and peach. In Australia, it has

been observed on plum (P. sdicina) and, in Great Britain, on almond and sweet

cherry.

One of the characteristic symptoms of copper deficiency is shoot dieback. In

early summer terminal growth ceases, mottling and chlorosis (fig. I6I) may

develop, and the terminal leaves become brown at the tips and margins, giving

the shoots a withered appearance (fig 162). Eventually, many of the terminal

HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 333

leaves fall as the tips of the shoots are killed back (fig. 158 pi. 9, D).

Sometimes in the current season, but mostly in the following season, the lateral

buds below the dieback are forced into growth. These shoots die back in

the same manner, and the repetition of the dieback over a period of years causes

affected trees to have a bushy, stunted appearance.

The bark of affected trees may be rough and corky, but the extent of such

injury may depend on the species and variety. In plum, hard, rough, irregular,

and dark-colored fissures develop in the bark, and reddish-brown gum often

exudes from the ruptured fissures. In almond, severe rough bark also occurs, and

considerable gumming of trunks and lower parts of main branches occurs in

late winter and early spring in Nonpareil (fig. 163) and Ne Plus Ultra.

Trees of Texas (Mission) almond show dark, rough bark but seldom produce

gum.

The copper level in the leaves from deficient trees is, in general, about 3 ppm

or less.

Plum trees showing symptoms of copper deficiency have been cured by

application of copper sulfate to the soil and by spraying the young leaves with

Bordeaux mixture. For copper-deficient almond, good correction has been

obtained by application of copper sulfate and CuEDTA to the soil or by foliar

spray of Bordeaux mixture or CuEDTA. For diagnostic purposes, copper sulfate can be injected into holes bored in the trunk.

Soil applications have generally varied from 1 pound to 5 pounds of copper

sulfate placed in the bottom of a circular trench or spaded in around the base

of each tree, the exact quantity depending on the size of the tree and the fixing

power of the soil. CuEDTA, ^ to 1 pound per tree as a broadcast treatment,

has been used on almond with success. Sometimes response from soil treatments

may not become evident the first season.

Foliar sprays in early spring with Bordeaux mixtures of 5-5-100 to 10-10-100

have been reported to give good correction on plum and almond. Almond has

even responded to Bordeaux as dilute as 1-1-100. Also with almond, CuEDTA

at one-quarter pound per 100 gallons of water has been effective. Higher rates

of CuEDTA were found to be phytotoxic to the leaves.

The holes used for the injection of dry copper sulfate are spaced about 4

inches apart around the trunk, and excessive injury is avoided by keeping the

material away from the cambium and the bark. This is done by inserting the

copper sulfate in gelatin capsules or forcing it through a tube. Wooden plugs

can then be driven into the holes.

FIGURE 158.—A-C. Plant parts showing symptoms of zinc deficiency: A, Peach; B, apricot;

C, sweet cherry. In each illustration deficient parts (lefi) are compared with healthy

parts (right). D, Prune shoots with tip killing due to copper deficiency.
334 VIRUS DISEASES OP STONE FRUIT

FIGURE 159.—Limb on peach tree affected by zinc deficiency showing typical

tosetted growth.

Boron Deficiency (C. G. Woodbridge)

Most stone fruit species are affected by boron deficiency. Marked deficiency

is characterized by the dying back of new shoots usually in the spring but

sometimes later in the season {204, 277, 278, 431). The buds may swell in

early spring then die and slough off. Whole trees may die, but this usually

takes several years (figs. 164 and 165). Lateral shoots may develop below the

dead portion, giving the branch a witches'-broom effect. Dieback due to boron

deficiency may be mistaken for winter injury; however, in early spring with

boron deficiency the cambium is white, whereas with winter injury the cambium

is discolored.

Leaves on shoots affected with dieback may scorch, curl, and die (fig. 166).

Sometimes rosettes of leaves may occur and these symptoms may be confused

with 2inc deficiency. Boron-deficient sweet cherry leaves are narow and frequently have irregular serations (fig. 167). Observations and diagnosis can

readily be confirmed with chemical analysis of the affected tissue. If the boron
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 335

FIGURE 160.—Sweet cherry tree in Utah, showing small chlorotic leaves and severe

dieback due to zinc deficiency.
336 VIRUS DISEASES OF STONE FRUIT

FIGURE 161.—^Leaves of Santa Rosa plum showing chlorosis and scorching characteristic

of copper deficiency.

FIGURE 162.—Copper-deficient almond shoots showing tip and marginal necrosis of

terminal leaves, that give the shoots a withered appearance.
HANDBOOK NO. 437, U. S. DEPARTMENT OP AGRICULTURE 337

content of leaves is below 20 ppm on a dry-weight basis, boron deficiency can

be suspected.

Symptoms of boron deficiency appear first on fruit, but seldom is the entire

crop affected. Fruit may show surface cracking, shriveling, and malformation

(101). Water-soaked areas in the flesh are common in prunes and plums, but

internal browning and corky tissue are found in apricot, and gumming occurs

on almond fruit.

Preventive sprays are used in most areas where boron deficiency is known to

occur. Soil applications of boron compounds have also successfully prevented

boron deficiency.

Boron-Excess Injury (C. G. Woodbridge)

Most stone fruit species are affected. The most striking feature associated

with boron toxicity in apricot is the greatly enlarged nodes on 1- and 2-year-old

twigs (fig. 168). Internodes may be somewhat shorter than usual and gumming may occur. The bark is frequently rough and may slough off. Tips of

shoots may die during the summer, and the leaves near the tip may turn black

and fall. Small twigs, leaf petioles, and the lower side of leaves may show necrosis. Fruit ripens early. Scablike protuberance and corking of the fruit are associated with high boron.

FIGURE 163.—Scaffold limb of Nonpareil almond showing rough bark and gumming

characteristic of copper deficiency.
338 VIRUS DISEASES OF STONE FRUIT

Dieback of cherry twigs (fig. 169) is also caused by an excesive amount of

boron. Gumming is common. Growth is neghgible. Leaves affected with boron

toxicity may have necrotic areas near the midrib or in the lamina of the leaf

(fig. 170). Opening of the flower buds is delayed.

FIGURE 164.—Young peach tree showing moderate dieback in the spring on shoots of

the previous year's growth due to boron deficiency.
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 339

FIGURE I65.—^Terminal dieback on sweet cherry due to boron deficiency. The terminal

bud started to grow in the spring but died later, following partial defoliation.

Small necrotic spots on the underside of the main rib of peach, cherry, and

almond leaves are common symptoms of boron toxicity (fig. 171). In severe

leaves turn yellow and drop prematurely. Twigs are frequently cankered and

cases, gummed. Fruits are malformed and the kernels develop poorly (fig.

172).

On prune trees affected with boron toxicity the nodes swell, but not as much

as on apricot, and the bark cracks and curls (fig. 168 and fig. 153, B and fig.

173).

Spurs develop slowly and the leaves are small. Leaves feel coarse, the midrib is

thick, and many small necrotic patches appear and fall out. The latter symptom

is more striking in peach. Fruit is small and ripens prematurely. Diagnosis

should be confirmed by tissue analysis. In leafy tissue, a boron content of over

80 ppm on a dry-weight basis is suspect.

Control measures depend upon the quality of the irrigation water. If the water

is low in boron, excess boron may be leached out.
340 VIRUS DISEASES OF STONE FRUIT

FIGURE 166.—Boron deficiency in apricot leaves. The midrib is thickened, and the

leaves show a characteristic boatlike form.

FIGURE 167.—Leaves from sweet cherry tree growing in a low-boron sand culture,

compared with normal leaf, left. Affected leaves are narrower than normal and

serrations are irregular.
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 34I

Chloride-Excess Injury (R. M. Carlson and Omund Lilleland)

Almond, apricot, sweet cherry, peach, Japanese plum, and European plum

are known to be injured by excess chloride.

Trees growing in soils with moderate salt concentration may be stunted

without showing specific toxicity symptoms {286). This effect can be cumulative,

causing a slow, progressive decline. When exposed to high concentrations of

chloride, specific symptoms will develop; apricot leaves develop a cup shape

caused by upward rolling of the margins and the leaf tips, and leaf margins

scorch {40, 41, 397, 681). Almond, plum, and prune show tip and marginal

leaf scorch {41, 681). Excess chloride in cherry causes small, pale-green

leaves, marginal necrotic scorch, slender stems, and some leaf abscission {186,

511). The symptoms in peach are chlorosis, tip and marginal leaf burn, leaf

FIGURE 168.—Boron toxicity symptoms on apricot branch, showing enlarged nodes

and some stunting and killing of twigs.
342 VIRUS DISEASES OF STONE FRUIT

FIGURE 169.—^Dieback of sweet cherry twigs caused by an excessive amount of boron.

abscission, and dieback of branches (4i, 191, 283, 286, 397). Symptoms

may develop on only one side of a tree {397)- Soil analysis is not always

a reliable tool for diagnosis of chloride injury. Leaf analysis can be

used to confirm diagnosis by visual symptoms. Brown et al. {100) found

the lower limit of chloride content in leaves showing injury was about 1.0

percent (dry-weight basis) for apricot and peach, 0.6 percent for prune and

plum, 1.2 percent for Nonpareil almond, and 1.8 percent for Texas almond.

Deciduous trees generally show some detrimental effect if foliar chloride

concentrations exceed 0.3 percent.

The form of chloride in the root media can greatly influence the amount of

chloride damage to the tree. Wadleigh et al. (681) showed that excess chloride

damage to stone fruits is much more severe when calcium chloride is the source

compared with isosmotic solutions of sodium chloride.

Excess chloride injury can also occur through foliar absorption of chloride

from sprinkler-applied irrigation water. Ehlig and Bernstein {197) showed that

sodium or calcium chloride in water sprinkled on trees caused necrosis of leaf

tips and partial defoliation of almond and plum. Twig tips and fruiting spurs

of almond, plum, and apricot were partially killed by sodium or calcium chloride

in this experiment.

Leaching the soil to remove excess chloride and use of low chloride irrigation

water are suggested as control measures.

Sodium-Excess Injury (Omund Lilleland)

Almond, apricot, sweet cherry, peach, and Japanese plum are known to be

injured by excess sodium.
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 343

FIGURE 170.—Sweet cherry leaves showing symptoms of boron toxicity. Necrotic areas

are commonly near the midrib but may be elsewhere in the leaf lamina.

FIGURE 171.—Severe boron toxicity on young peach shoot showing necrotic spots along

the stem and petioles.
344 VIRUS DISEASES OF STONE FRUIT

FIGURE 172.—Boron toxicity in peach fruit, showing malformation and poor

kernal development.

Several types of leaf scorch (397, 399) are caused by excess sodium. Burning at the tip of the leaf is frequently characteristic of early stages of injury

(fig. 154, C and D). Trees may be stunted but remain alive for a number of

years, or they may die in one season. Analysis of scorched leaves often shows

0.5 percent or more of sodium in the dry matter. A low potassium content is

frequently associated with a high sodium content. Chemical analysis of the

roots of injured trees reveals accumulation of sodium in the wood. Injury may

occur on soils which contain as low as 250 ppm of total soluble salts.

Leaching the soil with nonsaline irrigation water and additions of gypsum,

sulfur, and similar materials, depending upon soil conditions, are suggested

as corrective measures.

Arsenic Injury (N. R. Benson)

All fruit species show marked reduction in growth when planted on soils

containing excess arsenic. The effect is believed to be toxicity to the roots. In

addition to growth retardation, some species also exhibit symptoms on the

leaves. Peach and apricot are most easily injured; sweet cherry is only

moderately damaged ; and plum {Prunus domestica) shows no foliage symptoms
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 345

even when planted on soils that contain so much arsenic that growth is severely

restricted.

As a general rule, arsenic toxicity symptoms on peach do not become apparent

until midsummer and appear first on the older or basal leaves. The younger,

terminal leaves frequently remain normal for a while or throughout the season.

The first indication of injury is the development of brown to reddish-brown

spots along the leaf margins. These spots also appear in the leaf blade between

the veins. Later these necrotic islands fall from the leaf, leaving irregularshaped holes—a shot hole effect similar to that caused by the X-disease virus

(fig. 153, E). In fact, the symptoms are so much alike, the arsenic injury has

often been mistaken for X-disease (403, 566). The injured tissue around the

leaf margin may drop out, leaving a ragged margin. In severely affected trees,

defoliation takes place later in the season, but any fruits on a tree remain

attached and ripen somewhat prematurely (fig. 153, F). The fruits do not attain

full size and are astringent in flavor. A similar injury results from arsenical

sprays applied to peach trees.

Symptoms in apricot resemble those in peach but with less tendency for

defoliation. Symptoms on cherry are much less severe and are usually confined

to interveinal browning.

At the present time there appears to be no practical method of removing

arsenic from the soil. Therefore, emphasis has been placed on reducing arsenic

FIGURE 173.—Boron toxicity on 2-year-old prune twigs on which bark cracked, curled

outwards, and in some cases was sloughed ofï. Normal twig on left.
346 VIRUS DISEASES OF STONE FRUIT

absorption by the tree and of increasing the tolerance of trees for arsenic.

This has been accomphshed by continued high nitrogen fertihzation and occasional applications of zinc sulfate to the soil. The addition of sulfur to the

soil in addition to the zinc sulfate on alkaline soils increased the effectiveness of

the treatment (639). Also effective, especially on alkaline or calcareous soils

when soil application of zinc sulfate was least effective, were sprays of zinc

EDTA and other chelates (26). The rate of application of zinc sulfate for soil

application was 5 to 8 pounds per tree. Sprays of zinc EDTA consisting of 2.5

pounds of material per 100 gallons were applied in June and July. Applications

of zinc sulfate to the soil may be repeated as necessary but should not be required

more often than every 3 to 4 years. Sprays may be required annually.
HERBICIDE INJURIES THAT RESEMBLE

VIRUS DISEASES

W. V. WELKER

Many of the symptoms of herbicide injury are similar to those caused by virus

disorders and mineral deficiencies. In general, these injuries are the result of

incorrect use of herbicides. Injury from an herbicide may occur when the

desired dosage is exceeded through error, as when the sprayer is improperly

calibrated, or when an inaccurate delivery system is used. Although a twofold to

threefold tolerance factor to avoid injury to crops is usually present in recommendations for the use of herbicides, foliar symptoms may occur before the

critical level is reached at which yields are reduced. Injury seldom occurs when

recommendations for herbicide use are carefully followed.

Young trees with small root systems are more susceptible to herbicide injury

than older trees with well-developed root systems. Many of the recommendations stipulate that applications of herbicides should be delayed for varying

periods from the time the trees are planted. Injury is also more apt to occur on

light-textured soils than on heavy-textured soils. The amount of clay and

organic matter in a soil influences the availability of an herbicide and its rate

of downward movement with water.

The amount and distribution of rainfall can also influence the appearance of

injury symptoms. Frequent, light showers alternating with dry periods usually

result in less downward movement of herbicides than a heavy, soaking rain.

Deep disking just prior to applying an herbicide can result in injury with

compounds that are normally safe. Rains may wash the herbicide into the base

of the cut, thus placing the herbicide deeper than normal and also concentrating

it. Many of the herbicides used in orchards rely upon depth protection for most

of their selectivity. Deep disking can eliminate much of the depth protection.

Injury symptoms vary for a given herbicide depending upon the amount

of herbicide available at any one time. At a low availability level an herbicide

may show bleaching of the leaf color in a characteristic pattern. At a high

availability level it may show none of this ; burning or scorching of the leaf may

be the only symptom exhibited.

In evaluating plant injury symptoms, all aspects of the situation should be

carefully considered. Such aspects include nutritional deficiencies or excesses,

root pruning, debarking, and the presence of insects, diseases, and nematodes.

Simazme [2-chloro-4, 6-bis (ethylamino)-j--tria2Íne} injury on peaches is

characterized by a mottling of the interveinal area of the leaf. This usually

begins with chlorosis that appears in the peripheral area of the leaf and progresses toward the midrib. The midrib and main veins as well as the tissue

immediately adjacent to them remain green. The affected area becomes bright

347
348 VIRUS DISEASES OF STONE FRUIT

yellow. In cases of severe injury, the mottling may not develop as far as the

midrib. A scorching may develop at the margin and envelop most of the leaf;

this is followed by leaf drop. Mild symptoms of mottling may not affect the

ability of the tree to carry a normal crop (fig. 174).

Terbacil [3-/íí/-butyl-5-chloro-6-methyluracil} injury in peach begins

with the loss of green from the main veins. This occurs in mature leaves as well

as newly expanding leaves. The veins turn a golden yellow. The tissue

immediately adjacent to the veins is next affected, and the yellowing spreads

until the entire leaf may become yellow. Exposure to higher dosages may result

in little yellowing other than the veins. Leaf scorch may become the dominant

injury symptom. Leaf scorch usually begins at the periphery of the lower half

of the leaf and may envelop the entire leaf. Abscission of the leaves may follow.

Quite often, vegetative buds break following leaf drop. These new shoots

have shortened internodes and produce leaves that are much reduced in size

(fig. 175).

FIGURE 174.—Peach leaves showing interveinal mottling and chlorosis resulting from

simazine toxicity.
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 349

FIGURE 175.—Peach leaves showing terbacil injury: Top, Vein clearing at low dosage;

bottom, leaf scorch at high dosage.
350 VIRUS DISEASES OF STONE FRUIT

Isocil [5-bromo-3-isopropyl-6-methyluracil] injury to peach very closely

resembles that of terbacil with vein clearing and yellowing of the adjacent

tissue. The injury may occur more quickly over the tree than with terbacil. This

may be due to isocil's solubility in water, which is approximately three times

as great as terbacil (fig. 176).

