Boli Capsun Si Arbusti

FOOD AND AGRICULTURE ORGANIZATION INTERNATIONAL PLANT
OF THE UNITED NATIONS GENETIC RESOURCES INSTITUTE
FAO/IPGRI TECHNICAL GUIDELINES
FOR THE
SAFE MOVEMENT OF
SMALL FRUIT GERMPLASM
Edited by
M. Diekmann, E.A. Frison and T. Putter
In collaboration with the
Small Fruit Virus Working Group
of the
International Society for
Horticultural Science
2
CO N T E N T S
Introduction 4
Contributors 6
General Recommendations 8
Technical Recommendations 8
A. Pollen 8
B. Seed 9
C. In vitro material 9
D. Vegetative propagules 9
E. Disease indexing 10
F. Therapy 11
Descriptions of Pests 13
Fragaria spp. (strawberry) 13
Viruses 13
1. Ilarviruses 13
2. Nepoviruses 14
3. Pallidosis 15
4. Strawberry crinkle virus (SCrV) 17
5. Strawberry latent C virus (SLCV) 18
6. Strawberry mild yellow-edge 19
7. Strawberry mottle virus (SMoV) 21
8. Strawberry pseudo mild
yellow-edge virus (SPMYEV) 22
9. Strawberry vein banding
virus (SVBV) 23
Diseases of unknown etiology 25
1. Chlorotic fleck 25
2. June yellows of strawberry 26
3. Leafroll 28
4. Vein yellowing 29
Prokaryotic diseases - ‘MLOs’ 30
1. Aster yellows 30
2. Strawberry green petal 31
3. Witches-broom and multiplier
disease
33
Prokaryotic diseases - bacteria 35
1. Strawberry angular leaf spot 35
2. Strawberry bacterial wilt 36
3. Marginal chlorosis of strawberry 37
Fungal diseases 38
1. Alternaria leaf spot 38
2 Anthracnose 39
3. Fusarium wilt 40
4. Phytophthora crown rot 41
5. Strawberry black root rot 42
6. Strawberry red stele (red core) 43
7. Verticillium wilt 44
Ribes spp. (currant, gooseberry) 45
Viruses 45
1. Alfalfa mosaic virus (AMV) 45
2. Cucumber mosaic virus (CMV) 46
3. Gooseberry vein banding virus
(GVBV) 48
4. Nepoviruses 50
5. Tobacco rattle virus (TRV) 51
Diseases of unknown etiology 53
1. Black currant yellows 53
2. Reversion of red and black currant 54
3. Wildfire of black currant 56
4. Yellow leaf spot of currant 57
Prokaryotic disease 58
Full blossom of currant 58
Fungal diseases 59
1. American powdery mildew 59
2 Anthracnose (leaf spot) 60
Rubus spp. (blackberry, raspberry) 62
Viruses 62
3
1. Blackberry calico virus (BCV)
(see also wineberry latent virus) 62
2. Black raspberry necrosis virus
(BRNV) 63
3. Bramble yellow mosaic virus 65
4. Cucumber mosaic virus (CMV) 66
5. Ilarviruses 67
6. Nepoviruses 68
7. Raspberry bushy dwarf virus
(RBDV) 70
8. Raspberry leaf mottle virus (RLMV) . 72
9. Raspberry leaf spot virus 73
1.
2.
3.
4 .
5 .
6 .
10.
11.
12.
13.
Raspberry vein chlorosis virus
(RVCV) 75
Raspberry yellow spot virus
(RYSV) 76
Rubus yellow net virus (RYNV) 77
Wineberry latent virus (WLV) (see
also blackberry calico virus (BCV)) 78
Prokyarotic diseases - 'MLOs'
1. Boysenberry decline
2. Rubus stunt
Prokyarotic diseases - bacteria
1. Crown and cane gall
2. Fireblight
3. Hairy root
Fungal diseases
1. Blackberry rust
2. Cane and leaf rust
80
80
82
83
83
84
85
85
85
86
3.
3. Downy mildew 87
4. Late leaf rust 88
5. Orange rust 88
6. Phytophthora root rot 90
7. Verticillium wilt
(bluestem or bluestripe wilt) 91
8. White root rot 92
Vaccinium spp. (blueberry, cranberry) 93
Viruses 93
Blueberry red ringspot virus
(BRRV) 93
Blueberry scorch virus (BBScV) 95
Blueberry shock ilarvirus (BSIV) 96
Blueberry shoestring virus (BSSV) 97
Nepoviruses 98
Ringspot of cranberry 100
Disease of unknown etiology 101
Blueberry mosaic 101
Prokaryotic diseases - ‘MLOs’ 102
1. Blueberry stunt (BBS) 102
2. Cranberry false blossom 104
3. Witches’-broom 106
Prokaryotic disease - bacteria 107
Crown gall 107
Fungal diseases 108
1.
2.
4.
5.
6.
7.
8.
9.
Botryosphaeria stem canker 108
Cottonball (Hard rot,
Tip blight) 109
Fusicoccum Canker
(Godronia canker) 110
Mummy berry disease 111
Phomopsis canker of blueberry 112
Phytophthora root rot 113
Rose bloom 114
Twig blight 116
Upright dieback
(Phomopsis canker of
cranberry) 117
Pests of small fruit
Arthropods
Nematodes
118
118
119
Appendix 1: Institutions maintaining small fruit
germplasm 121
4
INT RODUCT I ON
Collecting, conservation and utilization of plant genetic resources and their global
di st ri but i on are essent i al component s of i nt ernat i onal crop i mprovement
programmes.
Inevitably, the movement of germplasm involves a risk of accidentally introducing
plant quarantine pests* along with the host plant material; in particular, pathogens
that are often symptomless, such as viruses, pose a special risk. In order to
minimize, this risk, effective testing (indexing) procedures are required to ensure
that distributed material is free of pests that are of quarantine concern.
The ever-increasing volume of germplasm exchanged internationally, coupled with
recent rapid advances in biotechnology, has created a pressing need for crop-
specific overviews of the existing knowledge in all disciplines relating to the
phytosanitary safety of germplasm transfer. This has prompted FAO and IPGRI to
launch a collaborative programme for the safe and expeditious movement of
germplasm, reflecting the complementarity of their mandates with regard to the
safe movement of germplasm. FAO, as the depository of the International Plant
Protection Convention of 1951, has a long-standing mandate to assist its member
governments to strengthen their Plant Quarantine Services, while IPGRI’s mandate
- inter alia - is to further the collecting, conservation and use of the genetic
diversity of useful plants for the benefit of people throughout the world.
The aim of the joint FAO/IPGRI programme is to generate a series of crop-specific
technical guidelines that provide relevant information on disease indexing and
other procedures that will help to ensure phytosanitary safety when germplasm is
moved internationally.
The technical guidelines are produced by meetings of panels of experts on the crop
concerned, who have been selected in consultation with the relevant specialized
institutions and research centres. The experts contribute to the elaboration of the
guidelines in their private capacities and do not represent the organizations to
whom they belong. FAO, IPGRI and the contributing experts cannot be held
responsible for any failures resulting from the application of the present guidelines.