Bromadl [5-bromo-3-Jíír-butyl-6-methyluracil], being closely related to

isocil and terbacil, affects peaches in much the same manner. The peach seems

to have less tolerance to bromacil than to either isocil or terbacil. Injury symptoms appear first as a yellowing of the veins and then leaf scorch. The yellowing

of the tissue adjacent to the veins usually does not develop nearly as well as in

terbacil or isocil (fig. 177).

Dalapon [2, 2-dichloropropionic acid] may induce a number of injury symptoms. Tip burn may occur over any portion of the tree. At higher dosages tip

burn may be accompanied by marginal leaf burn. The entire margin may become

scorched. Leaf scorch may also appear between the veins. The new growth may

appear lighter in color, have a shiny appearance, and show some twisting. The

young leaves may fail to elongate (fig. 178).

Amitrole [3-amino-l,2,4-tria2ole] induces in peach the same basic symptom

as it does in so many other species—whitening of the leaves. Amitrole inhibits

FIGURE 176.—Peach leaves showing vein clearing and leaf scorch resulting from

isocil toxicity.
HANDBOOK NO. 437, U. S. DEPARTMENT OP AGRICULTURE 351

FIGURE 177.—Peach leaves showing vein clearing and leaf scorch resulting from

bromocil toxicity.

chlorophyll formation, thus the lack of chlorophyll appears in the new growth.

At higher dosages, the older leaves may exhibit scorching in blotches beginning

at the margins. This scorching does not engulf the entire margin. Leaf abscission may occur shortly after leaf scorch appears( fig. 179).

Dkhlobenil [2,6-didiloroben2onitrile] injury in peach appears as small,

necrotic spots along the margins of the fully expanded mature leaf. The dark

necrotic area is surrounded by a light chlorotic area. The necrotic spots are

quite small when they first appear and tend to enlarge with time (fig. 180).

Dicamba [3, 6-dichloro-o-anisic acid] affects terminal leaves of peach by

inhibiting their unfolding. A characteristic symptom of dicamba injury in most

species is cupping of the leaves. The peach exhibits a similar response as the

folded leaves take on a crescent shape with the midrib as the axis. The elongation of the leaves may not be influenced at low dosage. The leaves Üiat are

folded may appear to be wilting as they droop ; however, examination will show

that they are firm and turgid. At higher dosages, necrosis of the growing point

may occur. Leaf burn may begin with the apical leaves. It usually starts at the

base of the leaf, either along the leaf margin or the midrib, and progresses

acropetally. Necrosis may also occur in the stem, starting at the tip and progressing basipetally (fig. 181).
352 VIRUS DISEASES OF STONE FRUIT

FIGURE 178.—Peach leaves showing dalapon injury: Top, marginal necrosis at low

dosage; bottom, marginal and interveinal necrosis at high dosage.
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 353

FIGURE 179.—Peach leaves showing necrotic blotches resulting from amitrole toxicity.
354 VIRUS DISEASES OF STONE FRUIT

FIGURE 180.—Peach leaves showing marginal necrosis resulting from

dichlorobenil toxicity.

FIGURE 181.—^Peach shoot showing dicamba injury: Crescent-shaped leaves and necrosis

of growing point and leaves.
AIR POLLUTION INJURIES TO STONE

FRUIT TREES

H. E. HEGGESTAD

Air pollution injury to vegetation is often confused with injury from other

causes, especially virus diseases and nutritional disorders. Plants are very sensitive to air pollution; however, species vary considerably in their sensitivity to

specific pollutants. Interest in air pollution has increased in the past decade.

Vegetation injury by toxicants in photochemical smog is now recognized to be

a national problem (441).

As with vegetation generally, little is known about the economic impact of

air pollution on stone fruits. Certain markings resulting from acute injury can

be attributed to specific pollutants. Emphasis in this section is on the effects of

fluorides (which seem to be the pollutant of most concern to us) on stone

fruits. The information on the effects of other air pollutants is reviewed.

Fluoride

Fluoride causes injury to leaves of many species of Prunus and to fruits of

some species. Fluoride injury to peach fruit is known as soft suture, although

other agents may cause similar symptoms.

The problem was first recognized in the United States in the early 1940's

(394^ 463, 302). Leaf injury was severe near certain industries. Principal

sources of fluoride are: industries that manufacture aluminum and steel; phosphate rock processing; brick and pottery plants; chemical industries that use

fluorides; and rocket fuel combustion. Although procedures for reducing

fluoride pollution at the source have been improved, the number and size of

some of the industries emitting fluoride have increased. Fluorides may be toxic

to sensitive species when the concentration in air is a half part per billion or less.

Sensitive species show leaf necrosis when concentrations in the leaf have

accumulated to about 50 parts per million or more.

Prunus species are among the most sensitive plant species to fluoride air

pollution. Apricot generally is highly sensitive but, Moorpark and Tilton

apricot are less sensitive. Other sensitive plants are Italian Prune (P. domestica),

peach, sloe plum, and mahaleb cherry. Sweet cherry has been classified as a

tolerant species {86). Apparently, oriental flowering cherry (P. serrulata) and

myrobalan plum (P. cerasifera) are also quite tolerant. A black tip condition of

peach fruit, described as similar to soft suture, was reported in 1952 {428).

Although 25 percent of fruits showed injury in orchards near a steel plant, no

leaf scorch was observed, except on apricots near one of the orchards. Later,

Benson {35) presented evidence that soft suture of peaches may be caused by

fluorides. Bolay and Bovey {86) describe a dark-brown to black lesion of the

stylar end of apricot and cherry attributed to fluorides.

355
356 VIRUS DISEASES OF STONE FRUIT

Fruit injury results when peach trees are exposed to fluoride fumes of relatively low concentrations, especially during the pit-hardening period. Most

foliage necrosis, however, is associated with the accumulation of fluorides.

Exposure to very low concentrations for long periods of time, or shorter periods

at high concentrations, may be equally injurious. The amount of fluoride

accumulated in the tissue is the critical parameter (3, 86, 463).

The first symptom of fluoride injury is wilting at the edges of leaves, usually

followed by a brown or tan marginal scorch. Injury induced by hydrogen

fluoride to Belle of Georgia peach leaves is shown in figure 182. A sharply

defined, reddish-brown band often separates the necrotic tissue from the adjacent

healthy tissue. The marginal scorch resembles that attributed to sodium excess

and magnesium deficiency. Leaf margins may cup upward. Necrotic areas may

dry and fall away. Defoliation may occur. Leaf injury is intensified by lack of

rain and unfavorable soil conditions, such as gravel spots or too heavy soil (.502).

Actually, drought may cause similar injuries in the absence of fluoride. With

fluoride, the necrosis is confined more to the leaf margins than with drought.

Under some conditions, chlorosis develops following exposure to fluorides, as

shown on Belle of Georgia peach in figure 183. Somewhat similar chlorosis

may be due to magnesium deficiency and, no doubt, other causes. Cupping

and shriveling of leaf tips also occurs, as shown on Moorpark apricot in figure

184. If fluoride is the cause of injury, analysis of leaf tissue should reveal

elevated concentrations of fluoride. The more sensitive species may develop leaf

necrosis when fluoride in the tissue is less than 50 ppm; however, more than

50 ppm are usually required. Plants in a tolerant class, such as sweet cherry,

may store over 500 ppm in leaves without visible injury (So). Controlled

fumigation studies by Adams et al. (3) revealed greater injury from daily

exposure for 8 hours to 1.5 parts per billion (ppb) than exposure for 8 hours

FIGURE 182.—Necrosis of peach leaves resulting from fluoride toxicity.
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 357

FIGURE 183.—Chlorosis of peach leaves resulting from fluoride toxicity.

every third day at 5 ppb or for 4 hours every third day to 10 ppb hydrogen

fluoride. They state that plants exposed at the lowest level every day had less

chance for recovery between fumigations. Field studies in Ontario (193)

provide additional information on fluoride levels and injury to peach leaves and

fruit.

The first symptom of fluoride injury to fruits is reddening of the skin along

the suture and usually near the stylar end about 2 weeks before fruits are mature.

The flesh is also reddish, ripens faster, and becomes soft (figs. 185 and 186).

Soft suture is sometimes known as suture red spot. Cracks in the skin may

develop, and the affected portion is bruised easily and is subject to decay.

Although fluorides cause soft suture, a very similar syndrome is caused by

growth regulators and perhaps other agents. Fruit affected by 2,4,5-trichlorophenoxyacetic acid (2,4,5-T) may show growth protuberances as well as soft suture

(fig. 187). According to Benson (33), fruit injury induced by fluorides can be

distinguished from injury caused by growth regulating compounds, such as 2,

4-dichlorophenoxyacetic acid (2,4-D). In addition to uneven growth and

ripening, the injury by the growth regulators is usually most severe toward the

stem end of the fruit.
358 VIRUS DISEASES OF STONE FRUIT

FIGURE 184.—^Apricot shoot showing cupping and shriveling of tips of leaves resulting

from fluoride toxicity, right; normal shoot, left.

Best control of fluoride injury is obtained with the use of proper scrubbers to

reduce fluoride emissions at the source. Soft suture of peach may be controlled

95 percent or more by one to three sprays of lime or calcium chloride. Two

pounds of calcium chloride per 100 gallons of water applied at 2- to 3-week

intervals, beginning at pit hardening, is preferred. According to N. S. Benson

(personal communication), calcium chloride does not leave a fruit residue and

does not destroy insecticide effectiveness.

Sulfur Dioxide

Sulfur dioxide is a major air pollutant affecting vegetation. Primary sources are

the burning of fossil fuels, smelting of ores, production and refining of petroleum and natural gas, and manufacture and utilization of sulfur and sulfuric

acid. Zimmerman and Hitchcock (77.5) reported the results of controlled

fumigations with sulfur dioxide on 49 species of plants, including Prunus.

The concentration of the gas ranged from 0.2 to 1.1 ppm, and the time from

2 to 8 hours. With an exposure of 0.5 ppm sulfuric dioxide for 4 to 8 hours,

Moorpark apricot showed slight markings. Italian Prune was more susceptible;

it developed moderate markings. Italian Prune was approximately as susceptible

as buckwheat, smartweed, grape, and sweetpotato. On dicotyledonous plants,
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 359

the leaf tissue surrounding larger veins remains green; spotting results from

death of cells in interveinal areas. Injury to apricot and Sun High peach from

exposure to 3 Ppm sulfur dioxide for 4 hours is shown in figure 188.

Qironic injury appears as chlorosis; death of a few isolated cells is indicated

by white or brownish areas.

Field studies at Biersdorf, Germany, included observations on sweet cherry,

sour cherry, and plum. Levels of sulfur dioxide varied with distance from the

primary source, an iron sintering plant. The 24-hour average concentration at

the station nearest the source was about 0.15 ppm; and taking into account

only emission periods, the average was about 0.6 ppm. The pollutant caused a

marked reduction in growth of trees and in quality of fruit (268).

Ozone

Ozone is the major phytotoxicant in photochemical smog. Symptoms on

most dicotyledonous plants are either a fleck or stipple on the upper surface of

FIGURE 185.—Soft suture of peach fruit resulting from fluoride toxicity.
360 VIRUS DISEASES OF STONE FRUIT

fully expanded leaves. Chlorosis and loss of leaves is usually a part of the

syndrome. There is very little information about effects on stone fruits. Injury

by mites resembles fleck caused by ozone.

Elberta peach was one of 37 plant species fumigated with ozone by Hill et al.

FIGURE 186.—Cross section of peach fruit with soft suture resulting from fluoride

toxicity, showing, at top, a darkened area in the flesh.

FIGURE 187.—Peach fruit showing growth protuberances, predominantly at the stem end,

resulting from 2,4,5-T toxicity.
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 361

(314). Plants were exposed for 2 hours to ozone treatments, ranging from

0.13 to 0.41 ppm. Peach was intermediate in sensitivity. The injury was

described as ""a mild chlorotic upper-surface mottling along veins." In addition,

dark lesions and shot-holing may develop, as shown in figure 189. The injury

resulted from exposure to 0.6 ppm ozone for 2 hours. The dark lesions and

shot-holing developed more rapidly than the mottling along veins, which was

FIGURE 188.—Leaves of peach, left, and apricot, right, injured by exposure to sulfur

dioxide 3 ppm for 4 hours.
362 VIRUS DISEASES OF STONE FEUIT

more pronounced on leaves a few days after the photograph (fig. 189) was

taken.

FIGURE 189.—Peach leaves showing chlorosis and dark lesions with shotholing resulting

from ozone toxicity; normal leaf on left.
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 353

Plum trees were injured in Switzerland by ozone in the vicinity of a water

reservoir where ozone treatment of drinking water was underway (396). Apparently, sufficient ozone escaped to the air to reach phytotoxic levels in the valley.

The leaves of plums were chlorotic, especially between the larger veins. There

was considerable tip and border necrosis. Italian Prune trees were more sensitive

to ozone than cherry trees tested under the same conditions.

Researchers in California (336) listed about 115 plant species as either susceptible or resistant to photochemical smog. Perhaps the primary toxicant in

the smog was ozone. Apricot was rated susceptible, and cherry, peach, and

plum resistant.

The use of ozone to preserve peach and other fruits was investigated by

Spalding (623). Except for inhibiting surface mycelium, no significant effect

was found on the fungi that were causing rhizopus and brown rots of peaches,

when ozone concentrations of up to 10 ppm were maintained for 5 days.

This dosage of ozone, however, resulted in injury to peaches described as

sunken and browned tissue in the region of the stomata. Ozone caused death of

tissue and loss of moisture. The fruit had a pebbly appearance (fig. 190).

Little or no injury to fruit occurred when the concentration of ozone was

reduced to 0.5 ppm and lower.

Other Pollutants

Peroxyacetyl nitrate was identified about 10 years ago as a primary phytotoxicant in photochemical smog (441). Typically, the injury is a glazing or

bronzing of the undersurface of leaves. No reports are available on the

sensitivity of Prunus species.

Ethylene is a common air pollutant, with motor vehicle exhaust and the

manufacture of certain plastics as primary sources. Symptoms on plant species

include epinasty, chlorosis, necrosis, leaf and bud abscission, and failure of

FIGURE 190.—Injury to peach fruit, right, resulting from exposure to high concentration

of ozone during storage. Normal fruit, left.
364 VIRUS DISEASES OF STONE FRUIT

flowers to open. Heck et al. (288) determined the response of 89 species,

including peaches, to relatively high concentrations. Tests with peach seedlings

revealed them to be one of the more sensitive of plant species.

Nitrogen dioxide, chlorine, aldehydes, and ammonia are other pollutants

receiving attention by researchers, but no specific information on the sensitivity

of Prunus species seems to be available. The possibility of effects of combinations

of pollutants also must be considered. Literature references and more detail

on air pollution injury to vegetation are found in recent reviews (93, 289, 732).

Contact type chemicals, such as arsenite, used for defoliants on such crops as

potatoes prior to harvest, have caused varying types of injury to nearby fruit

orchards as a result of drift of the chemicals. Trees nearby may lose nearly

all leaves. At greater distances, the side of the trees nearest the sprayed area

will show most injury. Increased injury is usually associated with improper

formulations and application techniques.
LITERATURE CITED^

(1) ANONYMOUS.

1959. CURRENT RESEARCH AND INVESTIGATIONS. N.Z. Orchardist 32(10):

299-301.

(2)

1968. PLANT QUARANTINE ANNOUNCEMENTS. CANADA. Food and Agr.

Organ. Plant Prot. Bui. 16: 94-95.

(3) ADAMS, D. F., HENDRIK, J. W., and APPLEGATE, H. G.

1957. RELATIONSHIP AMONG EXPOSURE PERIODS, FOLIAR BURN, AND FLUORINE CONTENT OF PLANTS EXPOSED TO HYDROGEN FLUORIDE. Agr.

and Food Chem. 5: 108-116.

(4) AFANASIEV, M. M.

1963. "SHORT STEM" CONDITIONS IN LAMBERT CHERRIES. (Abstr.) Phytopathology 53: 1137.

(5)

(6)

1965. LAMBERT MOTTLE AND SHORT STEM VIROSES OF SWEET CHERRIES IN

MONTANA. Zast. bilja (Belgrade) 16: 401-403.

(7)

1967. EFFECT OF TEMPERATURE AND LENGTH OF INCUBATION ON SYMPTOM

DEVELOPMENT OF LAMBERT MOTTLE OF SWEET CHERRIES. Plant Dis.

Reptr. 51: 269-270.

1968. SEPARATION OF LAMBERT MOTTLE FROM PRUNUS RINGSPOT VIRUS IN

PRUNUS SEROTINA. Plant Dis. Reptr. 52: 184-185.

(8) and HAMILTON, R. I.

1965. "SHORT STEM" VIROSIS OF SWEET CHERRIES. Plant Dis. Reptr. 49:

253-255.

(9) and MILLS, I. K.

1957. THE SPREAD OF LAMBERT MOTTLE VIROSIS IN LAMBERT AND PEERLESS

VARIETIES OF SWEET CHERRIES IN MONTANA. Plant Dis. Reptr. 41:

517-520.

(10) and MILLS, I. K.

1961. "SHORT STEM" VIROSIS OF SWEET CHERRIES. Northwest Assoc. Hort.,

Ent., and Plant Path. Rept. 22: 8.

(11) and MORRIS, H. E.

1951. VIRUS DISEASES OF SWEET CHERRIES IN MONTANA. Plant Dis. Reptr.

35: 191.

(12) ALBRIGO, L. G., CLAYPOOL, L. L., and URIU, K.