By their nature, they reflect the consensus of the crop specialists who attended the
* The word ‘pest’ is used in this document as it is defined in the revised edition of the International Plant
Protection Convention. It encompasses all harmful biotic agents ranging from viroids to weeds.
5
meeting, based on the best scientific knowledge available at the time of the
meeting. The experts that have contributed to this document are listed after this
introduction.
The technical guidelines are written in a short, direct, sometimes ‘telegraphic’ style,
in order to keep the volume of the document to a minimum and to facilitate
updating. The guidelines are divided into two parts: The first part makes general
recommendations on how best to move germplasm of the crop concerned and
mentions available intermediate quarantine facilities when relevant. The second
part covers t he i mport ant pest s and di seases of quarant i ne concern. The
information given on a particular pest or disease does not pretend to be exhaustive
but concentrates on those aspects that are most relevant to quarantine. Where
possible, acronyms for viruses are according to Hull et al. (1991)**
The present guidelines were developed at a meeting held in Corvallis, Oregon
from 13 to 15 August, 1992 in collaboration with the Small Fruit Virus Working
Group of the International Society of Horticultural Science (ISHS). The meeting
was hosted by the USDA-ARS National Clonal Germplasm Repository.
** Hull, R., Milne, R.G. & Van Regenmortel, M.H.V. 1991. A list of proposed standard acronyms for
plant viruses and viroids. Arch. Virol. 120:151-164.
6
CONTRI BUTORS
Peter R. Bristow
Washington State University
7612 Pioneer Way East
Puyallup, WA 98371-4998
USA
Tel. (1-206) 840-4529
Fax (1-206) 840-4671
A. Teifion Jones
Scottish Crop Research Institute
Invergowrie
Dundee DD25DA
Scotland, UK
Tel. (44-382) 562731
Fax (44-382) 562426
e-mail [email protected]
Richard H. Converse
USDA
Agriculture Research Service
Horticultural Crops Research
Laboratory
3420 NW Orchard Avenue
Corvallis, OR 97330-5098
USA
Tel. (1-503) 754-6078
Fax (1-503) 750-8764
Emile A. Frison
IPGRI
Via delle Sette Chiese 142
00145 Rome
Italy
Tel. (39-6) 51892221
Fax (39-6) 5750309
e-mail [email protected]
Graeme Guy
Department of Agriculture
Swan Street
Burnley 3121, Victoria
Australia
Tel. (03) 810 1511
Fax (03) 819 5653
Kim Hummer
USDA-ARS-NCGR
33447 Peoria Road
Corvallis, OR 97330
USA
Tel. (1-503) 750-8712
Fax (1-503) 750-8717
e-mail hummerk.bcc.orst.edu
John L. Maas
USDA, ARS
Fruit Laboratory
B-004, Room-111, BARC-W
Beltsville, MD 20705
USA
Tel. (1-301) 504-7653
Fax (1-301) 504-5062
Robert R. Martin
Agriculture Canada
6660 NW Marine Drive
Vancouver
British Columbia V6T 1X2
Canada
Tel. (1-604) 224-4355
Fax (1-604) 666-4994
e-mail [email protected]
Joseph Postman
USDA-ARS-NCGR
33447 Peoria Road
Corvallis, OR 97333
USA
Tel. (1-503) 750-8712
Fax (1-503) 750-8717
e-mail [email protected]
Tonie Putter
Plant Protection Service
FAO
Rome
Italy
Tel. (39-6) 57974022
Fax (39-6) 57973152
e-mail [email protected]
Donald C. Ramsdell
Department of Botany and Plant
Pathology
Michigan State University
East Lansing, MI 48824
USA
Tel. (1-517) 355-0483
Fax (1-517) 353-1926
e-mail [email protected]
7
OB S E R V E R S
Joseph Foster
NPGQC
Building
Beltsville, MD 20705
580 BARC-E
USA
Tel. (1-301) 504-8485
David A. Raworth
Agriculture Canada
6660 NW Marine Drive
Vancouver
British Columbia V6T 1X2
Suzanne Hurtt
USDA, ARS, National Germplasm
Resources Laboratory
Building 580 BARC-East
13004 Baltimore Avenue
Beltsville, MD 20705-2350
USA
Tel. (1-301) 504-8630
Fax (1-301) 504-8397
Canada
Tel. (1-604) 224-4355
Fax (1-604) 666-4994
Sara Spiegel
Department of Virology
The Volcani Center
Bet Dagan
50-250
Israel
Tel. (972-3) 9683561
Fax (972-3) 9604180
e-mail [email protected]
Richard Stace-Smith
Agriculture Canada
6660 NW Marine Drive
Vancouver
British Columbia V6T 1X2
Canada
Tel. (1-604) 224-4355
Fax (1-604) 666-4994
Laurene Levy
USDA, ARS, National Germplasm
Resources Laboratory
Room 106, Building 011A, BARC-W
Beltsville, MD 20705
USA
Tel. (1-301) 504-5437
Fax (1-301) 504-5435
Edward V. Podleckis
USDA, ARS, National Germplasm
Resources Laboratory
Room 252, Building 011A, BARC-W
Beltsville, MD 20705
USA
Tel. (1-301) 504-6209
Fax (1-301) 504-5435
Garry Wood
The Horticulture and Food Research
Institute of New Zealand Ltd.
Private Bag 92169
Auckland
New Zealand
Tel. (64-9) 849-3660
Fax (64-9) 846-3330
8
GENERAL RECOMMENDATI ONS
Plant material should be obtained directly from the lowest risk source
available: This could be one of the institutions listed below where virus-
tested germplasm is maintained, or one of the other sources listed in the
same country or continent than to move it over or longer distances.
All material should be kept in containment and undergo indexing as well as
therapy procedures, if necessary, and retesting before being released.
Germplasm that is infected with a pathogen of quarantine concern which
cannot be eradicated readily should be maintained in containment until
sui t abl e t herapy met hods become avai l abl e and have been appl i ed
successfully. In case healthy germplasm is available from other sources, the
infected material should be destroyed.
TECHNI CAL RECOMMENDATI ONS
Small fruit germplasm can be moved as pollen, seed, in vitro material or as
vegetative propagules.
A. Pollen
Pollen should be collected from pathogen-tested plants in containment.
Pollinated mother plants and progeny seedlings derived from other pollen
sources should be tested for pollen-transmitted viruses and virus-like agents
known to occur in that crop.
Imported pollen, found to carry arthropod pests
bees, should be destroyed or treated and retested.
and fungal pathogens of
9
B. Seed
Seed should be free of pulp, air-dried, inspected for the absence of insect
pests and fumigated when necessary.
Seed may be surface-disinfected with 0.5% sodium hypochlorite for 10
minutes at room temperature to avoid externally seed-borne pathogens.
Seeds should be germinated in sterilized potting media and
insect-proof facility.
grown in an
Seedlings should be tested for seed-transmitted viruses.