1966. THE EFFECT OF NITROGEN LEVEL ON DEVELOPMENT AND MATURITY

OF ROYAL APRICOT FRUITS. Amer. Soc. Hort. Sei. Proc. 89: 53-60.

(13) ALCORN, S. M., WILHELM, S., and THOMAS, H. E.

1955. A MOSAIC DISEASE OF HIMALAYA BLACKBERRY. Phytopathology 45:

272-274.

(14) ALLEN, W. R.

1964. SEROLOGICAL AND PHYSICOCHEMICAL COMPARISONS BETWEEN VIRUSES

OF THE PRUNUS NECROTIC RINGSPOT AND PFEFFINGER (RASP LEAF)

TYPES. Phytopathology 54: 455-459-

(15)

1968. TOMATO BUSHY STUNT VIRUS FROM PRUNUS AVIUM L. II. SEROLOGICAL TYPING AND THE CHARACTERIZATION OF ANTIBODY TYPES AND

ACTIVITIES. Can. J. Bot. 46: 230-233.

(16) and DAVIDSON, T. R.

1967. TOMATO BUSHY STUNT VIRUS FROM PRUNUS AVIUM L. L FIELD

STUDIES AND VIRUS CHARACTERIZATION. Can. J. Bot. 45: 2375-2383.

(17) ANTHON, E. W., and WOLFE, H. R.

1951. ADDITIONAL VECTORS OF WESTERN X-DISEASE. Plant Dis. Reptr.

33: 345-346.

^ References reviewed only through 1969 publication.

365
366 VIRUS DISEASES OF STONE FRUIT

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1964. CHLOROTIC LEAFSPOT FROM A MECHANICALLY TRANSMISSIBLE VIRUS

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1954. NECROTIC LEAF SPOT OF PEACH AND ITS EFFECT ON JUNE-BUDDED

STOCK. Calif. Dept. Agr. Bul. 43: 13-17.
400 VIRUS DISEASES OF STONE FRUIT

(693) and BREECE, J. R.

1955. EVIDENCE OF RETENTION OF PEACH YELLOW BUD MOSAIC VIRUS IN

SOIL. (Abstr.) Phytopathology 45: 696.

(694) and BREECE, J. R.

1956. PEACH CALICO, ONE OF MANY VIRUS DISEASES OF STONE FRUITS

Calif. Dept. Agr. Bui. 45: 256-258.

(695) BREECE, J. R., and SCHLOCKER, ARCHIE.

1958. STUBBY TWIG, A NEW VIRUS DISEASE OF PEACH AND NECTARINE IN

CALIFORNIA. Phytopathology 48: 465-468.

(696) BREECE, J. R., TRAYLOR, J. A., and WILLIAMS, H. E.

1961. THE OCCURRENCE OF APRICOT RING POX VIRUS IN PLUM IN CALIFORNIA. Plant Dis. Reptr. 45: 796-797.

(697) ct al.

1960. OBSERVATIONS ON THE PASSAGE OF PEACH NECROTIC LEAFSPOT AND

RINGSPOT VIRUSES THROUGH PEACH AND NECTARINE SEEDS AND

THEIR EFFECTS ON THE RESULTING SEEDLINGS. Plant Dis Reptr

44: 117-119. '

(698) and SCHLOCKER, ARCHIE.

1953. PEACH YELLOW BUD MOSAIC. Calif. Dept. Agr. Bui. 42- 266-267

(699) TRAYLOR, J. A., and WILLIAMS, H. E.

1963. THE NATURAL OCCURRENCE OF PEACH ASTEROID SPOT VIRUS IN A

NATIVE PRUNUS (P. ANDERSONII L.) IN CALIFORNIA AND NEVADA

Phytopath. Medit. 2: 196-198.

(700) TRAYLOR, J. A., WILLIAMS, H. E., and WEINER, A. C.

1968. INVESTIGATIONS OF CHERRY RASP LEAF DISEASE IN CALIFORNIA

Plant Dis. Reptr. 52: 618-622.

(701) WILLIAMS, H. E., and MILLICAN, A. A.

1957. VIRUS-FREE NURSERY STOCK. Calif. Dept. Agr. Bui 46- 177-180

(702) WALKER, E. A.

1939. RED SUTURE DISEASE OF PEACH REPORTED FROM MARYLAND Plant

Dis. Reptr. 23: 254.

(703) WALLACE, ARTHUR, ed.

1962. A DECADE OF SYNTHETIC CHELATING AGENTS IN INORGANIC PLANT

NUTRITION. Edwards Bros., Ann Arbor, Mich. 195 pn

(704) WALLACE, T.

1961. THE DIAGNOSIS OF MINERAL DEFICIENCIES IN PLANTS BY VISUAL

SYMPTOMS. New York, N.Y. 125 pp.

(705) WANN, F. B.

1941. CONTROL OF CHLOROSIS IN AMERICAN GRAPES. Utah Agr. Exp. Sta.

(706) WATERWORTH, H. E., and FULTON, R. W.

1964. VARIATION AMONG ISOLATES OF NECROTIC RINGSPOT AND PRUNE

5T-'^n55-TÍ60^ ^^^^"^"^^^ ^^^^ ^^^^ CHERRY. Phytopathology

(707) • and GiLMER, R. M.

1969. DARK GREEN EPINASTY OF CHENOPODIUM QUINOA, A SYNDROME

59^^3^3T3^3^8'^ ^^^^^ LATENT IN APPLE AND PEAR. Phytopathology

(708) WAY, R. D., and GiLMER, R. M.

1958. POLLEN TRANSMISSION OF NECROTIC RINGSPOT VIRUS IN CHERRY

Plant Dis. Reptr. 42: 1222-1224.

(709) and GiLMER, R. M.

1963. REDUCTIONS IN FRUIT SETS ON CHERRY TREES POLLINATED WITH

53^^3^9V4Tl^ "^^^^^ ^^ ^^^^ ^"^^^^ YELLOWS. Phytopathology

(710) WEINBERGER, J. H., and THOMPSON, L. A

1962. INHERITANCE OF CERTAIN FRUIT AND LEAF CHARACTERS IN TAPANESE PLUMS. Amer. Soc. Hort. Sei. Proc 81- 172-179

(711) WEINTRAUB, M.

1961. PURIFICATION AND ELECTRON MICROSCOPY OF THE PEACH YELLOW

BUD MOSAIC VIRUS. Phytopathology 51: 198-200.
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 401

(712) and WILLISON, R. S.

1953. STUDIES ON STONE-FRUIT VIRUSES IN CUCURBIT HOSTS. III. THE

EFFECT OF CUCURBIT EXTRACTS ON INFECTIVITY. Phytopathology

43: 328-332.

(.713) and WILLISON, R. S.

1954. STUDIES OF STONE-FRUIT VIRUSES IN CUCURBIT HOSTS. V. THERMAL

INACTIVATION OF SOME ISOLATES. Phytopathology 44: 538-542.

(714) WELSH, M. F.

1961. TERMINOLOGY OF PLANT VIRUS DISEASES. Can. J. Bot. 39: 1773-

1780.

(715) and MAY, JAMES.

1965. DETECTION OF VIRUS INFECTION IN IMPORTED CHERRY AND APRICOT

CLONES. Can. Plant Dis. Surv. 45: 85-88.

(716) and WILKS, J. M.

1951. INDUCED MODIFICATION OF SYMPTOM SEVERITY IN LITTLE CHERRY.

Phytopathology 41: 136-138.

(717) WILDE, W. H. A.

1960. INSECT TRANSMISSION OF THE VIRUS CAUSING LITTLE CHERRY DISEASE. Can. J. Plant Sei. 40: 707-712.

(718) WiLKS, J. M., and MiLBRATH, J. A.

1956. COMPARATIVE STUDIES OF THE VIRUS DISEASES WESTERN XDISEASE

LITTLE CHERRY AND LITTLE CHERRY. Phytopathology 46: 596-599.

(719) and REEVES, E. L.

1960. FLOWERING CHERRY, A RESERVOIR OF THE LITTLE CHERRY VIRUS.

Phytopathology 50: 188-190.

(720) and STEWART, J. A.

1961. RESPONSE OF LITTLE CHERRY-INFECTED CHERRY TREES TO ZINC

TREATMENTS. Can. J. Plant Sei. 41: 517-522.

( 721 ) and WELSH, M. F.

1955. SWEET CHERRY FOLIAGE INDICATOR HOSTS FOR THE VIRUS THAT

CAUSES LITTLE CHERRY. Can. J. Agr. Sci. 35: 595-600.

(722) and WELSH, M. F.

1961. HOST RANGE STUDIES OF THE LITTLE CHERRY DISEASE VIRUS. Can.

J. Plant Sei. 41: 544-548.

(723) and WELSH, M. F.

1964. APPARENT REDUCTION OF LITTLE CHERRY DISEASE SPREAD IN

BRITISH COLUMBIA. Can. Plant Dis. Surv. 44: 126-130.

(724) WILLIAMS, H. E., and MILBRATH, J. A.

1955. FRECKLE FRUIT OF SWEET CHERRY. (Abstr.) Phytopathology 45:

696.

(725) TRAYLOR, J. A., and WAGNON, H. K.

1962. RECOVERY OF VIRUS FROM REFRIGERATED FRUIT TREE AND GRAPEVINE POLLEN COLLECTIONS. (Abstr.) Phytopathology 52: 367.

(726) TRAYLOR, J. A., and WAGNON, H. K.

1963. THE INFECTIOUS NATURE OF POLLEN FROM CERTAIN VIRUS-INFECTED

STONE FRUIT TREES. (Abstr.) Phytopathology 53: 1144.

(727) TRAYLOR, J. A, and WAGNON, H. K.

1967. EVIDENCE OF THE RETENTION OF CHERRY RASP LEAF VIRUS IN SOIL IN

CALIFORNIA. (Abstr.) Phytopathology 57: 103.

(728) WILLISON, R. S.

1944. STRAINS OF PRUNE DWARF. Phytopathology 34: 1037-1049.

(729)

1945. A LINE-PATTERN VIROSIS OF SHIRO PLUM. Phytopathology 35:

991-1001.

(730)

(731)

(732)

1946. PEACH BLOTCH. Phytopathology 36: 273-276.

1951. PEACH BLOTCH. In Virus Diseases and Other Disorders with Viruslike Symptoms of Stone Fruits in North America. U.S. Dept. Agr.

Agr. Handb. 10, pp. 93-94.

1962. CROSS PROTECTION AND INTERFERENCE WITH SOME STONE-FRUIT

VIRUSES. Can. J. Bot. 40: 1041-1049.
402 VIRUS DISEASES OF STONE FRUIT

(733) BERKELEY, G. H., and HILDEBRAND, E. M.

1951. TATTER LEAF. In Virus Diseases and Other Disorders with Viruslike Symptoms of Stone Fruits in North America. U.S. Dept. Agr.

Agr. Handb. 10, pp. 141-146.

(734) and WEINTRAUB, M.

1953. STUDIES ON STONE-FRUIT VIRUSES IN CUCURBIT HOSTS. I. A METHOD

OF EVALUATING THE INFECTIVITY OF INFECTIOUS JUICE. Phytopathology 43: 175-177.

(735) and WEINTRAUB, M.

1954. STUDIES ON STONE-FRUIT VIRUSES IN CUCURBIT HOSTS. IV. SOME

EFFECTS OF HYDROGEN ION CONCENTRATION AND DILUTION ON

INFECTIVITY. Phytopathology 44: 533-537.

(736) and WEINTRAUB.

1957. PROPERTIES OF A STRAIN OF CUCUMBER MOSAIC VIRUS ISOLATED FROM

PRUNUS HOSTS. Can. J. Bot. 35: 763-771.

(737) WEINTRAUB, M., and FERGUSON, j. D.

1956. PURIFICATION AND ELECTRON MICROSCOPY OF VIRUSES CAUSING

CHERRY YELLOWS AND RELATED DISEASES. Can. J. Bot. 34: 86-103.

(738) WEINTRAUB, M., and TREMAINE, J. H.

1959. SEROLOGICAL AND PHYSICAL PROPERTIES OF STONE FRUIT VIRUSES.

I. PREPARATIVE AND SEROLOGICAL TECHNIQUES. Can T Bot 37 •

1157-1165. * '

(739) WILSON, E. E.

1952. DEVELOPMENT OF BUD FAILURE IN THE JORDANOLO VARIETY OF

ALMOND. (Abstr.) Phytopathology 42: 520.

(740)

1954. SEED TRANSMISSION TESTS OF ALMOND BUD-FAILURE DISORDERS.

(Abstr.) Phytopathology 44: 510.

(741) and SCHEIN, R. W.

1956. THE NATURE AND DEVELOPMENT OF NONINFECTIOUS BUD-FAILURE

IN ALMOND. Hilgardia 24: 519-542.

C742) and STOUT, G. L.

1944. A BUD-FAILURE DISORDER IN ALMOND TREES. CALIF DEPT AGR

Bui. 33: 60-64.

(743) and STOUT, G. L.

1950. OBSERVATIONS ON THE BUD-FAILURE DISORDER IN JORDANOLO, A

NEW VARIETY OF ALMOND. (Abstr.) Phytopathology 40: 970

(744) and STOUT, G. L. J f &y

1951. DRAKE ALMOND BUD FAILURE. In Virus Diseases and Other Disorders

with Viruslike Symptoms of Stone Fruits in North America. U.S

Dept. Agr. Agr. Handb. 10, pp. 191-194.

(745) and WAGNON, H. K.

1955. A PEACH DISORDER POSSIBLY RELATED TO THE VIRUS BUD FAILURE

DISEASE OF ALMOND. Phytopathology 45' 323-326

(746) WILSON, N. S., and COCHRAN, L. C.

1952. YELLOW SPOT, AN ERIOPHYID MITE INJURY ON PEACH. Phytopathology 42 : 443-447.

(747) JONES, L. S., and COCHRAN, L. C.

1955. AN ERIOPHYID MITE VECTOR OF THE PEACH MOSAIC VIRUS. Plant Dis

Reptr. 39: 889-892.

(748) WISCONSIN AGRICULTURAL EXPERIMENT STATION.

1945. HOW IMPORTANT IS NECROTIC RING SPOT OF SOUR CHERRY? Wis

Agr. Exp. Sta. Ann. Kept. (Bui. AGG) 61: 23-24

(749) WOLFE, H. R.

1955. TRANSMISSION OF WESTERN X-DISEASE VIRUS BY THE LEAFHOPPER

COLLADONUS MONTANUS (VAN D.). Plant Dis. Reptr 39- 298-299

(750 and ANTHONY, E. W.

1953. TRANSMISSION OF WESTERN X-DISEASE VIRUS FROM SWEET AND SOUR

CHERRY BY TWO SPECIES OF LEAFHOPPERS. J. Econ. Ent 46- 1090- 1092. . . y

(751) ANTHON, E. W., KALOOSTIAN, G. H., and JONES, L. S.

1951. LEAFHOPPER TRANSMISSION OF WESTERN X-DISEASE. T Econ Ent

AA: 616-619.
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 403

(752) WOOD, F. A.

1968. SOURCES OF PLANT-PATHOGENIC AIR POLLUTANTS. Phytopathology

58: 1075-1084.

(753) YARWOOD, C. E.

1952. DELETERIOUS ACTION OF WATER IN PLANT VIRUS INOCULATIONS.

Nature 169: 502.

(754)

(755)

(756)

(757)

(758)

1953. QUICK VIRUS INOCULATION BY RUBBING WITH FRESH LEAF DISCS.

Plant Dis. Reptr. 37: 501-502.

1956. MECHANICAL TRANSMISSION OF PEACH YELLOW BUD MOSAIC VIRUS.

Plant Dis. Rcptr. 40: 299.

1957. CONTACT TRANSMISSION OF PEACH RINGSPOT VIRUS. PhytOpatholoey

47: 539.

1957. JUICE TRANSMISSION OF VIRUSES TO PEACH. (Abstr.) Phytopathology 47: 38.

1957. MECHANICAL TRANSMISSION OF FRUIT TREE VIRUSES. Can. Phytopathology Soc. Proc. 25: 19-20.

-759) and SYLVESTER, E. S.

1959. THE HALF-LIFE CONCEPT OF LONGEVITY OF PLANT PATHOGENS.

Plant Dis. Reptr. 43: 125-129.

(760) and THOMAS, H. E.

1954. MECHANICAL TRANSMISSION OF FRUIT TREE VIRUSES. (Abstr.)

Phytopathology 44: 511.

(761) YOUNG, H. C.

1951. INDEXING HOSTS FOR SOUR-CHERRY RINGSPOT AND YELLOWS. PHYTOpathology 41: 479-480.

(762) ZAWADSKA, BARBARA

1965. OBSERVATIONS AND PRELIMINARY EXPERIMENTS ON FRUIT TREE

VIRUS DISEASES IN POLAND. Zast. bilja (Belgrade) 16: 513-516.

(763)

1968. STUDIES ON POME AND STONE FRUIT TREE VIRUSES IN POLAND WITH

SPECIAL EMPHASIS ON VARIETIES RECENTLY INTRODUCED FROM

EASTERN COUNTRIES. Rcs. Inst. Pomol., Skierniewice, Rept. E 21-

CR-27 (1967), p. 24. (Processed.)

(764) ZELLER, S. M.

1934. CHERRY MOTTLE LEAF. Greg. Stare Hort. Soc. Ann. Rept. 26: 92-95.

(.765) CORDY, C. B., and MILBRATH, J. A.

1951. ALBINO. In Virus Diseases and Other Disorders with Virusliice Symptoms of Stone Fruits in North America. U.S. Dept. Agr. Agr. Handb.

10, pp. 103-105.

(766) and EvANS, A. W.

1941. VEIN CLEARING, A TRANSMISSIBLE DISEASE OF PRUNUS. Phytopathology 31: 463-467.

(767) KIENHOLZ, J. R., and MILBRATH, J. A.

1951. BLACK CANKER. In Virus Diseases and Other Disorders with Viruslike

Symptoms of Stone Fruits in North America. U.S. Dept. Agr. Agr.

Handb. 10, pp. 137-138.

(768) and MILBRATH, J. A.

1942. BANDED CHLOROSIS, A TRANSMISSIBLE DISEASE OF CHERRY. Phytopathology 32: 634-635.

(769) and MILBRATH, J. A.

1945. TRANSMISSION OF PEACH WART TO SWEET CHERRY. Phytopathology

35: 607-609.

(770) and MILBRATH, J. A.

1947. MILD RUSTY MOTTLE OF SWEET CHERRY ( PRUNUS AVIUM). Phytopathology 37: 77-84.

(771) and MILBRATH, J. A.

1948. WESTERN X-DISEASE OF MONTMORENCY CHERRY AND ITS RELATION TO

BUCKSKIN OF SWEET CHERRY. (Abstr.) Phytopathology 38: 920.
404 VIRUS DISEASES OF STONE FRUIT

(772) and MILBRATH, J. A.

1951. MILD RUSTY MOTTLE. In Virus Diseases and Other Disorders with

Viruslike Symptoms of Stone Fruits in North America. U.S. Dept.

Agr. Agr. Handb. 10, pp. 116-119.

(773) MILBRATH, J. A., and CORDY, C. B.

1944. ALBINO CHERRY, A VIRUS DISEASE IN SOUTHERN OREGON. (Abstr.)

Phytopathology 34: 937.

(774) MILBRATH, J. A., and KIENHOLZ, J. R.

1947. BLACK CANKER OF CHERRY. (Abstr.) Phytopathology 37: 366.

(775) ZIMMERMAN, P. W., and HITCHCOCK, A. E.

1956. SUSCEPTIBILITY OF PLANTS TO HYDROFLUORIC ACID AND SULFUR

DIOXIDE GASES. Boyce Thompson Inst. Contrib. 18: 263-279.
APPENDIX

COMMON AND SCIENTIFIC NAMES OF

PLANTS MENTIONED IN THE TEXT^

ALMOND

ALMOND, DESERT

ALMOND, FEN2X

ALMOND, FLOWERING

ALMOND, DWARF FLOWERING

ALMOND, RUSSIAN

ALMOND, TANGUT

APPLE

APRICOT

APRICOT, ANSU

APRICOT, DESERT

APRICOT, JAPANESE

BALSAMAPPLE

BEAN, COMMON

BEAN, PINTO

BLACKBERRY, HIMALAYA

BRISTLY OXTONGUE

BUSHCHERRY, CHINESE (KOREAN)

CARROT

CASTOR BEAN

CATJANG

CELERY

CHEESEWEED

CHERRY, ALMOND

CHERRY, AMUR

CHERRY, BITTER

CHERRY, BITTER (VAR. MOLLIS)

CHERRY, BLACK

CHERRY, CAPOLLIN

CHERRY CATALINE

CHERRY, CHINESE FLOWERING

CHERRY, DESFONTAINES

CHERRY, DUKE

CHERRY, GROUND

CHERRY, HOLLYLEAF

Prunus dulcís (Mill.) D. A. Webb

P. fasciculata (Torr.) Gray

P. fenzliana Fritsch

P. triloba Lindl.

P. glandulosa Thunb.

P. tenella Batsch

P tangutica (Batal.) Koehne

Malus sylvestfis Mill.

Prunus armeniaca L.

P. armeniaca var. ansu Maxim.

P. ftemontii S. Wats.

P. mume Sieb. + Zuce.

Momordica balsamina L.

Phaseolus vulgaris L.

P. vulgaris L.

Rubus procerus P. J. Muell.

Picris echioides L.

Prunus japónica Thunb.

Daucus carota L.

Ricinus communis L.

Vigna unguculata supp cylindrica (L.)

Van Esetline

Apium graveolens var. dulce (Mill.) Pers.

Malva parviflora L.

Prunus glandulosa Thunb.

P. maackii Rupr.

P. emarginata (Hook.) Walp.

P. emarginata var. mollis (Doug, ex Hook.)

Brew. & Wats.

P. serótina Ehrh.

P. serótina var. salicifolia ( HBK ) Koehne

(syn. P. capuli Cav.)

P. lyonii Sarg.

P. pseudocerasus Lindl.

P. xfontanesiana (Spach) Schneid.

{P. avium L. x P. mahaleb L.)

P. avium L. x P. cerasus L.

P. fruticosa Pall.

P. ilicifolia (Nutt.) Walp.

-^Names checked by the Plant Taxonomy Laboratory, Agricultural Research Service, U.S.

Department of Agriculture.

405
406 VIRUS DISEASES OF STONE FRUIT

CHERRY, JAPANESE FLOWERING

FUJI CHERRY

SIEBOLD CHERRY

TAKANE CHERRY

CHERRY, MAHALEB

CHERRY, MANCHU

CHERRY, MAZZARD

CHERRY, ORIENTAL FLOWERING

HIGAN CHERRY

SARGENT CHERRY

YOSHINA CHERRY

CHERRY, PIN

CHERRY, SAND

CHERRY, SAND, PURPLE LEAF

CHERRY, SOUR

CHERRY, SOUR, DOUBLE

FLOWERING

CHERRY, SWEET

CHERRY, WESTERN SAND (BESSEY)

CHOKECHERRY, AMUR

CHOKECHERRY, EASTERN

CHOKECHERRY, GREAT PLAINS

CHOKECHERRY, WESTERN

COWPEA

CRAB APPLE, BIGFOOT

CUCUMBER

CURRANT, COMMON RED

DODDER

DOLICHOS

FULLER'S TEASEL

GLOBE AMARANTH

GOOSEFOOT

GRAPE

GROUNDCHERRY

GUAR

HEDGENETTLE

HOP

JIMSON-WEED

KERRIA, JAPANESE

LAURELCHERRY, COMMON

LAURELCHERRY, ZABEL

LAURELCHERRY, PORTUGUESE

MAPLE, RED

MILKWEED, COMMON

MOUNTAIN ASH

NECTARINE

PARSLEY

P. incisa Thunb.

P. sieboldii (Carr.) Wittm.

P. nipponica M^tsum.

P. ssiori F. Schmidt

P. mahaleb L.

P. tomentosa Thunb.

P. avium L.

P. serrulata Lindl.

P. serrulata var. lannesiana (Carr.) Rehd.

P. subhirtella Miq.

P. sargenta Rehd.

P. yedoensis Matsum.

P. pensylvanica L.

P. pumila L.

P. cistena N. E. Hanson

P. cerasus L.

P. cerasus f. rhexi (Kirchn.) Voss.

P. avium L.

P. besseyi Bailey

P. maackii Rupr.

P. virginiana L.

P. virginiana var. melanocarpa{K. Neis.)

Sarg.

P. virginiana var. demissa (Nutt. ex

Torr. & Gray) Torr.

Vigna unguiculata (L.) Walp.

Malus platycarpa Rehd.

Cucumis sativus L.

Ribes sativum Syme

Cuscuta campestris Yunck.

C. subinclusa Dur. & Hilg.

Dolichos biflorus L.

Dipsacus fullonum L.

Gomphrena globosa L.

Chenopodium amar anticolor Coste & Reyn.

Vitis spp.

Physalis floridana L.

Cyamopsis tetragonoloba (L.) Taub.

Stachys bullata Benth.

Homulus americanus Nutt.

Datura stramonium L.

Kerria japónica (L.) DC.

Prunus laurocerasus L.

Prunus laurocerasus f. zabeliana Spaeth

P. lusitanica L.

Acer rubrum L.

Asclepias syriaca L.

Sorbus spp. L.

Prunus pérsica var. nectarina (Ait.) Maxim.

Petroselinum crispum (Mill.) Nym.
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 407

PEACH

PEACH, DAVID

PEACH, DESERT

PEACH, FLAT

PEACH, KANSU

PEACH, PURPLELEAF

PEACH, SMOOTHPIT

PEAR

PERIWINKLE

PETUNIA

PLANTAIN

PLUM, AMERICAN

PLUM, APRICOT

PLUM, BOKAR

PLUM, BEACH

PLUM, CHICKASAW

PLUM, DAMSON (BULLACE)

PLUM, EUROPEAN (PRUNE)

PLUM, FLATWOODS

PLUM, HOG

PLUM, HORTULAN

PLUM, HYBRIDS

PLUM, JAPANESE

PLUM, KLAMATH

PLUM, MARIANNA

PLUM, MEXICAN

PLUM, MYROBALAN

PLUM, PURPLELEAF

PLUM, SLOE

PLUM, WILDGOOSE

PORTUGAL LAUREL

QUINCE

QUINOA

RASPBERRY, RED

SEASIDE DAISY

SERVICEBERRY

SESBANIA

SNAPDRAGON

SQUASH

CULTIVATED STRAWBERRY

STRAWBERRY, SAND

SWEET BASIL

TITHONIA

TOBACCO

TOMATO

ZINNIA

Prunus pérsica (L.) Batsch

P. davidiana (Carr.) Franch.

P. andersonii Gray

P. pérsica f. compressa ( Loud. ) Rehder

P. kansuensis Rehd.

P. pérsica f. atropurpúrea Schneid.

P. mira Koehne.

Pyrus communis L.

Vinca rosea L.

Petunia hyhrida Vilm.

Plantago spp.

Prunus americana Marsh.

P. simoni Carr.

/*, bokhariensis Royle ex Schneid.

P. maritima Marsh.

P. angustifolia Marsh.

P. insititia L.

P. domestica L.

P. umbellata Ell.

P. umbellata V2LÏ. injucunda (Small.) Sarg.

P. reverchonii Sarg.

P. hortulana Bailey

P. besseyi Bailey x P. salicina Lindl.

P. salicina Lindl. x P. simonii Carr.

P. salicina Lindl.

P. subcordata Benth.

P. cerasifera Ehrh. x P. munsoniana

Wight & Hedr.

P. mexicana S. Wats.

P. cerasifera Ehrh.

P. cerasifera cu. Atropurpúrea syn. P. pissardi

Carr.

P. spinosa L.

P. munsoniana Wight & Hedr.

P. lusitanica L.

Cydonia oblonga Mill.

Chenopodium quinoa Willd.

Rubus idaeus L.

Erigeron glaucus Ker

Amelanchior spp. Med.

Sesbania exaltata (Raf.) Cory

Antirrhinum majus L.

Cucúrbita maxima Duchesne, + 3 other spp.

called squash

Pragaria x ananassa Duch.

F. chiloensis (L.) Duchesne

Ocimum basilicum L.

Titbonia speciosa (Hook.) Grisef.

Nicotiana tabacum L.

N. glutinosa L.

N. rustica L.

N. megalosiphon Heurck & Muell.-Arg.

Lycopersicon esculentum Mill.

7Annia elegans Jacq.
CONTRIBUTORS

Aichele, M. D. Washington Department of Agriculture, Prosser, Wash. 99350

Allen, W. R. Research Branch, Canada Department of Agriculture, Vineland

Station, Ontario

Anthon, E. W. Department of Entomology, Washington State University,

Wenatchee, Wash. 98801

Ballinger, W. E. Department of Horticultural Science, North Carolina State

University, Raleigh, N.C. 27607

Benson, N. R. Department of Horticulture, Washington State University,

Wenatchee, Wash. 98801

Blodgett, E. C. Formerly Washington Department of Agriculture, Prosser,

Wash. 99350

Cameron, H. R. Department of Botany and Plant Pathology, Oregon State

University, Corvallis, Oreg. 97331

Carlson, R. M. Department of Pomology, University of California, Davis,

Calif. 95616

Chandler, W. H. Formerly Department of Horticulture, University of California, Los Angeles, Calif. 90024

Cheney, P. W., Agricultural Research Service, U.S. Department of Agriculture,

Wenatchee, Wash. 98801

Childers, N. F. Department of Horticulture and Forestry, Rutgers — The State

University, New Brunswick, N.J. 08903

Cochran, L. C. Department of Botany and Plant Pathology, Oregon State

University, Corvallis, Oreg. 97331

Compton, O. C. Department of Horticulture, Oregon State University, Corvallis,

Oreg. 97331

Davidson, O. W. Formerly Department of Horticulture and Forestry, Rutgers—

The State University, New Brunswick, N.J. 08903

Davidson, T. R. Research Branch, Canada Department of Agriculture, Vineland

Station, Ontario

Fogle, H. W. Agricultural Research Service, U.S. Department of Agriculture,

Beltsville, Md. 20705

Fridlund, P. R. Department of Plant Pathology, Washington State University,

Prosser, Wash. 99350

Fulton, R. W. Department of Plant Pathology, University of Wisconsin,

Madison, Wis. 53706

Gilmer, R. M. Department of Plant Pathology, Cornell University, Geneva,

N.Y. 14456

Hansen, A. J. Research Branch, Canada Department of Agriculture, Summerland, British Columbia

408
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 409

Hansen, C. J. Department of Pomology, University of California, Davis,

Calif. 95616

Heggestad, H. E. Agricultural Research Service, U.S. Department of Agriculture, Beltsville, Md. 20705

Helton, A. W. Department of Plant Science, University of Idaho, Moscow,

Idaho 83843

Hutchins, L. M. Agricultural Research Service, U.S. Department of Agriculture,

Beltsville, Md. 20705

Johnson, F. Department of Plant Pathology, Washington State University,

Puyallup, Wash. 98371

Kahn, R. P. Agriculture Quarantine Inspection Program, APHIS, U.S. Department of Agriculture, Glenn Dale, Md. 20769

KenKnight, G. E. Agricultural Research Service, U.S. Department of Agriculture, Shreveport, La. 71105

Kester, D. E. Department of Pomology, University of California, Davis.

Calif. 95616

Kirkpatrick, H. W. Agricultural Research Service, U.S. Department of Agriculture, Byron, Ga. 31008

Klos, E. J. Department of Botany and Plant Pathology, Michigan State University, East Lansing, Mich. 48823

Kochan, W. J. Department of Plant Science, University of Idaho, Parma, Idaho

83660

Lilleland, O. Formerly Department of Pomology, University of California.

Davis, Cahf. 95616

Mircetich, S. M. Agricultural Research Service, U.S. Department of Agriculture,

Davis, Calif. 95616

Moore, J. D. Department of Plant Pathology, University of Wisconsin.

Madison, Wis. 53706

Nichols, C W. Bureau of Plant Pathology, California Department of Agriculture, Sacramento, Calif. 95814

Nyland, G. Department of Plant Pathology, University of California, Davis,

Cahf. 95616

Parish, C. L. Agricultural Research Service, U.S. Department of Agriculture,

Wenatchee, Wash. 98801

Parker, K. G. Formerly Department of Plant Pathology, Cornell University,

Ithaca, N.Y. 14850

Pine, T. S. Agricultural Research Service, U.S. Department of Agriculture,

Davis, Cahf. 95616*

Proebsting, E. L. Formerly Department of Pomology, University of California.

Davis, Cahf. 95616

Proebsting, E. L. Jr. Department of Horticulture, Washington State University,

Prosser, Wash. 99350

* Deceased.
410 VIRUS DISEASES OF STONE FRUIT

Schlocker, A. Bureau of Plant Pathology, California Department of Agriculture,

Sacramento, Calif. 95814

Smith, R. L. Department of Soils and Meteorology, Utah State University,

Logan, Utah 84321

Traylor, J. A. Bureau of Plant Pathology, California Department of Agriculture,

Sacramento, Calif. 95814

Tremaine, J. H. Research Branch, Canada Department of Agriculture, Vancouver, British Columbia

Uriu, K. Department of Pomology, University of California, Davis, Calif.

95616

Wadley, B. N. Agricultural Research Service, U.S. Department of Agriculture,

Logan, Utah 84321

Wagnon, H. K. Bureau of Plant Pathology, California Department of Agriculture, Sacramento, Calif. 95814

Walker, D. R. Department of Plant Science, Utah State University, Logan,

Utah 84321

Weigle, C. G. Bureau of Plant Pathology, California Department of Agriculture, Sacramento, Calif. 95814

Welker, W. V. Jr. Agricultural Research Service, U.S. Department of Agriculture, New Brunswick, N.J. 08903

Welsh, M. F. Research Branch, Canada Department of Agriculture, Summerland, British Columbia

Williams, H. E. Bureau of Plant Pathology, California Department of Agriculture, Sacramento, Calif. 95814

Wilson, N. S. Agricultural Research Service, U.S. Department of Agriculture,

Riverside, Cahf. 92502

Woodbridge, C. G. Department of Horticulture, Washington State University,

Pullman, Wash. 99163
REFERENCES TO RELEVANT LITERATURE

PUBLISHED AFTER CLOSING DATE

FOR RECEIPT OF MANUSCRIPTS

ANONYMOUS.

1968. PEACH ROSETTE IN THE M.I.A. Agr. Gaz. N.S.W. 79: 606.

1969. ANNUAL REPORT, EAST MALLING RESEARCH STATION. 199 pp.

1970. RAPPORT D'ACTIVITE, CENTRE DE RECHERCHES AGRONOMIQUES DE L'ETAT.

Gembloux. 1970.