C. In vitro material
In vitro material should be derived from pathogen-tested sources.
In vitro material obtained from other sources should be tested for viruses
and other systemic pathogens known to occur in that crop.
For the movement of in vitro material, neither charcoal, fungicides or
antibiotics should be added to the medium.
In vitro material should be shipped in transparent containers and visually
inspected for bacteria, fungi and arthropods. contaminated material should
be treated or destroyed.
D. Vegetative propagules
Vegetative propagules should be derived directly from sources that have
been pathogen-tested following the recommendations in this guide and
found free from i n f e c t i o n .
Vegetative propagules from sources not tested for pathogens should only be
used when in vitro material or seed is not available.
Runner tips or stem cuttings should be obtained in preference to roots,
rooted cuttings or rooted plants.
10
E.
Vegetative propagules should be washed free of soil, visually inspected, and
treated for external arthropod and nematode pests by either fumigation with
an ovicidal material or dipping in an appropriate insecticide.
Vegetative propagules should be established in a sterilized potting mix and
maintained in a containment facility. A systemic insecticide (e.g. aldicarb or
oxamyl) should be placed in the root zone at the time of planting to kill any
possible arthropods and foliar nematodes within the plant tissue.
Once established, vegetative
tidelines outlined below.
Disease indexing
propagules should be indexed according to the
Many of the pathogens found in small fruit species are latent and cannot be
detected by visual assessment. It is essential that all material, including plants
derived from tissue culture, be extensively tested.
To optimize the sensitivity of the biological tests, donor source plants and indicator
plants should be actively growing and be free from pests and diseases. These
conditions are best provided in insect-proof glasshouse facilities with good
temperature control to maintain 20-25°C and supplementary high light intensity
during 14-18 h per day.
Mechanical inoculation. Tests are best made in early spring when plants are
actively growing. Soft, young donor plant leaves or, where possible for Vaccinium,
flower petals, should be homogenized in a 2% nicotine alkaloid solution in water.
Concentrated nicotine alkaloid is a very hazardous and poisonous substance and
should be handled with great care. If finger inoculation is used, plastic gloves
should be worn, and inhalation of the fumes be avoided as much as possible. In
many cases 0.05 M phosphate buffer with 2% polyvinyl pyrrolidone (PVP; MW
40,000) is a good alternative. A suitable abrasive should be used either in the
extraction buffer (e.g. Celite) or dusted on the test plant leaves prior to inoculation
(e.g. 300-mesh carborundum). Test plants should be inoculated as soon as the
extract is made and should be rinsed with water immediately after inoculation.
Cucumber cotyledons should be inoculated before the tip of the first true leaf is
11
exposed more than 3-4 mm; Chenopodium quinoa should be inoculated when less
than 15 cm tall; Nicotiana bethamiana should be used when 3-6 leaves are suitable
for inoculation and before flower buds appear. Plants should be observed for
symptoms for up to three weeks after inoculation.
Graft-inoculation. Actively growing donor and recipient plants should be used.
Bottle grafts are often used for Ribes, Rubus and Vaccinium and leaflet grafts for
Fragaria. Grafts are considered successful if leaflet grafts appear viable after two
weeks and bottle grafts after three to four weeks. Depending on the virus and host
species, sympt oms may appear af t er i ncubat i on t i mes r angi ng f r om weeks
(Fragaria) to two growing seasons (reversion disease in Ribes). Details are given in
the respective descriptions.
F. Therapy
Thermotherapy applied to well established plants for several weeks, followed by
excision of explants from treated plants, is the method of choice for the four
genera. Explants are regenerated on a nutrient medium in vitro to fully developed
plants. It should be noted that not all plants resulting from a thermotherapy are
pathogen-free. Therefore, successfully regenerated plants should be indexed
according to the procedures recommended in these guidelines. In the case of
commercial varieties, evaluation for trueness to horticultural type is necessary.
Fragaria
Well rooted plants in large porous pots should be placed in a growth chamber at
ambient temperature. A gradual 2°C increase per day should be employed to a
constant 38°C. Plants should be held at 38°C for at least 21 days (longer if the virus
is heat stable, e.g. strawberry veinbanding virus). Explants of 0.5 mm or smaller
should be excised and regenerated on a nutrient medium in vitro to whole plants.
Testing for pathogens should be done after plants have gone through natural
winter dormancy.
Vaccinium
Vaccinium corymbosum is very sensitive to high temperature. Plant growth at
38°C is improved by placing plants in a CO
2
-enriched atmosphere (1200 ppm CO
2
) .
New shoot cuttings 10-20 mm long are taken after 6 weeks of growth under these
conditions. After treating cut ends with rooting hormone (1000 ppm IBA), cuttings
12
are successfully regenerated in mist propagation beds. The pH of the rooting
medium in the mist bed should be between 3.5 and 5.5.
Rubus
After 3 weeks of thermotherapy at 36-38°C meristem tips of 0.5 mm should be
excised and regenerated. Alternatively, Rubus primocane tips, 5 mm long, can be
mist-bed propagated after a longer treatment period (6-8 weeks), following rooting
hormone dip treatment of the base of cuttings. Also root pieces may be heat-
treated.
Ribes
Use adequate nutrients to assure vigorous growth. Ribes may not tolerate constant
temperatures above 35°C during thermotherapy. Three weeks at 36°C has been
adequate to eliminate several viruses of Ribes. In cases where meristem culture is
difficult for tissue culture, prolonged exposure (up to 6 weeks) at temperatures
below 36°C may permit production of some clean plants from 5-10 mm shoot tips.
General References
Caruso, F.L. & Ramsdell, D.C. (eds.). 1994. Compendi um of Bl ueberry and
Cranberry Diseases. APS Press (in press).
Conver se, R. H. ( ed. ) . 1987. Virus Diseases of Small Fruits. Uni t ed St at es
Department of Agriculture, Agriculture Handbook No. 631, Washington,
D.C.
Converse, R. H. 1992. Modern approaches to strawberry virus research. Ac t a
Hortic. 308:18-30.
Ellis, M.A., Converse, R.H., Williams, R.N. & Williamson, B. (eds.). 1991.
Compendium of Raspberry and Blackberry Diseases and Insects. APS Press,
St. Paul.
Frazier, N.W. 1974. Six new strawberry indicator clones evaluated for the detection
and diagnosis of twelve graft-transmissible diseases. Plant Dis. Reptr 5 8:28-
31.
Hancock, J.F., Maas, J.L., Shanks, C.H., Breen, P.J. & Luby, J.J. 1991. Strawberries
(Fragaria). pp. 489-546. In: Genetic Resources of Temperate Fruit and Nut
Crops. Eds. J.N. Moore and J. R. Ballington, Jr. Acta Hortic. 290.
Maas, J.L. (ed.). Compendium of Strawberry Diseases. APS Press, St. Paul.
Spiegel, S., Frison, E.A. & Converse, R.H. 1993. Recent developments in therapy
and virus-detection procedures for international movement of clonal plant
germ plasm. Plant Dis. 7 7:1176-1180.
13
DESCRIPTIONS OF PESTS
Fragaria spp. (strawberry)
Viruses
1. Ilarviruses
Two ilarviruses are reported in Fragaria - tobacco streak virus (TSV) and Fragaria
chiloensis ilarvirus (FCIV). They have quasi-isometric particles of 22-35 nm in
diameter; for FCIV bacilliform particles up to 57 nm long have also been reported.
Symptoms
TSV is symptomless or causes mild transient symptoms on commercial strawberry
cultivars. FCIV is symptomless in F. chiloensis.
Host range
TSV occurs in commercial strawberry cultivars and is known to have a wide
natural host range including both herbaceous and woody plants. FCIV occurs in
wild F. chiloensis.
Geographical distribution
TSV was reported from Australia, Israel and North America; occurs probably
worldwide. FCIV was detected in Chile in the Andes and coastal mountain areas.
Transmission
Thrips (Frankliniella occidentalis and Thrips tabaci) have been reported as vectors
of TSV in several annual crops. No vectors are known for FCIV. Both viruses are
transmitted through pollen and seed.
Therapy
Heat therapy (38°C) for six weeks followed by tissue culture of meristem tips 0.5
mm in length should eliminate TSV in a high percentage of resulting plants.
Indexing
ELISA is reliable for leaves, seeds and pollen. Leaflet grafted F. vesca indicator
clones show symptoms 10-30 days after grafting. New growth may appear normal
but plants remain infected.
14
References
Kaiser, W.J., Wyatt, S.D. & Pesho, G.R. 1982. Natural hosts and vectors of tobacco
streak virus in eastern Washington. Phytopathology 7 2:1508-1512.
Spi egel , S. , Mart i n, R. R. , Legget t , F. , t er Borg, M. & Post man, J. 1993.
Characterization and geographical distribution of a new ilarvirus from
Fragaria chiloensis. Phytopathology 83:991-995.
Stace-Smith, R., Converse, R.H. & Johnson, H.A. 1987. Tobacco streak virus in
strawberry. pp. 57-60. In: Virus Diseases of Small Fruits. Ed. R.H. Converse.
United States Department of Agriculture, Agriculture Handbook No. 631,
Washington, D.C.
2. Nepoviruses
Five nepoviruses are important in Fragaria spp.: arabis mosaic (ArMV), raspberry
ringspot (RRSV), strawberry latent ringspot (SLRSV), tomato black ring (TBRV)
and tomato ringspot (ToRSV). Virus particles are isometric, about 30 nm in
diameter, profiles angular.
Symptoms
Newly infected plants may show blotchy leaf mottling and occasional necrosis on
leaf tissue; infected plants become progressively stunted and eventually die.
Fig. 1. Necrosis of young leaves in Fragaria vesca var.
semperflorens ‘Alpine’ two weeks after grafting from a plant
infected with tobacco streak virus. (Dr. R.H. Converse,
Horticultural Crops Research Laboratory, Corvallis)
15
Host range
Nepoviruses occur in Fragaria spp. and many other wild and cultivated hosts. The
experimental host range includes many commonly used test plants.
Geographical distribution
AMV, RRSV, SLRSV and TBRV occur in strawberry in Europe. ToRSV occurs in
native F. chiloensis along the coast of northern California and in commercial
strawberry in North America.
Transmission
In nature transmitted by nematode vectors belonging to the Dorylaimidae. A high
level of pollen and seed transmission occurs in Fragaria spp.
Therapy
No information is available for Fragaria.
Indexing
Nepoviruses are readily detected by ELISA. However, many serological variants
ar e des cr i bed t hat may not r eact wi t h al l ant i s er a. Nepovi r us es can be
mechanically transmitted to herbaceous hosts, which are satisfactory for virus
detection but not for identification.
Reference
Sections on nepoviruses in: Virus Diseases of Small Fruits. Ed. R.H. Converse.
Uni t ed St at es Depar t ment of Agr i cul t ur e, Agr i cul t ur e Handbook No. 631,
Washington, D.C.
3. Pallidosis
Cause
The pallidosis agent (PA) is a probable virus of undetermined morphology and
identity. Pallidosis disease (PD) is associated with several high molecular weight
double-stranded RNA (dsRNA) bands of 4.3-5.2 x 10
6
daltons in diseased plants.
Symptoms
In strawberry cultivars PA is either latent or causes very mild, non-diagnostic
symptoms.
16
Fig. 2. Pallidosis disease - left:
distorted, chlorotic leaves in graft-
inoculated F. virginiana clone UC-10;
right: healthy plant. Dr. R.H. Converse,
Horticultural Crops Research
Laboratory, Corvallis)
Host range
Fragaria spp.
Geographical distribution
Australia (probably introduced from the US), Canada and USA.
Transmission
PA is seed-borne in F. vesca and spreads in the field by unknown means.
Therapy
Meristem tip culture.
Indexing
PA causes epinasty, distortion, chlorosis and dwarfing in graft-inoculated F .
virginiana clones UC-10 or UC-11, and no symptoms in graft-inoculated F. vesca
clones. ‘The presence of dsRNA bands in the 4.3-5.2 x l0
6
dalton range allows
presumptive identification of PA in complex infections where other viruses can
mimic the symptoms of PA on clones UC-10 or UC-11.
References
Fulton, J.P. 1987. Strawberry pallidosis. pp. 55-56. In: Virus Diseases of Small
Fruits. Ed. R.H. Converse. United States Department of Agriculture,
Agriculture Handbook No. 631, Washington, D.C.
17
Yoshikawa, N. & Converse, R.H. 1990. Strawberry pallidosis disease: distinctive
dsRNA species associated with latent infections in indicators and in diseased
strawberry cultivars. Phytopathology 8 0:543-548.
4. Strawberry crinkle virus (SCrV)
A rhabdovirus with membrane-bound bacilliform particles, 69 x 190-380 nm.
Symptoms
Infected cultivars may be symptomless. Sensitive strawberry cultivars may have
dwarfed, distorted, crinkled, or otherwise deformed leaves with chlorotic to
necrotic vein-associated spots. Symptoms are more severe when other viruses are
present.
Host range
Fragaria spp.
Geographical distribution
Worldwide.
Transmission
By strawberry aphids (mainly Chaetosiphon fragaefolii) in a persistent circulative
f as hi on. Ther e i s a 14 days mi ni mum l at ent per i od f r om acqui s i t i on t o
transmission.
Fig. 3. Strawberry crinkle in Fragaria
vesca clone UC-4. (Dr. R.H. Converse,
Horticultural Crops Research
Laboratory, Corvallis)
18
Therapy
Thermotherapy and meristem tip culture.
Indexing
Leaflet grafting onto clones of F. vesca. Symptoms vary from slight angular
epinasty to severe leaflet crinkling. Petiole and stolon lesions, often causing
bending at the lesion, are diagnostic symptoms for SCrV infection.