1971. BIOLOGICAL AND CHEMICAL RESEARCH INSTITUTE, RYDALMERE. Biology

Branch-Plant Pathology Section. Kept. Dept. Agr. N.S.W. 1969-1970: 158-

168.

ACKERMANN, P.

1968. KROUZKOVITOST—NOVA VIROZA MERUNKY. (RINGSPOT, A NEW VIRUS

DISEASE OF APRICOT.) Zahr. Listy 61(7) : 202. (Abs. in Referat. Zh. Rasten,

1968(12), 1032, 1968.)

AGRIOS, G. N.

1961. FACTORS CONDUCIVE TO POOR STOCK-SCION UNION AND VIRUS-LIKE SYMPTOM DEVELOPMENT IN DWARF PEACH. Dis. Abstr. 21: 2848-2849.

ALDWINKLE, H. S., and ARNESON, P. A.

1972. STEM PITTING OF PEACH IN NEW YORK. Plant Dis. Reptr. $6: 616-617.

ALLEN, W. R.

1963. COMPARISON OF STRAINS OF PRUNUS NECROTIC RINGSPOT AND PRUNE

DWARF VIRUSES WITH VIRUSES OF THE PFEFFINGER (RASP LEAF) TYPE.

Phytopathology 53: 1436-1442.

DiAS, H. F., and DAVIDSON, T. R.

1969. VIRUS DISEASE PROBLEMS IN ONTARIO FRUIT ORCHARDS AND VINEYARDS.

Canada Agr. 14: 18-20.

and TREMAINE, J. H.

1965. CHARACTERISTICS OF ANTIGENS AND ANTIBODIES ASSOCIATED WITH THE

PRUNUS NECROTIC RINGSPOT VIRUS IMMUNE SYSTEM. Virology 25: 122-

132.

ATKINSON, J. D.

1971. DISEASES OF TREE FRUITS IN NEW ZEALAND. Diseases of Fruit Trees in

New Zealand. Wellington, New Zealand, A. R. Shearer, Govt. Printer.

AZAD, R. N.

I960. 'LINE PATTERN' DISEASE OF PLUM ( PRUNUS DOMESTICA L.). Indian

Jour. Agr. Sei. 29: 61-62.

BARNETT, O. W. JR.

1968. A DIFFERENTIAL RESPONSE OF CERTAIN LABILE VIRUSES TO STABILIZING

AGENTS. 101 pp. Thesis, Univ. Wis.

and FULTON, R. W.

1969. SOME CHEMICAL PROPERTIES OF PRUNUS NECROTIC RINGSPOT AND TULARE

APPLE MOSAIC VIRUSES. Virology 39: 556-561.

411
412 VIRUS DISEASES OF STONE FRUIT

BARRAT, J. G., MIRCETICH, S. M., and FOGLE, H. W.

1968. STEM PITTING OF PEACH. Plant Dis. Reptr. 52: 91-94

BASAK, W., and MiLLIKAN, D. F.

1968. RINGSPOT DISEASE OF PRUNUS EFFUSA 'KRASSA SEVERA'. THIS RESEMBLES

PRUNUS NECROTIC RINGSPOT AND APPLE CHLOROTIC RINGSPOT VIRUSES

IN SOME OF ITS PROPERTIES BUT IT MAY BE A NEW VIRUS. Seventh European Symposium of fruit tree virus diseases, Aschersleben 10-16, July, 1967.—

TagBer, dt. Akad. LandwWiss. Berl. 97, 1968. (221-225).

1969. VIRUS DISEASES OF FRUIT PLANTS. (93-96). Biul. Inst. Ochr. RosL, Poznan,

44: 454. Engl., Russ. Summary 48: 2114.

BAUMANN, GISELA

1968. STONE FRUIT VIRUSES IN THE ORNAMENTAL SHRUBS OF THE GENUS PRUNUS.

Seventh European Symposium of fruit tree virus diseases, Aschersleben 10-16

July, 1967. TagBer. dk. Akad. LandwWiss. Berl. 97, 1968. (211-220).

BERCKS, R., and KUNZE, L.

1969. ÜBER DEN NACHWEIS DES TABAKMOSAIKVIRUS IN SUSSKIRSCHEN. (ON THE

IDENTIFICATION OF TOBACCO MOSAIC VIRUS IN SWEET CHERRIES.) NachrBl.

dt. PflSchutzdienst., Stuttg. 21: 66-67.

and MiSCHKE, W.

1963. UNTERSUCHUNGEN ÜBER DIE GEWINNUNG VON PARTIELL GEREINIGTEM

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BERNHARD, R., MARENAUD, C, and SUTIC, D.

1969. LE PECHER GF 305 INDICATEUR POLYVALENT DES VIRUS DES ESPECES A

NOYAU. Ann. PhytOpath. 1: 603-617.

BLATTNY, C, and ZiMANDL.

1968. CZECHOSLOVAKIAN MOUNTAIN ISOLATION FOR VIRUS-FREE FRUIT TREES.

Seventh European Symposium of fruit tree virus diseases, Aschersleben 10-16

July, 1967. TagBer. dt. Akad. LandwWiss. Berl. 97: 333-337.

1969. VLIV VIROVYCH CHOROB NA JAKOST PLODU OVOCYNCH STROMU. II. PECKOVB

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2. STONE FRUIT.) Ziva 18: 15-17.

BLODGETT, E. C, ISMEN, F. H., GOMEC, B., ALAY, K., ALTINYAY, N., and WAGNON, H. K.

1970. AMASYA CHERRY DISEASE IN TURKEY. PI. Prot. Bull. F.A.O. 18:49-52.

and AlCHELE, M. D.

1971. THE EATON-BUG DISEASE OF SWEET CHERRY. Plant Dis. Reptr. 55:344-346.

BOCK, K. R.

1967. STRAINS OF PRUNUS NECROTIC RINGSPOT VIRUS IN HOP (HUMULUß

LUPULUS L.). Ann. Appl. Biol. 59: 437-446.

BOLWYN, B.

1968. RELATION OF BORON TO CHERRY ROSETTE DISEASE IN OREGON, AND THB

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Bos, L.

1969. ANNUAL REPORT FOR 1968, INSTITUTE FOR PHYTOPATHOLOGICAL RBSEARCH, WAGENINGEN. 169 pp. Engl. Summary 48: 3249.

1968. ANNUAL REPORT FOR 1967, INSTITUTE FOR PHYTOPATHOLOGICAL RBSEARCH, WAGENINGEN. 189 pp. Engl. Summary 47: 1.
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BOZARTH, R. F.

1971. COMPARATIVE PROPERTIES OF NECROTIC RINGSPOT VIRUS FROM CHERRY

AND PEACH. Phytopathology 61: 532-537.

CAMERON, H. R.

1969. STEM PITTING OF ITALIAN PRUNE. Plant Dis. Reptr. 53: 4-6.

CASPER, R., and KUNZE, L.

1972. SEROLOGISCHER REIHENTEST AUF BEFALL MIT PRUNUS NECROTIC RINGSPOT

VIRUS ZUM NACHWEIS DER STECKLENBERGER KRANKHEIT. Nachrichtenblatt

Deutsch. Pflanzenschutz. Stuttgart 24: 2-24.

1972. SEROLOGISCHER REIHENTEST AUF BEFALLMIT PRUNUS NECROTIC RINGSPOT

VIRUS ZUM NACHWEIS DER STECKLENBERGER KRAKHEIT. Nachr Bl. Deutsch.

Pflanzenschutz Braunschweig 24: 20-24.

CASTELAIN, C. and MORVAN, G.

1970. UTILISATION DU PRUNUS SPINOSA L. POUR LA DETECTION DU VIRUS DES

TACHES FOLIAIRES CHLOROTIQUES DANS LES ARBRES FRUITIERS A NOYAUX.

(THE USE OF P. SPINOSA FOR DETECTING APPLE CHLOROTIC LEAFSPOT

VIRUS IN STONE FRUIT TREES.) Ann. Phytopath. 2: 349-363.

CHAMBERLAIN, E. E.

1971. OUTWITTING THE VIRUS. Jour. R.N.Z. Inst. Hort. N.S. 2: 115-126.

CHAMBERLAIN, E. E., ATKINSON, J. D., WOOD, G. A. and HUNTER, J. A.

1971. OCCURRENCE OF CHERRY GREEN RING MOTTLE VIRUS IN NEW ZEALAND.

N.Z. Jour. Agr. Res. 14: 499-508.

CHENEY, P. W., and PARISH, C. L.

1969. A GRAFT-TRANSMISSIBLE ANOMALY OF CHERRY. Phytopathology 59: 10.

AiCHELE, M. F., PARISH, C. L. and BLODGETT, E. C.

1967. THE SPUR CHERRY VIRUS. Phytopathology 57: 1004.

AiCHELE, M. D., PARISH, C. L., and BLODGETT, E. C.

1969. HOST RANGE OF THE SPUR CHERRY VIRUS. Plant Dis. Reptr. 53:984-988.

PARISH, C. L., and COYIER, D. L.

1970. HOST RANGE STUDIES OF THE CHERRY SHORT STEM VIRUS FROM OREGON.

Plant Dis. Reptr. 54: 651-655.

CIVEROLO, E. L., and MiRCETICH, S. M.

1972. A PEACH ISOLATE OF PRUNUS NECROTIC RINGSPOT VIRUS. Phytopathology

62: 529-532.

CROPLEY, R.

1968. FRUIT TREE VIRUSES IN BRITAIN—OUR KNOWLEDGE AND IGNORANCE.

Sei. Hort. 20: 95-100.

1968. THE IDENTIFICATION OF PLUM POX (SHARKA) VIRUS IN ENGLAND. Plant

Path. 17: 66-70.

1971. PLUM POX (SHARKA DISEASE). Rep. E. Mailing Res. Sta. 1970: 153-158.

DAVIDSON, T. R., and RUNDANS, V.

1972. DETECTION OF NECROTIC RINGSPOT AND PRUNE DWARF VIRUSES BY

INDEXING DORMANT CHERRY BUDS ON HERBACEOUS PLANTS. Canad.

Jour. Plant Sei. 52: 915-920.

1972. INCIDENCE OF NECROTIC RINGSPOT AND PRUNE DWARF VIRUSES IN WILD

PRUNUS SPECIES. Canad. Jour. Plant Sei. 52: 907-913.
414 VIRUS DISEASES OF STONE FRUIT

DEMSKI, J. W., and BOYLE, J. S.

1968. ABSENCE OF NECROTIC RINGSPOT VIRUS OF SOUR CHERRY IN WEED HOSTS.

Phytopathology 58: 125-126.

1969. SEROLOGICAL RELATIONSHIPS OF SOME VIRUS ISOLATES FROM SOUR CHERRY

USING ANTISERA FROM MICE AND RABBITS. Phytopathology 59: 996-998.

1968. SPREAD OF NECROTIC RINGSPOT VIRUS IN A SOUR CHERRY ORCHARD. Plant

Dis. Reptr. 52: 972-974.

DiAS, H. F.

1972. A SAP-TRANSMISSIBLE VIRUS ASSOCIATED WITH DISEASES OF PEACH AND

GRAPE. Proc. Canad. Phytopathol. Soc. 39: 29.

DocEA, E., FRATILA, ELISABETA, MOTIU, ANA, and IGNAT, VOICA.

1970. OBSERVATII ASURPA ATACULUI PRODUS DE PRUNUS VIRUS 7 CHRISTOFF

(ANNULUS PRUNI CHRISTOFF) LA UNELE SOIURI DE PRUN. Lucr. Stunt.

Inst. Agron. "Nicolae Balcescu" Ser. B. 13: 191-200.

DOWLER, W. M., JONES, R. K., and FERREE, R. J.

1968. STEM PITTING OF PEACH IN SOUTH CAROLINA. Plant Dis. Reptr. 52: 907.

DUNEZ, J., MARENAUD, C, DELBOS, R., and LANSAC, MiCHELINE.

1972. VARIABILITY OF SYMPTOMS INDUCED BY THE APPLE CHLOROTIC LEAF SPOT

(CLSV)—A TYPE OF CLSV PROBABLY RESPONSIBLE FOR BARK SPLIT DISEASE

OF PRUNE TREES. Plant Dis. Reptr. 56: 293-295.

FESTIG, H.

1969. ISPOLJAVANJE SIMPTOMA VIRUSA SARKE NA SIJANCIMA NEKIH VOCAKA

INFICIRANIH INOKULUMIMA RAZLICITOG PORIJEKLA. Zag. Eilja 20' 215-

221.

FOGLE, H. W., MIRCETICH, S. M., and CiVEROLO, E. L.

1968. STEM PITTING IN PRUNUS, A NEW DISORDER IN THE EAST. Phytopathology

58: 884.

FRAZIER, N. W., and JENSEN, D. D.

1970. STRAWBERRY, AN EXPERIMENTAL HOST OF PEACH WESTERN X DISEASE.

Phytopathology 60: 1527-1528.

FRIDLUND, P. R.

1968. EFFECTS OF HIGH TEMPERATURE ON GRAFT TRANSMISSION OF THE PRUNUS

RINGSPOT VIRUS. Phytopathology 58: 1192-1193.

1968. IR-2, A GERM PLASM BANK OF VIRUS-FREE FRUIT TREE CLONES. HortScience

3: 227-229.

and BOTTORFF, F. O.

1968. VIRUS GUMMOSIS OF APRICOT CAUSED BY SOME PRUNE DWARF VIRUS

STRAINS. Phytopathology 58: 119-120.

1970. SYSTEMIC INVASION OF PRUNUS BUDSTICK BY THE GREEN RING MOTTLE

VIRUS. Plant Dis. Reptr. 54: 917-920.

1970. TOP-KILLING OF KWANZAN FLOWERING CHERRY AFTER INOCULATIONS WITH

TWELVE PRUNUS VIRUSES. Plant Dis. Reptr. 54: 1073-1074.

1970. TEMPERATURE EFFECTS ON VIRUS DISEASE SYMPTOMS IN SOME PRUNUS,

MALUS AND PYRUS CULTIVATORS. Bull. Wash. Agr. Expt. Sta. 726.
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 415

1971. FAILURE OF HOT-WATER TREATMENT TO ELIMINATE PRUNUS VIRUSES.

Plant Dis. Reptr. 55: 738-740.

FRITZSCHE, R., and KEGLER, H.

1968. NEMATODEN ALS VEKTOREN VON VIRUSKRANKHEITEN DER OBSTGEWACHSE.

Deutsche Acad. Landwirtsch. Wiss. Berlin 97: 289-295.

FRY, P. R., and WOOD, G. A.

1969. PEACH ROSETTE, A VIRUS IN N.Z. STONE FRUIT. Orchard N.Z. 42: 397-400.

1970. LITTLE CHERRY VIRUS IN NEW ZEALAND. N.Z. Jour. Agr. Res. 13: IH118.

1971. PRUNUS NECROTIC RINGSPOT AND PRUNE DWARF VIRUSES IN NEW ZEALAND.

N.Z. Jour. Agr. Res. 14: 515-525.

FULTON, R. W.

1968. SEROLOGY OF SOME VIRUSES ISOLATED FROM CHERRY, PLUM, APPLE, AND

ROSE. Seventh European Symposium of fruit tree virus diseases. Aschersleben

10-16 July, 1967—TagBer. dt. Akad. LandwWiss. Berl. 97: 273-276.

GAVALAS, N. A.

1970. SYMPTOMS OF STEM PITTING ON PEACH TREES IN GREECE. Plant Dis. Reptr.

54: 73-75.

GRANETT, A. L., and GiLMER, R. M.

1971. MYCOPLASMAS ASSOCIATED WITH X-DISEASE IN VARIOUS PRUNUS SPECIES.

Phytopathology 61: 103(>-1037.

GYORGY, BEATRIX, and NEMETH, MARIA

1968. SEROLOGICAL DIAGNOSIS OF THE PLUM POX VIRUS ON APRICOTS. AN ANTISERUM PREPARED BY THE SEPHADEX PURIFICATION METHOD FROM PEACH

FRUIT AND LEAVES PROVED SUITABLE FOR INDEXING APRICOT TREES.

Seventh European Symposium of fruit tree virus diseases, Aschersleben 10-16

July, 1967—TagBer, dt. Akad. LandwWiss. Berl. 97, 1968. (269-271)

HANSEN, A. J.

1972. HOST RANGE AND IDENTITY OF CHERRY RASPLEAF VIRUS IN BRITISH

COLUMBIA. Phytopathology (Abstr.) 62: 763.

HELTON, A. W., and HUBERT, J. J.

1968. INDUCING SYSTEMIC RESISTANCE TO CYTOSPORA INVASION IN PRUNUS

DOMESTICA WITH LOCALIZED PRUNUS RINGSPOT VIRUS INFECTIONS. Phytopathology 58: 1423-1424.

HtRTEA, GH., and MlNOIU, N.

1967. INFLUENTA VIRUSULUI VARSATULUI PRUNELOR ASUPRA ACTIVITII UNOR

ENZIME SI A RESPIRATIEI LA PRUN. Ann. Inst. Cercet. Prot. Plant 5: 139-

149.

HUANG, JENIFER and NYLAND, G.

1970. THE MORPHOLOGY OF A MYCOPLASMA ASSOCIATED WITH PEACH X-DISEASB.

(Abstr.) Phytopathology 60: 1534.

INOUE, H., and BUKOVAC, M. J.

1971. PEACH FRUIT DEFORMATION INDUCED WITH 2-M CHLOROPHENOXY PROPIONAMIDE. Jour. Amer. Soc. Hort. Sei. 96: 728-730.

JENSEN, D. D.