Reference
Frazier, N.W., Sylvester, E.S. & Richardson, J. 1987. Strawberry crinkle. pp. 20-25.
In: Virus Diseases of Small Fruits. Ed. R.H. Converse. United States Department of
Agriculture, Agriculture Handbook No. 631, Washington, D.C.
5. Strawberry latent C virus (SLCV)
A rhabdovirus with membrane-bound bacilliform particles, 68 x 190-380 nm.
Symptoms
Infected cultivars may be symptomless. In indicator plants F. vesca clone UC-5
SLCV produces diagnostic symptoms of severe epinasty in new leaves, followed
by dwarfing, mottling and distortion of subsequent leaves without epinasty; clones
UC-4 and UC-6 are symptomless.
Fig. 4. Symptoms of strawberry
latent C virus several months after
grafting on Fragaria vesca ‘EMK’.
(Dr. R.H. Converse, Horticultural
Crops Research Laboratory,
Corvallis)
19
Host range
Fragaria spp.
Geographical distribution
Eastern North America and Japan.
Transmission
In nature SLCV is persistently transmitted by Chaetosiphon fragaefolii aphi d
.
Experimentally, it also has been transmitted by leaflet grafting and by dodder.
Therapy
Thermotherapy and meristem tip culture.
References
McGrew, J.W. 1987. Strawberry latent C. pp. 29-30. In: Virus Diseases of Small
Fruits. Ed. R.H. Converse. United States Department of Agriculture,
Agriculture Handbook No. 631, Washington, D.C.
Yoshikawa, N., Inouye, T. & Converse, R.H. 1986. Two types of rhabdovirus in
strawberry. Ann. Phytopathol. Soc. Japan 52
2
:437-444.
6. Strawberry mild yellow-edge
Cause
A luteovirus with isometric particles of 25 nm diameter and a potexvirus with rod-
shaped particles of about 14 x 500 nm are associated with the disease.
Fig. 5. Symptoms of strawberry mild
yellow-edge disease in Fragaria vesca
clone UC-4 45 days after grafting:
mottling of young leaves and
premature senescence. (Dr. R.H.
Converse, Horticultural Crops
Research Laboratory, Corvallis)
20
Symptoms
Strawberry cultivars are symptomless carriers of strawberry mild yellow-edge
disease (SMYED). In combination with other viruses, symptoms vary and include
chlorosis, stunting and marginal or overall chlorosis.
Host range
In addition to cultivated strawberries, SMYED has been found in nature in F.
chiloensis in Chile and in several Duchesnea spp. in Japan.
Geographical distribution
Worldwide.
Transmission
Naturally by aphids, mostly in the genus Chaet os i phon, in a persistent or
circulative manner. C. fragaefolii seems to be the major vector. Experimentally,
SMYED can be graft- or aphid-transmitted to F. vesca indicators.
Therapy
Thermotherapy and meristem tip culture.
Indexing
Leaflet grafting onto sensitive clones of F. vesca. Clone UC-4 and ‘Alpine’ seedlings
usually show typical symptoms within 3 weeks after inoculation while clone UC-6
remains symptomless. Potex virus particles can be detected in crude sap of
SMYED-infected plants by ELISA and by immunosorbent electron microscopy.
References
Converse, R.H., Martin, R.R. & Spiegel, S. 1987. Strawberry mild yellow edge. pp.
25-29. In: Virus Diseases of Small Fruits. Ed. R.H. Converse. United States
Department of Agriculture, Agriculture Handbook No. 631, Washington,
D.C.
Hadidi, A., Montasser, M.S., Levy, L., Goth, R.W., Converse, R.H., Madkour, M.A.
& Skrzeckowski, L.J. 1993. Detection of potato leafroll and strawberry mild
yellow-edge luteoviruses by reverse transcription-polymerase chain reaction
amplification. Plant Dis. 77:595-601.
Jelkmann, W., Martin, R.R., Lesemann, D.E., Vetten, H.J. & Skelton, F. 1990. A new
potexvirus associated with strawberry mild yellow-edge disease. J. Gen.
Virol. 71:1251-1258.
Spiegel, S. & Martin, R.R. 1992. Detection of strawberry mild yellow-edge disease
in micropropagated strawberry plantlets. Acta Hortic. 308:61-68.
21
7. Strawberry mottle virus (SMoV)
A virus with isometric particles about 32-37 nm in diameter.
Symptoms
SMoV exhibits great strain variation. Severe strains of SMoV may reduce vigour
and fruit yield. SMoV frequently occurs along with other aphid-borne viruses
which results in more severe symptoms.
Host range
Fragaria spp., Duchesnea chrysantha, D. indica and Potentilla sundaica.
Geographical distribution
Worldwide.
Transmission
SMoV is transmitted naturally in a semipersistent manner by Chaetosiphon spp.
and Aptis gossypii SMoV is experimentally transmitted by these and five other
gener a of aphi ds. Mechani cal t ransmi ssi on t o C. qui noa i s possi bl e but
inconsistent.
Therapy
SMoV is one of the easiest of the strawberry viruses to eliminate by thermotherapy.
Entire plants grown at constant 37°C were freed of SMoV in 10-14 days. Meristem
tip culture was effective in eliminating SMoV from cultivars.
Fig. 6. Symptoms of a moderate
strain of strawberry mottle virus in
fragaria vesca ‘EMC’. (Dr. R.H.
Converse, Horticultural Crops
Research Laboratory, Corvallis)
22
Indexing
Leaflet grafting or transmission by C. fragaefolii to F. vesca clones UC-4, UC-5 and
UC-6, as well as F. vesca ‘Alpine’ seedlings. Initial symptoms on young leaves vary
from asymmetric net vein chlorosis and epinasty to leaf tip necrosis. Mild strains
cause persistent leaf mottling symptoms. Intermediate strains cause fine vein
clearing and fusing but no mottle. Leaves are small and distorted.
References
Mellor, F.C. & Krczal, H. 1987. Strawberry mottle. pp. 10-16. In: Virus Diseases of
Small Fruits. Ed. R.H. Converse. United States Department of Agriculture,
Agriculture Handbook No. 631, Washington, D.C.
Yoshikawa, N. & Converse, R.H. 1991. Purification and some properties of
strawberry mottle virus. Ann. Appl. Biol. 118:565-576.
8. Strawberry pseudo mild yellow-edge virus (SPMYEV)
A carlavirus with rod-shaped particles, 12 x 625 nm.
Symptoms
Infected strawberry cultivars are symptomless.
Host range
Fragaria spp., Duchesnea chrysantha, D. indica, and Rubus parvifolius.
Geographical distribution
Japan, USA.
Fig. 7. Stippling symptom on an old
‘leaf of Fragaria vesca ‘Alpine’,
characteristic of strawberry pseudo
mild yellow-edge virus infection. (Dr.
R.H. Converse, Horticultural Crops
Research Laboratory, Corvallis)
23
Transmission
Naturally transmitted by the aphids Chaetosiphon fragaefolii and Aphis gossypii
in a semipersistent manner.