1968. INFLUENCE OF HIGH TEMPERATURES ON THE PATHOGENICITY AND SURVIVAL OF WESTERN X-DISEASE VIRUS IN LEAF-HOPPERS. Virology 36: 662-

667.
416 VIRUS DISEASES OF STONE FRUIT

JONES, B. M., and JANSON, B. F.

1969. NEW PEACH DISEASE IN OHIO ORCHARDS. Ohio Report Jan.-Feb. 1969:

11-13.

JONES, L. S., WILSON, N. S., BURR, W., and BARNES, M. M.

1970. RESTRICTION OF PEACH MOSAIC VIRUS SPREAD THROUGH THE CONTROL OF

THE VECTOR MITE ERIOPHYES INSIDIOSUS. Jour. Econ. Ent. 63: 1551-1552.

JORDOVIC, M.

1968. UDEO SADNICA U SIRENJU SARKE KLJIVE. Zast. Bilja 19: 273-277.

1968. REAKCIJA PLODOVA PRUNUS TOMENTOSA NA VIRUS SARKE SLJIVE. Zast.

Bilja 19: 59-61.

1969. SISTEMICNO KRETANJE VIRUSA SARKE U STABLU POZEGACE. Zast. Bilja

20: 123-130.

FESTIC, H., and RANKOVIC, M.

1969. ISPITIVANJA PRUNUS SPINOSA L. KAO DOMACINA VIRUSA SARKE (PRETHODNO SAOPSTENJE). Zast. Bilja 20: 253-259.

KABLE, P. F., and PARKER, K. G.

1968. CHERRY VIRUSES TRANSMITTED TO MILKWEED FROM INFECTED PEACH AND

KWANZAN CHERRY. Phytopathology 58: 1443-1444.

KEGLER, H., PROLL, E., SCHMIDT, H. B., and OPEL, H.

1969. NACHWEIS DES TABAKNEKROSEVIRUS (TOBACCO NECROSIS VIRUS) IN OBSTGEHOLZEN. Phytopath. Z. 65: 21-42.

KEGLER, H., SCHMIDT, H. E., and SCHIMANSKI, H. H.

1968. DER NACHWEIS WEITERER VIRUSKRANKHEITEN AN OBSTGEHOLZEN IN DER

DEUTSCHEN DEMOKRATISCHEN REPUBLIK. NachrBl. dt. PflSchutzdienst,

Berl., N.F. 22: 168-175.

KiRKPATRiCK, H. C, LINDNER, R. C, and CHENEY, P. W.

1968. SYMPTOMLESS INFECTION OF STONE FRUITS WITH A MECHANICALLY TRANSMISSIBLE VIRUS FROM ROSE. PI. Dis. Reptr. 52: 499-502.

KiSHi, K., TAKANASHI, K., and ABIKO, K.

1968. STUDIES ON VIRUS DISEASES OF STONE FRUITS. I. PEACH NECROTIC RINGSPOT AND PRUNE DWARF VIRUS IN JAPAN. Ann. Phytopath. Soc. Japan 34:

143-150.

TAKANASHI, K., and ABIKO, K.

1969. STUDIES ON VIRUS DISEASES OF STONE FRUITS: II. DISTOIBUTION OF PEACH

NECROTIC RINGSPOT VIRUS AND PRUNE DWARF VIRUS. Bull. Hort. Res.

Stn. Hiratsuka, Ser. A 8: 141-154.

KLEINHEMPEL, H.

1968. ZUR ANALYSE VON VIREN IN JOHANNIS- UND STACHELBEERBESTANDEN DER

DEUTSCHEN DEMOKRATISCHEN REPUBLIK. Arch. Gartenb. 16: 151-159.

KRISTENSEN, H. R.

1968. BLOMME-POX- EN ONDARTED VIRUSSYGDOM. Erhversvfrugtavleren 1968:

141-150.

1968. VIRUSSYGDOMME HOS FRUGTTRAEER. Gartnertidende 84: 295-302.

KRISTENSEN, H. R.

1970. A BIBLIOGRAPHY OF PAPERS ON VIRUS DISEASES OF DECIDUOUS FRUIT TREES

1967-1970. 49 pp.
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 417

KUNZE, L.

1969. DER EINFLUSS DER STECKLENBERGêR KRANKHEIT AUF DEN ERTRAG VON

SAUERKIRSCHEN. Sonderdruck Erwerbobstbau 11: 3.

and KRCZAL, H.

1968. VERSUCHE ZUR ÜBERTRAGUNG DES SCHARKAVIRUS DURCH DIE PFIRSICHBLATTLAUS MYZUS PERSICAE SULZ. NachrB. dt. PflSchutzdienst., Stuttg.,

20: 97-98.

LEWIS, F. H., STOUFFER, R. F., and HEWETSON, F. N.

1968. A SERIOUS NEW DISORDER OF PEACH TREES. Plant Dis. Reptr. 52: 292-294.

LuKENs, R. J., MILLER, P. M., WALTON, G. S., and HITCHCOCK, S. W.

1971. INCIDENCE OF X DISEASE OF PEACH AND ERADICATION OF CHOKECHERRY.

Plant Dis. Reptr. 55: 645-647.

MACOVEI, A.

1969. REAPINDIREA ACTÚALA A VIRUSULII PLUM POX (SHARKA) IN ROMANIA.

Studii Cere. Biol. Ser. Bot. 21: 311-316.

1971. ELECTRON MICROSCOPIC EVIDENCE OF PINWHEEL STRUCTURES IN NICOTIANA CLEVELANDII GRAY. Cells infected with plum pox virus. Rev. Roum.

Biol. Botanique 16: 331-334.

1971. STADIUL ACTUAL AL CUNOSTINTELOR PRIVITOARE LA VIRUSAL VARSATULUI

PRUNULUI (PLUM POX) CU REFERIRÉ SPECIALA LACERCETARILE EFECTÚATE

IN ROMANIA. Studii Cerc. Biol. Ser. Bot. 23: 71-80.

MARCUS, O.

1969. ERGEBNISSE ZEHNJAHRINGER VIRUSKONTROLLEN IN KURHESSISCHEN OBSTBAUMSCHULEN. NachrBl. dt. PflSchutzdienst., Stuttg., 21: 38-41.

MARENAUD, C, and DUNEZ, J.

1969. CONTRIBUTION A L'ETUDE DES VIRUS TRANSMIS PAR NEMATODES CHEZ LES

ARBOES FRUITIERS A NOYAU. Ann. Phytopath. 1: 591-602.

MCCRUM, R. C.

1968. PRUNUS VIRGINIANA A NATURAL HOST FOR A MOSAIC VIRUS OF APPLE.

Plant Dis. Reptr. 52: 794.

MEGAHED, E.-S. and MOORE, J. D.

1969. INACTIVATION OF NECROTIC RINGSPOT AND PRUNE DWARF VIRUSES IN

SEEDS OF SOME PRUNUS SPP. Phytopathology 59: 1758-1759.

MlNOIU, N.

1968. ELEMENTE NOI PRIVIND DIAGNOSTICAREA SEROLOGICA A VIRUSULUI VARSATULUI LA PRUN (PRUNUS VIRUS 7 CHRIST). Ann. Inst. Cercet. Prot.

Plant 6: 179-188.

MIRCETICH, S. M., and FOGLE, H. W.

1969. STEM PITTING IN PEACH: TRANSMISSION AND NATURAL SPREAD. Phytopathology 59: 1555-1562.

and FoGLE, H. W.

1969. STEM PITTING IN PRUNUS SPP. OTHER THAN PEACH. Plant Dis. Reptf.

53: 7-11.

CIVEROLO, E. L., and FOGLE, H. W.

1971. RELATIVE DIFFERENTIAL EFFICIENCY OF BUDS AND ROOT CHIPS IN TRANSMITTING THE CAUSAL AGENT OF THE PEACH STEM PITTING AND INCIDENCE

OF NECROTIC RINGSPOT VIRUS IN PITTED TREES. Phytopathology 6l: 1270-

1275.
418 VIRUS DISEASES OF STONE FRUIT

FOGLE, H. W., and BARRâT, J. G.

1968. FURTHER OBSERVATIONS ON STEM PITTING IN PRUNUS. Plant Dis. Reptr.

52: 287-291.

MOTOI, E.

1968. CARACTERISTICILE UNOR IZOLATE DE VIRUS DE LA PIERSIC. Ann. Inst.

Cercet. Prot. PL 6: 189-195.

NYLAND, G., LOWNSBERRY, B. F., LOWE, S. K., and MITCHELL, J. F.

1969. THE TRANSMISSION OF CHERRY RASP LEAF VIRUS BY XIPHINEMA AMERICANUM. Phytopathology 59: 111-112.

OBATA, T.

1970. PRESENCE OF GREEN RING MOTTLE VIRUS IN JAPANESE SWEET CHERRY.

Res. Bull. PL Prot. Serv. Japan 8: 1-12.

OPEL, H., and KEGLER, H.

1968. UNTERSUCHUNGEN ÜBER HEMMECHANISMEN IN VIRUSINFIZIERTEN PFLANZEN. 3. MITT. PROBLEME DER MECHA NISCHEN ÜBERTRAGUNG VON OBSTVIREN AUF KRAUTIGE WIRTSPFLANZEN. PhytOpath. Z. 63: 75-95.

and KEGLER, H.

1969. TABLETTIERUNG EINS STABILIESIERUNGSGEMISCHES ZUR MECHANISCHEN

VIRUSUBERTRANGUNG BIEM OBST. Arch. Gartenb. 17: 155-159.

KEGLER, H., and RICHTER, J.

1969. VORKOMMEN UND CHARAKTERISIERUNG VON TMV-STAMMEN DES KERNOBSTES. Acta PhytOpath. Acad. Sei. Hung. 4: 1-12.

PARES, R. D.

1970. NEW RECORDS OF VIRUS AND VIRUS-LIKE DISEASES OF POME AND STONE

FRUIT IN NEW SOUTH WALES. Agr. Gaz. N.S.W. 81: 609-612.

PAULECHOVA-KRALIKOVA, KATARINA, and KEGLER, H.

1967. INVESTIGATIONS ON THE PROPERTIES OF A VIRUS ISOLATE FROM PRUNE

DWARF DISEASED PLUM TREES. Biología, Bratisl. 22: 673-677.

PAULSEN, A. Q., and FULTON, R. W.

1968. HOSTS AND PROPERTIES OF A PLUM LINE PATTERN VIRUS. Phytopathology

58: 766-772.

and FULTON, R. W.

1969. PURIFICATION, SEROLOGICAL RELATIONSHIPS AND SOME CHARACTERISTICS

OF PLUM LINE PATTERN VIRUS. Ann. Appl. Biol. 63: 233-240.

PEJKIC, B., and SUTIC, D.

1969. NEKE PROMENE PRI REDUKCIONOJ DEOBI MATERINSKIH CELIJA POLENA U

MIKROSPOROGENEZI KOD SLJIVE POZEGACE ZARAZENE VIRUSOM SARKE.

Zast. Bilja 19: 347-353.

PELET, F., BOVEY, R., and BAGGIOLINI, M.

1968. LA LUTTE CONTRE LA SHARKA DU PRUNIER. Agr. Romande 7: 51-52.

BOVEY, R., and BAGGIOLINI, M.

1968. LES SYMPTOMES DE LA SHARKA SUR LES PRUNIERS, PRUNEAUTIERS, ABRICOTIERS ET PECHERS. Agr. Romande 7: 80-84.

NEURY, G., PRAZ, P., and MARTIGNIER, P.

1969. OBSERVATIONS SUR LA DISSEMINATION DE LA SHARKA EN SUISSE ROMANDE.

Revue Suisse Vitic. Arboric. 1: 89-92.

PENA IGLESIAS, A.

1967-68. INVESTIGACIONES SOBRE LA 'VIRUELA' DEL ALBARICOQUERO PROBABLE

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HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 419

PENROSE, L. J., and PARES, R. D.

1969. STEM PITTING IN APRICOT ON PEACH STOCKS IN NEW SOUTH WALES.

Aust. J. Sei. 32: 107-108.

PiSKUN, N. I.

1969. 'SHARKA' SLIV NA UKRAINE. Zashch. Rast., Mosk. 13: 54.

PLESE, NACA and JURETIC, N.

1969. ISTRAZIVANJE O VIRUSIMA PROTENASTE PJEGAVOSTI TRANSJE. Acta Bot.

Croat. 28: 299-315.

RiLOVic, MARIJA, and WRISCHER, MERCEDES.

1969. NOVI DOMADARI I INTRACELULARNE INKLUZIJE VIRUSA SARKE. Zast.

Bilja 20: 144-150.

POP, I., COMAN, TATIANA, GHEORGHIU, EFTIMIA, and MOTOI, E.

1967. DATE OBTINUTE IN TESTAREA VIROZELOR POMILOR FRUCTIFERI IN

ROMANIA. Ann. Inst. Cercet. Prot. PL 5: 171-180.

POSNETTE, A. F., and CROPLEY, R.

1970. DECLINE AND OTHER EFFECTS OF FIVE VIRUS INFECTIONS ON THREE

VARIETIES OF PLUM (PRUNUS DOMESTICA L.). Ann. Appl. Biol. 65: lU114.

POSNETTE, A. F., CROPLEY, R., and SWAIT, A. A. J.

1968. THE INCIDENCE OF VIRUS DISEASES IN ENGLISH SWEET-CHERRY ORCHARDS

AND THEIR EFFECT ON YIELD. Ann. Appl. Biol. 61: 351-360.

PROESELER, G.

1968. UBERTRAGUNGSVERSUCHE MIT DEM LATENTEN PRUNUS-VIRUS UND DER

GALLMILBE BASATES FOCKEUI NAL. Phytopath. Z. 63:1-9-

PUTZ, C.

1969. LES VIROSES DES PETITS FRUITS. I. LES VIROSES DU FRAMBOISIER. Ann.

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RAMASWAMY, S., and POSNETTE, A. F.

1971. PROPERTIES OF CHERRY RING MOTTLE, A DISTINCTIVE STRAIN OF PRUNUS

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RANKOVIC, M.

1970. PROUCAVANJE I IDENTIFIKACIJA VIRUSA PROUZROKOVACA ENACIJA NA

LISCU BRESKVE. Zast. Bilja 21: 335-356.

and JORDOVIC, M.

1970. NEKA ISKUSTVA VIRUSA SARKE MEHANICKIM PRENOSENJEM NA ZELJASTE

BILJKE. Zast. Bilja 21: 157-163.

and JORDOVIC, M.

1970. JEDAN POGODAN METOD ZA PRECISCAVANJE VIRUSA SARKE. Zast. Bilja 21:

195-199.

RICHTER, J., and KEGLER, H.

1967. UNTERSUCHUNGER üBER RINGFLECKENKRANKHEITEN DER KIRSCHE. III.

SEROLOGISCHE UNTERSUCHUNGEN. Phytopath. Z. 60: 262-272.

and KLEINHEMPEL, H.

1967. SEROLOGICAL DETECTION OF NEPO VIRUSES IN FRUIT TREES. CHERRY LEAF

ROLL IN MAZZARD CHERRY, STRAWBERRY LATENT RINGSPOT IN PEACH, AND

ARABIS MOSAIC IN RED CURRANT. Seventh European Symposium of fruit

tree virus diseases, Aschersleben 10-16 July, 1967. TagBer. dt. Akad.

LandwWiss. Berl. 97: 277-282.
420 VIRUS DISEASES OF STONE FRUIT

SAHTIYANCI, S.

1969. REPORTS ON OUTBREAK OF PLUM POX VIRUS ON PLUM IN THE THRACE

REGION, A NEW RECORD FOR TURKEY. PI. Prot, Bull. F.A.O. 17: 67-69.

SAUNIER, R.

1969. REACTIONS DE DEUX VARIETIES PRECOCES DE PECHER A L'ELIMINATION DE

VIROSES DU TYPE RING-SPOT. C.r. hebd. Seanc. Acad. Sei., Paris 55: 262-269.

SAVULESCU, ALICE and MACOVEI, A.

1968. COMPARATIVE EXPERIMENTAL DATA CONCERNING PLUM POX AND PLUM

LINE PATTERN VIRUS IN RUMANIA. Seventh European Symposium of fruit

tree virus diseases, Aschersleben 10-16 July, 1967.—TagBer. dt. Akad.

LandwWiss. Berl. 97: 241-249.

SCHADE, CHRISTIANE

1968. UNTERSUCHUNGEN ZUM SEROLOGISCHEN NACHWEIS DES NEKROTISCHEN

RINGFLECKENVIRUS DER SAUERKIRSCHE. III. ZUR SEROLOGISCHEN VARIABILITÄT DES NEKROTISCHEN RINGFLECKENVIRUS DER SAUERKIRSCHE. Phytopath

Z. 62: 334-342.

1968. VIRUS DETECTION IN PLUM TREES IN VARIOUS SEASONS. Seventh European

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TagBer. dt. Akad. LandwWiss. Berl. 97: 283-288.

1971. DER NACHWEIS DES VIRUS DES NEKROTISCHEN UND DER CHLOROTISCHEN

RINGFLECKEN-KRANKHEIT IN KIRSCHEN MIT DER LATEXTEST ALS SCHNELLMETHODE. Arch. PflSchutz 7: 207-216.

1971. THE LATEXTEST—A RAPID METHOD FOR TRACING THE VIRUS OF NECROTIC

AND CHLOROTIC RINGSPOT IN CHERRIES. Archiv, f. Pflanzensch. 7: 207-216.

SCHIMANSKI, H. H.

1968. NATURAL INFECTION OF SEEDLING PLANTINGS OF THE GENUS PRUNUS BY

CHERRY RINGSPOT VIRUSES. Seventh European symposium of fruit tree virus

diseases, Aschersleben 10-16 July, 1967.—TagBer. dt. Akad. LandwWiss. Berl.