Therapy
Unknown.
Indexing
ELISA or dot immunoblot assay. Leaflet grafting onto F. virginiana clone UC-10
and F. vesca clones UC-4 and UC-5. On F. vesca, older leaves become mottled, may
exhibit vein yellowing or stippling, later turn necrotic, and die prematurely. These
symptoms closely resemble those caused on this indicator species by strawberry
mild yellow-edge disease.
References
Frazier, N.W. 1987. Strawberry pseudo-mild yellow edge. pp. 63-64. In: Virus
Diseases of Small Fruits. Ed. R.H. Converse. United States Department of
Agriculture, Agriculture Handbook No. 631, Washington, D.C.
Yoshikawa, N. & Inouye, T. 1986. Purification, characterization and serology of
strawberry pseudo mild yellow-edge virus. Ann. Phytopathol. Soc. Japan
52:643-652.
Yoshikawa, N., Poolpol, P. & Inouye, T. 1986. Use of dot immunobinding assay for
r api d det ect i on of st r awber r y pseudo mi l d yel l ow- edge vi r us. A n n .
Phytopathol. Soc. Japan 52:728-731.
9. Strawberry vein banding virus (SVBV)
A caulimovirus with isometric particles of 40-50 nm diameter.
Symptoms
Non-diagnostic chlorosis may develop in some susceptible strawberry cultivars.
Distinctive symptoms only occur in indicator plants.
Host range
Fragaria spp.
Geographical distribution
Australia, Brazil, Europe, Japan and North America.
24
Fig. 8. Symptoms of strawberry vein
banding virus infection in Fragaria
vesca ‘Alpine’. (Dr. R.H. Converse,
Horticultural Crops Research
Laboratory, Corvallis)
Transmission
In nature, SVBV is aphid-transmitted in a semipersistent manner, primarily by
Chaetosiphon fragaefolii. Five other aphid genera have transmitted this virus
experimentally.
Therapy
Thermotherapy and meristem tip culture.
Indexing
Leaflet grafting onto F. vesca clone UC-6 or F. virginiana clone UC-12. The virus is
very unevenly distributed among leaves of infected cultivars and indicator plants
and is best detected in symptom-bearing leaves. SVBV is detectable by dot
hybridization using homologous cDNA probes.
References
Frazier, N.W. & Morris, T.J. 1987. Strawberry vein banding. pp. 16-20. In: Virus
Diseases of Small Fruits. Ed. R.H. Converse. United States Department of
Agriculture, Agriculture Handbook No. 631, Washington, DC.
Stenger, D.C., Mullin, R.H. & Morris, T.J. 1988. Isolation, molecular cloning, and
detection of strawberry vein banding virus DNA. Phytopathology 7 8:154-
159.
25
Diseases of unknown etiology
1. Chlorotic fleck
Cause
Probably a virus.
Symptoms
Latent in most strawberry cultivars.
Host range
Fragaria spp.
Geographical distribution
Reported only from the state of Louisiana in the USA.
Transmission
Experimentally to F. vesca and F. virginiana by leaflet grafting and by the aphid
Aphis gossypii. Not mechanically transmissible.
Therapy
Thermotherapy, 35°C for 40 days or longer, and meristem tip culture.
Fig. 9. Chlorotic fleck symptoms in
Fragaria vesca indicator plant.
(Dr. R.H. Converse, Horticultural
Crops Research Laboratory,
Corvallis)
26
Indexing
By leaflet grafting to F. vesca and F. virginiana indicator clones. In F. vesca
indicators young leaves are distorted; vein clearing followed by small chlorotic
flecks is sometimes evident. Chlorotic fleck agent is not clearly distinguished from
other viruses by its symptomatology.
Reference
Fulton, J.P. 1987. Strawberry chlorotic fleck. p. 60. In: Virus Diseases of Small
Fruits. Ed. R.H. Converse. United States Department of Agriculture, Agriculture
Handbook No. 631, Washington, D.C.
2. June yellows of strawberry
Cause
Unknown. No viruslike particles nor other recognizable pathogens were observed
in tissues exhibiting symptoms of this non-graft-transmissible strawberry disorder.
However, a group of double-stranded RNA (dsRNA) species have been associated
with June yellows (JY) symptoms in strawberry.
Symptoms
Leaf blades of affected cultivated strawberry plants develop clearly delimited,
usually sectorial, chlorotic areas. Symptoms diminish in warm weather. White
streaks may also appear and persist in leaf blades. Plants affected with JY usually
become progressively stunted
over a few seasons and di e
prematurely.
Host range
Fragaria spp.
Geographical distribution
Worldwide.
Fig. 10. Symptoms of June yellows
disorder in ‘Cambridge Favourite’. Left:
leaf from a healthy plant; other leaves
show delimited chlorotic areas.
(Scottish Crop Research Institute,
Invergowrie)
27
Transmission
In seed and by vegetative propagation. JY behaves as if it were a genetic trait and
can be transmitted by either parent of a seedling. JY may not appear in the clonal
progeny of a seedling for a number of asexual generations and then reappear. JY is
not transmissible by grafting, by sap inoculation, or by vectors.
Therapy
JY has not been eliminated by thermotherapy or meristem tip culture.
Indexing
There is no satisfactory procedure for detecting JY in symptomless plants, such as
potential parental lines for breeding. The dsRNAs that have been associated with
JY are present at too low a level for routine testing and have only been found in
plants exhibiting JY symptoms. Progeny testing by selfing is the best currently
available technique for screening potential parents to avoid JY in seedlings. Much
otherwise excellent strawberry genetic material is currently unaccessible to plant
breeders because of the threat of JY transmission to progeny.
References
Hughes, J. d’A. 1989. Strawberry June yellows - a review. Plant Path. 38:146-160.
Watkins, C.A., Roberts, I.M. & Jones, A.T. 1992. Ultrastructural changes associated
with June Yellows in strawberry and with leaf yellowing symptoms of viral
and genetic origin in Fragaria, Rubus and Ribes. Ann. Appl. Biol. 121:151-
160
Watkins, C.A., Jones, A.T., Mayo, M.A., & Mitchell, M.J. 1990. Double-stranded
RNA analysis of strawberry plants affected by June yellows. Ann. Appl. Biol.
117:73-83.
Wills, A.B. 1987. Strawberry June yellows. pp. 69-72. In: Virus Diseases of Small
Fruits. Ed. R. H. Converse. Uni t ed St at es Depart ment of Agri cul t ure,
Agriculture Handbook No. 631, Washington, D.C.
28
3. Leafroll
Cause
Unknown. No viruslike particles or other identified pathogens were observed in
tissues exhibiting symptoms.
Symptoms
In cultivated strawberries and Fragaria indicator plants, the diagnostic symptom is
downward roiling of leaflet margins, varying from slight rolling to complete
inward rolling of both leaflets to form a tubular shape. Leaves are chlorotic, rugose
and exhibit vein clearing. All cultivars are susceptible, and there is no latency. The
disease, while limited in occurrence, is very damaging to infected plants.
Host range
Fragaria spp.
Geographical distribution
Northeastern part of North America and Kazakhstan.
Transmission
Natural spread occurs by unknown means. The agent is transmitted by grafting,
but not mechanically.
Therapy
Th i s d i s e a s e a g e n t i s n o t
inactivated by thermotherapy.
Fig. 11. Symptoms of strawberry
leafroll in Fragaria vesca clone UC-5.
(Dr. R.H. Converse, Horticultural Crops
Research Laboratory, Corvalis)
29
Indexing
Leafroll is self-evident in cultivated strawberries and in many Fragaria species. F
.
vesca clone UC-3 inoculated with leafroll by leaflet grafting is very susceptible,
whi l e F. vesca clones UC-4 and UC-6 are symptomless. After grafting, the
incubation period may be as long as six months.
Reference
Frazier, N.W. 1987. Strawberry leafroll. pp. 61-62. In: Virus Diseases of Small
Fruits. Ed. R.H. Converse. United States Department of Agriculture,
Agriculture Handbook No. 631, Washington, D.C.
4. Vein yellowing
Cause
Probably a virus.
Symptoms
In cultivated strawberries and Fragaria vesca indicator plants, the diagnostic
symptom is very striking vein yellowing. This symptom is obvious in spring and
autumn but is masked in summer. The disease is not damaging to infected plants.
Host range
Fragaria spp.
Geographical distribution
Japan.
Fig. 12. Strawberry vein yellowing
disease. (Dr. N. Yoshikawa, Iwate
University, Morioka)
30
Transmission
Natural spread occurs by unknown means. Experimentally, it is transmitted by
leaflet grafting. Aphid transmission tests using Chaetosiphon fragaefolii and Aphis
gossypii were negative. Not mechanically transmissible.
Therapy
Not reported.
Indexing
F. vesca clones UC-4, UC-5 or UC-6 show symptoms one to two weeks after
grafting of symptomless, infected leaflets.
Reference
Yoshikawa, N. & Inouye, T. 1988. Strawberry viruses occurring in Japan. Acta
Hortic. 236:59-67.
Prokaryotic diseases - ‘MLOs’
1. Aster yellows
Cause
Aster yellows (AY), a non-cultivable mollicute, often referred to as a mycoplasma-
like organism (MLO). Strawberry green petal MLO which is identical to clover
phyllody MLO, has been assigned to Type III, one of three major AY Types.
Symptoms
Cultivated strawberries become dwarfed, with chlorotic, cupped leaves, turning
red, later brown and flat on the ground. Flowers show virescent petals and various
degrees of phyllody and flower proliferation, depending on the AY strain, cultivar
and time of infection. No immunity or latency are known for AY in Fragaria.
Host range
In addition to Fragaria spp., AY has a host range of more than 300 species in 50
families.
Geographical distribution
North America. Similar diseases occur in Europe, Russia and Japan.
31
Transmission
By leafhoppers. Western North American strains of AY are transmitted by 27
leafhopper species, of which Macrosteles fascifrons, Colladonus montanus, and C.
geminatus have experimentally transmitted AY to or from Fragaria but do not
favour Fragaria as a host. Therefore other leafhoppers may be ‘important in the
spread of AY to strawberry in western North America. Eastern strains of AY are
only transmitted by M. fascifrons.
Therapy
No specific information for strawberry. In periwinkle, AY was eliminated by hot
water therapy.
Indexing
AY produces symptoms on all Fragaria species and cultivars tested, and generally
is eventually lethal in cultivars. AY is difficult to distinguish from green petal
when the two mollicutes are co-existent. Antisera against AY do not recognize
green petal ML0 (non-cultivable mollicute) and vice versa.
References
Chiykowski, L.N. 1987. Aster yellows in strawberry. pp. 31-34. In: Virus Diseases
of Small Fruits. Ed. R.H. Converse. United States Department of Agriculture,
Agriculture Handbook No. 631, Washington, D.C.
Clark, M.F. & Davies, D.L. 1984. Mycoplasma detection and characterization. pp
108-109. In: East Malling Res. Stn. Annu. Rpt. 1983.
Lee, I.M. & Davis, R.E. 1992. Mycoplasmas which infect plants and insects. pp. 379-
390. In: Mycoplasmas: Molecular Biology and Pathogenesis. Eds. I. Maniloff,
R.N. McElhaney, L.R. Finch and J.B. Baseman. Amer. Soc. for Microbiology.
Washington, D.C.
2. Strawberry green petal
Cause
A phloem-limited non-cultivable mollicute, often referred to as a mycoplasma-like
organism (MLO). The pathogen is also known to cause clover phyllody and was
recently classified as Type III of aster yellows MLO (non-cultivable mollicute).
32
Fig. 13. Strawberry green petal disease - green
flower petals and affected (above), dwarfed leaves
with chlorotic margins (below). (Dr. R.H. Converse,
Horticultural Crops research Laboratory, Corvallis)
Symptoms
In infected strawberry cultivars, petals adhere, turn green and eventually may turn
pink. In later stages of the disease petals may become leaflike (phylloid). Fruits
remain small, hard and green. Foliage is dwarfed, cupped and chlorotic. Plants
form few, shorter runners and die within a few months.
Host range
Fragaria spp. and several species of clover (Trifolium spp.).
Geographical distribution
North America (where it is particularly serious in northeastern Canada), Australia,
Europe, New Zealand, and Russia.
Transmission
The disease agent is transmitted in nature in a persistent manner by several
leafhopper species, but only Aphrodes bicinicta has been demonstrated to transmit
to and from strawberry. Other species such as Macrosteles fascifrons and species
of Euscel i s are involved in field spread in clover and other plant species.
Transmi t t ed experi ment al l y by dodder and graft -i nocul at i on, but not by
mechanical inoculation of sap extracts.
33
Therapy
Propagation of rapidly growing shoots from heat-treated plants was effective in
eradicating the agent from infected periwinkle. Application of tetracycline
antibiotics can cause the remission of symptoms.
Indexing
Green petal disease is evident in infected cultivars. It can be distinguished from
other aster yellows types by bioassay using dodder to infect celery, a differential
host in which the pathogen is symptomless. Can be detected and identified
serologically by ELISA from infected strawberry sap.
References
Chiykowski, L.N. 1962. Clover phyllody and strawberry green petal diseases,
caused by the same virus in eastern Canada. Can. J. Bot. 40:397-404.
Clark, M.F., Barbara, D.J. & Davies, D.I. 1983. Production and characteristics of
antisera to Spiroplasma citri and to clover-phyllody associated antigens
derived from plants. Ann. Appl. Biol. 103:251-259.
Lee, I.M. & Davis, R.E. 1992. Mycoplasmas which infect plants and insects. pp. 379-
390. In: Mycoplasmas: Molecular Biology and Pathogenesis. Eds. I. Maniloff,
R.N. McElhaney, L.R. Finch and J.B. Baseman. Amer. Soc. for Microbiology.
Washington, DC.