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and FUNK, T.

1968. UNTERSUCHUNGEN ÜBER DAS AUSMASS DER ÜBERTRAGUNG VON KIRSCHENRINGFLECKENVIREN DURCH DEN SAMEN VON VOGELKIRSCHEN (PRUNUS

AVIUM L.). Arch. Gartenb. 16: 143-150.

SCHMELZER, K.

1972. DAS KIRSCHENBLATTROLL-VIRUS (CHERRY LEAF-ROLL VIRUS) AUS DER BIRKE

(BETULA PÉNDULA ROTH). Cherry leaf-roll virus from Birch (Betula péndula Roth). Zentralblatt fur Bakteriologie, Parasitenkunde, Infektionskrankheiten und Hygiene. Abt. II. 127: 10-12.

1972. NACHWEIS DER VERWANDTSCHAFT ZWISCHEN HERKUNFTEN DES KIRSCHENBLATTROLL-VIRUS UND DEM ULMENMOSAIC-VIRUS. Zentralblatt fur Bakteriologie, Parasitenkunde, Infektionskrankheiten und Hygiene. Abt. II. 127:

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SCHMID, G.

1968. INVESTIGATION ON DETRIMENTAL CANKER OF SWEET CHERRIES. Seventh

European symposium of fruit tree virus diseases, Aschersleben 10-16 July,

1967.—TagBer. dt. Akad. LandwWiss. Berl. 97: 155-163.
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 421

1968. ZWETSCHGENBAUME JETZT AUF BEFALL VON SHARKA KONTROLLIEREN.

Schweiz. Z. Obstu. Weinb. 104: 431-434.

1968. DIE SHARKA EINE NEUEINGESCHLEPPTE VIRÓSE AN ZWETSCHGENBAUMEN.

Schweiz. Z. Obst- u. Weinb. 104: 121-123.

1969. DIE SHARKASITUATION IN 1968 IN DER DEUTSCHSPRACHIGEN SCHWEIZ.

Schweiz. Z. Obst- u. Weinb. 105: 312-319.

1970. DIE SHARKASITUATION IM JAHRE 1969 IN DER DEUTSCHSPRACHIGEN

SCHWEIZ. Schweiz. Z. Obst- u. Weinb. 106: 90-93.

1971. DIE SHARKASITUATION IM JAHRE 1970 IN DER DEUTSCHSPRACHIGEN

SCHWEIZ. Schweiz. Z. Obst- u. Weinb. 107: 107-109.

SEIDL, V.

1968. FURTHER EXPERIMENTS WITH APPLE PROLIFERATION VIRUS DISEASE.

Seventh European symposium of fruit tree virus diseases, Aschersleben 10-16

July, 1967.—TagBer. dt. Akad. LandwWiss. Berl. 97: 77-86.

SENEVIRATNE, S. N. DE., and POSNETTE, A. F.

1970. IDENTIFICATION OF VIRUSES ISOLATED FROM PLUM TREES AFFECTED BY

DECLINE, LINE PATTERN AND RINGSPOT DISEASES. Ann. Appl. Biol. 65:

115-125.

SMITH, S. H., and TRAYLOR, J. A.

1969. STEM PITTING OF YELLOW BUD MOSAIC VIRUS-INFECTED PEACHES. Plant

Dis. Reptr. 53: GGG-6G1.

SPRINGER, J. K. and others.

1972. INCIDENCE OF STEM PITTING OF PEACH IN FUMIGATED AND NONFUMIGATED

FIELD PLANTINGS. Plant Dis. Reptr. 56: 162-163.

STUBBS, L. L., and SMITH, P. R.

1971. THE ASSOCIATION OF PRUNUS NECROTIC RINGSPOT, PRUNE DWARF, AND

GREEN SUNKEN MOTTLE VIRUSES IN THE ROSETTING AND DECLINE DISEASE

OF PEACH. Aust. Jour. Agr. Res. 22: 771-785.

SUTIC, D., and BABOVIC, M.

1969. MONUCNOST IZOLACIJE VIRUSA SARKE I JEDNOG LATENTNOG VIRUSA IZ

ZARAZENIH, STABALA SLJIVE U TOKU ZIMSCOG MIROVANJA. Zast. Bilja

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TATJANA D. VERDEREVSKAJA.

1968. A SEVERE VIRUS DISEASE OF APRICOTS. Seventh European symposmm of

fmit tree virus diseases, Aschersleben 10-16 July, 1967.—TagBer. dt. Akad,

LandwWiss. Berl. 97: 173-180.

THOMAS, M., MARENAUD, C, and G. OLIVIER.

1971. THE SENSITIVITY OF SOME SPECIES OF THE PRUNUS GENUS TO CHLOROTIC

LEAF SPOT. Ann. Phytopath. 3: 73-85.

THOMSEN, A.

1968. FRUGTTRAE-VIRA INAKTIVERET VED TEMOTERAPI. Tidsskr. PlAvl. 72:141-

152.

1970. VIRUSINFEKTION HOS AEBLEGRUNDSTAMMER. Tidsskr. PlAvl. 73:619-628.

THORNBERRY, H. H.

1970. PEACH STEM PITTING IN ILLINOIS. Plant Dis. Reptr. 54:67-68.
422 VIRUS DISEASES OF STONE FRUIT

TiiTS, A.

1968. FURTHER INVESTIGATION ON THE VIRUS CAUSING PLUM POX-LIKE DISEASE.

Seventh European symposium of fruit tree virus diseases, Aschersleben 10-16

July, 1967.-TagBer. dt. Akad. LandwWiss. Berl. 97:251-254.

1968. FURTHER INVESTIGATIONS ON THE VIRUS CAUSING PLUM POX-LIKE DISEASE.

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VIRUS ON CERASUS TOMENTOSA (THUNB.) Wall.-Eeste NSV Tead Akad

Toim., Biol. Ser., 17:436-437.

1970. VIIRUSLIK PATOLOOGIA NING VILJAPUUDE JA MARJAKULTUURIDE

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TREMAINE, J. H.

1968. SOME PROPERTIES OF A CUCUMBER MOSAIC VIRUS STRAIN ISOLATED FROM

PRUNUS SPP. Phytopathology 58: 797-801.

TRIFONOV, D.

1969. LOKALISIERUNG UND WANDERUNG DES SCHARKAVIRUS (PLUM POX VIRUS)

IN PFLAUMENBÄUMEN. Zentbl. Bakt. ParasitKde Abt. 2 123:340-347.

1970. 2ARAZNOST NA NYAKOI VIDOVE PRUNUS S VIRUSITE OT GRUPATA

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VAN DOSTEN, H. J.

1970. HERBACEOUS HOST PLANTS FOR THE SHARKA (PLUM POX) VIRUS. Neth.

Jour. Plant Path. 76:253-260.

1970. THE ISOLATION OF SHARKA (PLUM POX) VIRUS FROM LEAVES AND

FRUITS OF PLUM WITH HERBACEOUS PLANTS. Neth. Jour Plant Path

76:99-103.

1972. DIAGNOSIS OF SHARKA (PLUM POX) BY INTERNAL AND EXTERNAL FRUIT

SYMPTOMS. Neth. Jour. Plant Path. 78:99-106.

1972. PURIFICATION OF PLUM POX (SHARKA) VIRUS WITH THE USE OF TRITON

X-100. Neth. Jour. Plant Path. 78:33-44.

VERDEREVSKAJA, TATJANA D. and KEGLER, H.

1971. STAMMNARBUNG (STEM PITTING) AN KERN- UND STEINOBST. NachrBl.

PflSchutzdienst DDR N.F. 25:153-157.

VUITTENEZ, A. and KUSZALA, J.

1971. ARABIS MOSAIC VIRUS ASSOCIATED TO AN ENATION DISEASE OF CHERRY

KIRSCH-VARIETIES, IN VOSGES MOUNTAINS (EASTERN FRANCE). Ann

Phytopathol. 3:485-491.

WADLEY, B. N.

1968. UNUSUAL DEATH RATE OF SWEET CHERRIES IN UTAH IN 1968. Utah State

Hort. Soc. Proc. 1968:22-23, 25, 26.

WADLEY, B. N.

1969. ROUGH FRUIT, A NEW VIRUS DISEASE OF SWEET CHERRIES. Phytopatholoey

59:213-215.
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 423

and ANDERSON, J. L.

1968. X-DISEASE OF SWEET CHERRIES. Utah Sci. 29:108-110.

WAGNON, H. K., TRAYLOR, J., WILLIAMS, H. E., and WEINER, A. C.

1968. INVESTIGATIONS OF CHERRY RASP LEAF DISEASE IN CALIFORNIA. Plant Dis.

Reptr. 52:618-622.

ZAWADZKA, BARBARA, and MILLIKAN, D. F.

1971. SYMPTOMATOLOGY AND SOME BIOLOGICAL EFFECTS OF THE SHARKA

DISEASE ON COMMON PRUNE IN POLAND. PhytOprotection 52:68-72.
HOST-DISEASE INDEX^

Page

Almond

Almond calico 104

Almond corky spot 259, 260

Almond virus bud failure . . 33, 34, 35,

36,37,38,39,40,41

Apricot ring pox 45

Asteroid spot 50

Boron deficiency 337

Boron-excess injury 339

Cherry mottle leaf 216

Cherry twisted leaf 222

Chloride-excess injury 341

Copper deficiency 331, 333, 334

336,337

Crazy-top 278

Drake almond bud failure 33

Iron chlorosis 327

Manganese deficiency 325

Muletail 278

Nitrogen deficiency 317

Noninfectious bud failure 278,280, 281

Peach mosaic 61, 66, 68, 70

Peach rosette 73,74

Peach yellows 91,93

Plum line pattern 166, 170

Potassium deficiency 320

Prunus ring spot 42,108,116

117,120, 123, Í24

Shatter-bud 278

Short stem 250

Sodium-excess injury 342

Stubby twig 139

X-disease 146

Yellow bud mosaic 156,160,161,

162,163,164

Zinc deficiency 327

Almond, desert

Asteroid spot 50

Peach mosaic 61

Prune dwarf 180

Prunus ring spot 105

Stubby twig 139

Yellow bud mosaic 156

Page

Almond, fenzl

X-disease 146

Almond, flowering

Peach rosette 73

Plum line pattern 166

Prune dwarf 180

Almond, dwarf flowering

Peach yellows 91

Prune dwarf 180

Almond, Russian

Pmne dwarf 180

Almond, tangut

Peach mosaic 61

Apple

Fruit pitting of sweet cherry 227

Prunus ring spot 27,104, i OS

Tobacco mosaic 256

Apricot

Apple chlorotic leaf spot 206

Apricot gumboil ... 261,262,263,264

Apricot gummosis 179

Apricot pox 45

Apricot pucker leaf 22, 43, 44

Apricot ring pox 22, 45,46, 47,

48,49\ 66,255

Apricot ring spot 45

Arsenic injury 344, 345,346

Asteroid spot 50, 53, 54

Boron deficiency 337,340

Boron-excess injury 337,341

Cherry mottle leaf 216

Cherry twisted leaf 222

Chloride-excess injury 341,342

Copper deficiency 333

Fluoride injury 355, 356, 338

Green ring mottle 193,196

Herbicide injury 314

Iron chlorosis 327

Manganese deficiency 325

Montmorency bark splitting . . 191,192

Ozone injury 363

Peach mosaic 61,65, 69

Peach rosette 73,74

5 Host here includes both plants that are infected by viruses and those that are

affected by noninfectious disorders.

424
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 425

Page

Apricot—Con.

Peach wart 88

Peach yellows 91,93

Phony 96

Pit pox 45

Plum line pattern 166

Potassium deficiency 320

Prune dwarf 179, 180

Prunus ring spot 126

Pucker leaf 43,44

Ring pox 45

Rusty mottle 242, 243, 246

Short stem 250

Sodium-excess injury 524,342

Spur cherry 252,253

Smbby twig 139

Sulfur dioxide injury 358,561

Tatter leaf 45

X-disease 146

Xylem aberration 257

Yellow bud mosaic 156,163

Zinc deficiency ... 327, 330, 331,332

Apricot, ansu

Asteroid spot 50

Peach mosaic 61

Apricot, desert

Peach mosaic 61

X-disease 146

Apricot, Japanese

Asteroid spot 50

Peach mosaic 61

Peach yellows 91

Phony 96

Prune dwarf 180

Yellow bud mosaic 156

Balsam apple

Cucumber mosaic virus 4

Plum line pattern 4

Prune dwarf 3,4,180

Prunus ring spot 3, 4,127,150

Bean, common

Apple chlorotic leaf spot 4

Cucumber mosaic 4

Cherry boron rosette 213

Fruit pitting of sweet cherry 227

Plum line pattern 4

Prunus ring spot 4

Rosette mosaic 135,136

Yellow bud mosaic . . 4,156

Page

Bean, pinto

Prunus ring spot 151

Blackberry, Himalaya

Yellow bud mosaic 156

Bristly oxtongue

Yellow bud mosaic 156

Bushcherry Chinese (Korean)

Peach mosaic 61

X-disease 146

Carrot

X-disease 146

Castor bean

Prune dwarf 4

Prunus ring spot 4

Yellow bud mosaic 4

Catjang

Plum line pattern 171,172

Celery

X-disease 146,154

Cheeseweed

Yellow bud mosaic 156

Cherry, almond

Peach yellows 91,93

Prune dwarf 180

Cherry, amur

Cherry mottle leaf 216

Plum line pattern 166

Prune dwarf 180

Short stem 250

Spur cherry 252

Cherry, bitter

Cherry mottle leaf 216, 218

Little cherry 232,237

X-disease 146

Cherry, bitter (var. mollis)

Little cherry 232

Cherry, black

Apricot ring pox 45

Cherry mottle leaf 216

Prune dwarf 180

Rusty mottle 243

Short stem 250

Spur cherry 252

X-disease 146

Cherry, capoUin

Short stem 250

Spur cherry 252

Cherry, cataline

Prune dwarf 180

Cherry, Desfontaines

Little cherry 232
426 VIRUS DISEASES OF STONE FRUIT

Page

Cherry, duke

Apple chlorotic leaf spot 206

Cherry mottle leaf 216

Green ring mottle 193,195

Little cherry 232

Peach calico 59

Peach mottle 71

Pink fruit 200

Prune dwarf 180

X-disease 131

Cherry, ground

Apple chlorotic leaf spot 206

Prune dwarf 180, 188

Cherry, hollyleaf

X-disease 146

Cherry, Japanese flowering

Fuji cherry

Little cherry 232

Siebold cherry

Little cherry 232

Ssiori cherry

Prune dwarf 180

Cherry mahaleb

Almond virus bud failure 34, 35

Asteroid spot 50

Cherry boron rosette 213

Cherry mottle leaf 216

Cherry rasp leaf 219,221

Cherry twisted leaf 222

Fluoride injury 355

Fruit pitting of sweet cherry . . 227, 228

Green ring mottle 194

Little cherry 232

Peach rosette 73,75

Plum line pattern 2,166, 167,169, 171

Prune dwarf 180, 186

Prunus ring spot i 06, 107, 117,

118,126

Rusty mottle 242,243

Spur cherry 252

Tobacco mosaic 256

Virus gummosis of Montmorency . 202

Weakpeach 144

X-disease . 146,150,151,154,236,237

Yellow bud mosaic 162

Cherry, Manchu

Apricot pucker leaf 43,44

Asteroid spot • 50

Cherry mottle leaf 216

Page

Cherry, Manchu—Con.

Green ring mottle 193

Little cherry 232

Montmorency bark splitting 22

Peach mosaic 61

Peach rosette 73

Peach wart 88,90

Peach yellows 91,93

Prune dwarf 180

Prunus ring spot 117, 118, 129

Rusty mottle 242,243

Spur cherry 252

X-disease 146

Yellow bud mosaic 156

Cherry, mazzard

Almond bud failure 34, 35

Cherry rasp leaf 219,220,221

Deep suture 307

Green ring mottle 193

Peach mottle 71

Peach rosette 73,74

Plum line pattern 170

Prune dwarf 180

Prunus ring spot 116,124, 126

Rough bark 240,241

Rusty mottle 242

Spur cherry 252

Yellow bud mosaic 163

X-disease 150,151,154,236

Cherry, Oriental flowering

Banded chlorosis of oriental

flowering cherry 166

Cherry mottle leaf 216

Epinasty of oriental flowering cherry 193

Fluoride injury 355

Green ring mottle 22,193,195,

196, i97, 198

High temperamre mottle 273

K & S little cherry 231

Little cherry 232, 235, 236

Peach mosaic 61

Peach wart 88,89

Plum line pattern \66J69. 170

Prune dwarf 22,180, 186,187

Prunus ring spot 22,106,115,

125A27,128

Rough bark 240

Rough bark of oriental flowering

cherry 193

Rusty mottle 243,246
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 427

Page

Cherry, Oriental flowering—Con.

Spur cherry 252

X-disease 146

Higan cherry

Little cherry 232

Yoshina cherry

Cherry mottle leaf 216

Little cherry 232

Plum line pattern 166

Cherry, pin

Little cherry 232

Plum line pattern 166

Prune dwarf 180

Prunus ring spot 105, 126

Short stem 250

X-disease 146

Cherry, sand

Peach rosette 73

Cherry, sand, purple leaf

Prunus ring spot 105

Cherry, sour

Albino 204,205

Almond virus bud failure 34, 35

Apple chlorotic leaf spot 206

Apricot ring pox 45

Boarder tree 179

Cherry mottle leaf 216

Cherry rasp leaf 219

Cherry ring spot 104

Cherry twisted leaf 222

Chlorotic mottle 179

Chlorotic ring spot 179

Constricting chlorosis 193

Cucumber mosaic 238,239

Green ring mottle 193,194,193,

196,198

Green ring yellows 193

High temperature mottle .... 272, 273

Little cherry 231, 232, 233, 236

Manganese deficiency 325,328

Montmorency bark splitting .. 191,192

Necrotic ring spot 104

Peach mottle 71, 72

Peach rosette 15,75

Peach wart 88,89

Physiological leaf drop 179

Pink fruit 22,200,202

Plum line pattern 166,167,169

Potassium deficiency 320, 322

Page

Cherry, sour—Con.

Prune dwarf 179,180,181,182,

183, 186,187,188,189,190

Prunus ring spot . . 104, 105,106, 107,

111,112,113,114,115,117,US,

119,120,121,126,127,129

Recurrent necrotic ring spot 104

Rusty mottle 242,245

Sour cherry yellows 179

Sour cherry decline 231

Spur cherry 252

Sulfur dioxide injury 359

Sweet cherry rough bark 254

Tatter leaf 104

Tobacco mosaic 256

Virus gummosis of Montmorency

202,203

Wilt & decline 145

X-disease 146,149,154,155

Xylem abberation 257

Zinc deficiency 327

Cherry, sweet

Albino 22,204,205

Almond virus bud failure 34, 35

Apple chlorotic leaf spot .... 206, 207

Apricot ring pox 45,47, 48, 49

Arsenic injury 344, 345

Asteroid spot 22, 50, 32, 33, 34

Black canker 209

Blossom anomaly of cherry . . 211,212

Boron deficiency 334,339,340

Boron-excess injury 338,339 342,343

Cherry blister bark 242

Cherry boron rosette .... 215,214,213

Cherry buckskin 145

Cherry mottle leaf .. 22,216,227,218

Cherry rasp leaf .... 22,161,219,220

Cherry ring spot 104

Cherry rugose mosaic 104

Cherry twisted leaf .. 22,222,223,224

Chloride-excess injury 341

Cockscomb 219

Copper deficiency 331

Crinkle leaf 306,307,308 309,

311,312,313

Cucumber mosaic 238

Curly leaf 306

Deep sumre 306,307,3iO,3ii

312,313

Eola rasp leaf 156

Fluoride injury 355,356
428 VIRUS DISEASES OF STONE FRUIT

Page I

Cherry, sweet—Con.

Freckle fruit 22,226

Fruit pitting 227,228, 229

Green ring mottle 193,196,198

Iron chlorosis 327

Lace leaf 104

Lambert mottle 242

Leaf enation 219

Little cherry 22, 231, 232,233,

234.235,236,237,317

Longleaf 306

Male trees 306

Manganese deficiency 325

Maple leaf 306

Mild rusty mottle 242,243

Montmorency bark splitting 191

Necrotic rusty mottle 242

Ozone injury 363

Plath bing 252

Peach mosaic 61

Peach mottle 71,72

Peach wart 88,89

Pink fruit 200

Plum line pattern 166, 170

Prune dwarf 179,180,284,186,

187, 188, 189

Prums ring spot 105, i06, 107,

111, 112,113, 118, 120,122,123, 125

Red bud 306

Rough bark 240,241

Rough leaf 306

Ruffled leaf 219

Rusty mottle 242,243,244,24^,

246,247,248

Severe rusty mottle 242

Short stem 22,250,2^i

Small bitter cherry 145

Sodium-excess injury 342,344

Spur bing 252

Spur cherry 22,252,2^3

Stecklenberger disease 104

Sulfur dioxide injury 359

Sweet cherry rough fruit . . 22,254,255

Tatter leaf 104,179

Tobacco mosaic 256

Utah dixie rusty mottle 50

Variegation 306,312

Virus gummosis of Montmorency . . 202

Western X-disease 145

White crinkle 306

Wild trees 306

Page

Cherry, sweet—Con.

X-disease 146,150,155

Xylem aberration 22,257,238

Yellow bud mosaic 156,161

Zinc deficiency 317,327,332,335

Cherry, western sand (Bessey)

Apricot ring pox 45

Peach mosaic 61

Peach rosette 73,75

Plum line pattern 166

Short stem 250

X-disease 146

Chokecherry, amur

Cherry mottle leaf 216

Plum line pattern 166

Prune dwarf 180

Short stem 250

Spur cherry 252

Chokecherry, eastern

Apricot ring pox 48

Peach rosette 73,75

Plum line pattern 166

Prune dwarf 180

Rusty mottle 243,246

X-disease . 145,146,151, Í52,153,154

Chokecherry, western

Apricot ring pox 45

Cherry twisted leaf 222,223,224

Redleaf 145

X-disease 146

Cowpea

Plum line pattern 171, Í 73

Rosette mosaic 135,136

Yellow bud mosaic 156, 157

Crabapple, big foot

Short stem 250

Cucumber

Cherry boron rosette 213

Cucumber mosaic 238,239

Plum line pattern 170, 171,173

Pmne dwarf 188

Prunm ring spot 104,130

Stubby twig 141

Yellow bud mosaic 156,157

Currant, common red

Yellow bud mosaic 156

Dolichos

Prunus ring spot 127,131

Fuller's teasel

Yellow bud mosaic 156
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 429

Page

Globe amaranth

Cherry rasp leaf 219

Prune dwarf 4

Prunus ring spot .... 4, 118,125,151

Rosette mosaic 135,136

Goosefoot

Apple chlorotic leaf spot 4, 207

Cherry rasp leaf 219,221

Cucumber mosaic 4

Fruit pitting of sweet cherry 227

Plum line pattern 4

Prunus ring spot A, 130,131

Rosette mosaic 135, 136

Yellow bud mosaic 4

Grape

Fmit pitting of sweet cherry 230

Rosette mosaic 135,136,137,138

Sulfur dioxide injury 358

Tobacco mosaic 256

Weak peach 144

Groundcherry

Cucumber mosaic 4

Plum line pattern 4, 170, 171,172

Guar

Prune dwarf 3,4, 180

Prunus ring spot ^,4,131

Hedge nettle

Yellow bud mosaic 156

Hop

Prunus ring spot 9, 27,104

Jimson-weed

Fruit pitting of sweet cherry 227

Kerria, Japanese

Yellow bud mosaic 156

Laurel cherry, Portuguese

Yellow bud mosaic 156

Maple, red

Peach rosette 73,75

Milkweed, common

Green ring mottle 194

X-disease 146

Mountain ash

Apple chlorotic leaf spot 27

Nectarine

Almond virus bud failure 34

Apricot ring pox 45

Asteroid spot 50,51

Green ring mottle 193

Peach calico 58

Peach mosaic 61, 62, 69

Peach stem pitting 77, 82, 84

Page

Nectarine—Con.

Peach wart 88, 89

Peach yellows 91

Stubby twig 139, 142

X-disease 146

Yellow bud mosaic 156,157

Parsley

X-disease 146

Peach

Almond virus bud failure . . 33, 34, 35,

37,40,41

Apple chlorotic leaf spot . . 27, 206, 207

Apple mosaic 104, 175

Apricot pucker leaf 43,44

Apricot ring pox 45

Arsenic injury 324, 345, 346

Asteroid spot 22, 50, 31, 53, 54, 55

Blister 88

Boron deficiency 338

Boron-excess injury .... 559,343,344

Calcium deficiency 319,322,324

Cherry boron rosette 213

Cherry mottle leaf 216

Cherry twisted leaf 222

Chimaera 290

Chloride-excess injury 341,342

Copper deficiency 331

Cucumber mosaic 238

Ethylene injury 364

False yellow leaf roll 139

Fluoride injury 355,3:56,3^7,358,

339, 360

Green ring mottle 193, 196, 198

Herbicide injury 314, 347,348,349,

330,331, 332, 333, 334, 357,360

Iron chlorosis 319,327

Little peach 91,93

Magnesium deficiency 3Í9,323,

326,325,356

Manganese deficiency 325

328, 329

Montmorency bark splitting 191

Muir peach dwarf 179

Nitrogen deficiency 317,3Í9

Nitrogen-excess injury 318

Ozone injury 361,362,363

Peach blotch 22,:56,57

Peach calico 22, 58, ^9

Peach false wart 288

Peach leaf casting yellows 145

Peach line pattern 166
430 VIRUS DISEASES OF STONE FRUIT

Page

Peach—Con.

Peach mosaic .. 22,61,62,63,64,6:5,

66, 61, 68, 69

Peach mottle 22,7i

Peach mule's ear 33

Peach necrotic leaf spot 104

Peach ring spot 104

Peach stunt 179

Peach rosette 22, 73, 74, 75

Peach rosette mosaic 135

Peach stem pitting . . 77,18, 79, SO, 81,

82, 83, 84, 83, 86

Peach variegation 290

Peach wart 22, 88, 89, 90

Peach willow twig 33

Peach yellow leaf roll 145

Peach yellow spot 292

Peach yellows ... 22,75,91,92,93,94

Phony 22,11>,%,91,98,99,100,

101, 102

Phony peach 96

Phosphorus deficiency 318,3Í9

Plum line pattern 166,167,175

Potassium deficiency 519, 320,321, 322

Prune dwarf 179,180,185,186,

187,188,189

Prunus ring spot 104,105, 107,

109,110, 111, 111, 118, 120,124,

125, 126, 127, 129,186

Red suture 22,91,^33,134

Rose mosaic 104

Rosette mosaic . . 22, 135,136,131,138

Rusty mottle 242,243

Short stem 250

Sodium-excess injury 324, 342

Spur cherry 252

Stipple spot 50

Smbby twig 22,139,140,141,142,143

Sulfur dioxide injury 359,361

Wart 88

Weak peach 22,144

Wild leaf 33

X-disease . 22, 145,146, W, 148, 149,

150,152,153,154,155, 317, 330, 345

Yellow bud mosaic 22, 156, 157,

138,139,160,161, 162,165

Yellow-red disease 145

Yellow-red virosis 145

Western X-disease 145

Western X red leaf 145

Winter's disease 156

Page

Peach—Con.

Winter's peach mosaic 156

Zinc deficiency 327,331,332,334

Peach, david

Cherry mottle leaf 216

Peach mosaic 61

Peach rosette 73

Peach yellows 91,93

Plum line pattern 166

Prune dwarf 180

X-disease 146

Peach, desert

Apricot ring pox 45

Asteroid spot 50,51

Plum line pattern 166

Yellow bud mosaic 156

X-disease 146

Peach, flat

Peach mosaic 61

Pear

Apple chlorotic leaf spot 27

Tobacco mosaic 256

Periwinkle

Little cherry 235

Peach rosette 73,75

X-disease 146,154

Petunia

Fruit pitting of sweet cherry 227

Plum line pattern 171

Rosette mosaic 135, 136

Plantain

Yellow bud mosaic 156

Plum, American

Peach mosaic 61, 69

Peach yellows 91, 93, 94

Prune dwarf 180, 187

Prunus ring spot 105

X-disease 146

Zinc deficiency 327

Plum, beach

Peach mosaic 61

X-disease 146

Plum, bokar

Asteroid spot 50

Peach mosaic 61

Plum, chickasaw

Asteroid spot 50

Peach mosaic 61

Peach rosette 73, 74, 76

Phony 96,97

I Weak peach 144
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 43I

Page

Plum, damson

Asteroid spot 50, 54

Peach mosaic 61

Peach rosette 73

Plum line pattern I66

Prune dwarf 180

Rosette mosaic 135,136

Rusty mottle 242, 243, 246

Stubby twig 139

X-disease 146

Yellow bud mosaic 163

Plum, European

Apple chlorotic leaf spot . . 27, 206, 207

Arsenic injury 344

Asteroid spot 50, 54

Boron deficiency 337

Boron-excess injury .... 324,339,343

Chloride-excess injury 341,342

Constriction disease . 268,269,270,271

Copper deficiency 532,333

Decline of Stanley prune 268

Fluoride injury 355

Iron chlorosis 327,330

Italian Prune leaf spot 274,273

Italian Prune sparse leaf 277

Little peach 93

Manganese deficiency 325

Nitrogen deficiency 317

Non-infectious plum shot hole 286, 287

Ozone injury 363

Peach mosaic 61,6A, 68

Peach rosette 73

Peach stem pitting 87

Peach yellows 91

Plum line pattern 2, 166, 167

Potassium deficiency .... 320, 322,323

Prune crinkle leaf 297,298

Prune diamond canker .. 176, i 77, 303

Prune dwarf 22,179,180,184,185,186

Prune leaf casting mottle . 299,300,301

Prune leaf mottle 299

Prune mosaic 179

Prune mottle 299

Prunus ring spot 113, 126

Pustular canker of Tragedy prune . 302

Rosette mosaic 135,136,138

Rusty mottle 246

Shoestring 179

Shot hole 274

Standard prune constricting mosaic

304

Page

Plum, European—Con.

Sulfur dioxide injury 358, 359

Willows 179

X-disease 146

Zinc deficiency 327

Plum, flatwoods

Peach mosaic 61

Peach rosette 73, 74

Plum, flowering

Apple chlorotic leaf spot 206

Plum, hog

Peach mosaic 61

Plum, hortulan

Peach mosaic 61

Peach rosette 73

Peach yellows 91,93

Phony 96

Plum, hybrids

Almond virus bud failure 34, 35

Apple mosaic 175

Apricot pucker leaf 43,44

Apricot ring pox 45,47

Italian prune leaf spot 274

Non-infectious plum shot hole 285,286

Peach mosaic 64, 68

Peach rosette 73,75

Peach wart 88,89,90

Plum line pattern 22,166,167,168, 171

Plum rusty blotch 294

Plum white spot 22

Prune dwarf 180

Prunus ring spot . . . 106,108, 123,125

Red suture 134

Rosette mosaic 135,136

Shiro line pattern 166

Stubby twig 139

X-disease 146

Yellow bud mosaic 156

Plum, Japanese

Apple chlorotic leaf spot 207

Apricot ring pox 45

Asteroid spot 50,54,33

Chloride-excesis injury 341

Cherry mottle leaf 216

Cherry twisted leaf 222

Constriction disease 268

Copper deficiency 331,333,336

Iron chlorosis 327

Manganese deficiency 325

Nitrogen deficiency 317
432 VIRUS DISEASES OF STONE FRUIT

Page

Plum, Japanese—G)n.

Non-infectious plum crinkle leaf . . 283

Non-infectious plum shot hole 285,286

Peach mosaic 61,64

Peach rosette 73,75

Peach stem pitting 87

Peach yellows 91

Plum line pattern 166

Plum mosaic 166

Plum rusty blotch 294,293,296

Potassium deficiency 320

Prune dwarf 180, 185

Prunus ring spot 105

Red suture 133, 134

Rosette mosaic 135

Sodium-excess injury 342, 344

Smbby twig 139

X-disease 146

Zinc deficiency 327, 330, 331

Plum, Klamath

Peach mosaic 61

Plum line pattern 166

X-disease 146

Plum Marianna

Apricot pucker leaf 43,44

Peach rosette 75

Stubby twig 139

Plum, Mexican

Peach mosaic 61

Peach rosette 73

Phony 96

Plum, myrobalan

Asteroid spot 265

Cherry mottle leaf 216

Chlorotic fleck 265,266, 267

Fluoride injury 355

Peach mosaic 61

Peach stem pitting 87

Peach yellows 91

Plum line pattern 166,167, i69

Prune diamond canker 176

Prune dwarf 180, 186

Stubby twig 139

X-disease 146

Yellow bud mosaic 156

Plum, sloe

Asteroid spot 50

Fluoride injury 355

Plum line pattern 166

Page

Plum, wildgoose

Noninfectious plum shot hole .... 285

Peach mosaic 61, 69

Peach rosette 73

Peach yellows 91,93

Prune dwarf 180

X-disease 146

Pormgal Laurel

Yellow bud mosaic 156

Quinoa

Apple chlorotic leaf spot . . 22, 207, 208

Cherry rasp leaf 219,221

Cucumber mosaic virus 22

Prunus ring spot 130

Rosette mosaic 135,136

Tobacco mosaic 22,256

Raspberry, red

Apple chlorotic leaf spot 27

Yellow bud mosaic 156

Rose

Prunus ring spot 9,27,108

Yellow bud mosaic 156

Seaside daisy

Yellow bud mosaic 156

Serviceberry

Apple chlorotic leaf spot 27

Sesbania

Plum line pattern 4

Prune dwarf 3,4

Prunus ring spot 3,4

Snapdragon

Fruit pitting of sweet cherry 227

Squash

Cucumber mosaic 4

Prune dwarf 3,4,181,188

Prunus ring spot 3,4,7,130

Yellow bud mosaic 4

Strawberry, cultivated

X-disease 146

Strawberry, sand

Yellow bud mosaic 156

Sweet Basil

Fruit pitting of sweet cherry 227

Tithonia

Prune dwarf 4,181
HANDBOOK NO. 437, U. S. DEPARTMENT OF AGRICULTURE 433

Page

Tobacco

Nicotiana glutinosa

Peach rosette 73,75,135,136

N. megalosiphon

Plum line pattern 171, i 72, 174

N. rustica

Yellow bud mosaic 157

Page

N. tahaccum

Cucumber mosaic 258, 239

Fruit pitting of sweet cherry 227

Rosette mosaic 135,136

Yellow bud mosaic 157

Tobacco mosaic 256

X-disease 146

i^ U.S. GOVERNMENT PRINTING OFFICE 1975 0 479-462