Posnette, A.F. & Chiykowski, L.N. 1987. Strawberry green petal and similar
diseases. pp. 34-38. In: Virus Diseases of Small Fruits. Ed. R.H. Converse.
United States Department of Agriculture, Agriculture Handbook No. 631,
Washington, D.C.
Posnette, A.F. & Ellenberger, C.E. 1963. Further studies of green petal and other
leafhopper-transmitted viruses infecting strawberry and clover. Ann. Appl.
Biol. 51:69-83.
3. Witches’-broom and multiplier disease
Cause
A non-cultivable mollicute, often referred to as a mycoplasma-like organism (MLO).
Symptoms
Witches’-broom
(WB)
infected strawberries are dwarfed, bushy, sterile, have
numerous crowns, small leaves with spindly petioles, and severely broomed
daughter plants on short stolons. Strawberry plants infected with multiplier
disease (MD) are dwarfed with leaflets cupping upwards, and petioles short and
erect. Crown proliferation and short rulers are also characteristic. The few small
flowers that are formed bear normal-sized fruit.
34
Fig. 14. Witches’-broom and multiplier
disease in cv. ‘Sparkle’. (Dr. R.H.
Converse, Horticultural Crops Research
Laboratory, Corvallis)
Host range
WB and MD are known only in Fragaria spp.
Geographical distribution
North America.
Transmission
Leafhoppers are suspected but unproved vectors.
Therapy
No specific information for strawberry.
Indexing
Fragaria virginiana clone UC-12 is the best graft-inoculated indicator host for WB,
and F. chiloensis for MD. Both diseases cause severe crown proliferation and
dwarfing in graft-inoculated indicator plants.
References
Converse, R.H. 1987. Strawberry witches’-broom and multiplier diseases. pp. 66-
68. In: Virus Diseases of Small Fruits. Ed. R.H. Converse. United States
Department of Agriculture, Agriculture Handbook No. 631, Washington,
D.C.
35
Heimann, M.F., Spear, R.N., & Jeffers, S.N. 1992. Mycoplasmalike organisms
associated with strawberry multiplier disease. Phytopathology 82: 1 1 3 3
(abstract).
Sehgal, O.P. & Boone, D.M. 1963. Multiplier disease of strawberry in Wisconsin.
Plant Dis. Reptr 47: 46-48.
Pr okar yot i c di seases- bact er i a
1. Strawberry angular leaf spot
Cause
Xanthomonas fragariae Kennedy & King.
Symptoms
Minute water-soaked lesions on the lower leaf surface enlarge to become angular
spot s del i mi t ed by smal l vei ns. Lesi ons are t ransl ucent when vi ewed by
transmitted light, but dark green when viewed with reflected light. A viscous
bacterial exudate may form on lesions under high moisture conditions. When it
dries, the exudate forms a whitish, scaly film. Plants may be defoliated when
disease is severe.
Host range
Fragaria spp.
Geographical distribution
Brazil, Ethiopia, France, Italy (Sicily), USA, Venezuela.
Biology and transmission
Primary inoculum comes from overwintering leaf debris. The pathogen is very
resistant to desiccation and other adverse conditions. Very little is known about
the epidemiology.
Therapy
None is recommended.
Indexing
It is recommended, when clones are put into tissue culture, to routinely place the
initial explants for 2 or 3 weeks on a medium that promotes the growth of bacteria
36
(e.g. 40 g Tripticase Soy Agar in 1000 ml of water, or on media containing peptone
plus sucrose or glucose). Those meristems that remain free of bacterial growth are
transferred to a medium allowing meristem growth.
References
Bradbury, J.F. 1977. Xanthomonas fragariae. CMI Descriptions of Pathogenic Fungi
and Bacteria No. 558. Commonwealth Agricultural Bureaux, Slough.
Maas, J.L. 1984. Angular leaf spot. pp. 41-42. In: Compendium of Strawberry
Diseases. Ed. J.L. Maas. APS Press, St. Paul.
2. Strawberry bacterial wilt
Cause
Pseudomonas solanacearum E.F. Smith.
Symptoms
The earliest field symptoms are dropping of the older leaves of youngest plants.
Infected plants may show wilting during the hottest period of the day and recover
during cooler periods.
Host range
Not known if isolates of P. sol anacearum from strawberry are specific for
strawberry, or if isolates of P. solanacearum from other hosts are also pathogenic
to strawberry.
Geographical distribution
Japan, Taiwan.
Biology
Infected plants die within a few days after the appearance of the first symptoms.
Older plants appear resistant to the bacterium; P. solanacearum invades only a
limited number of xylem trachea cells even in young plants. Parenchymatous
tissues are attacked preferentially and large lysigenous cavities are formed and
become filled with bacteria.
References
Hsu, Y.H. 1987. Control of bacterial wilt of strawberry by planting with healthy
seedlings. Plant Prot. Bull. Taiwan 29 :199-201.
37
Kawaguchi, K., Ohta, K. & Goto, M. 1981. Studies on bacterial wilt of strawberry
plants caused by Pseudomonas solanacearum. 2. beta-D-glucogallin, the
antibacterial substance detected in the tissues of strawberry plants. Ann.
Phytopathol. Soc. Japan 47:520-527.
3. Marginal chlorosis of strawberry
Cause
An elongated bacterium has been uniquely associated with this disease.
Symptoms
Dwarfing of plants, cupping and yellowing of leaves, especially at leaflet margins.
Host range
Cultivated strawberry.
Geographical distribution
Widespread and serious in France and Spain in nurseries and in fruiting fields.
Transmission
Marginal chlorosis spreads in the field by unknown means.
Therapy
No information.
Indexing
Self-indicating.
Reference
Nourrisseau, J.G., Lansac, M. & Garnier, M. 1993. Marginal chlorosis, a new
disease of strawberries associated with a bacteriumlike organism. Plant Dis.
77:1055-1059.
38
Fungal diseases
1. Alternaria leaf spot
Cause
Alternaria alternata f.sp. fragaria Dingley.
Symptoms
Circular to irregular brown to black lesions, 2-5 mm in diameter, develop on upper
leaf surfaces and may have dark reddish purple margins. The lesions on the lower
leaf surface appear greyish brown. Elongate, dark, depressed lesions may occur on
and kill petioles and fruit.
Host range
Cultivated strawberries.
Geographical distribution
Belgium, France, Japan, Korea, Netherlands, New Zeal
Biology and transmission
This fungus species is not morphologically distinguishable from other A. alternata
and.
forms, however, the form attacking strawberry leaves is a distinct pathotype from
other Alternaria forms that commonly infect ripe strawberry fruit. Flowers and
fruits may also be infected, but this occurs less frequently. The disease spreads by
air-borne spores (conidia) from infected plant material. Disease development is
favoured by humid, warm conditions and overcrowding of plants. Cultivars differ
in susceptibility to Alternaria leaf spot; highly sensitive cultivars may be kilIed by
severe attacks.
References
Bal, E., Gilles, G., Creemers, P. & Verheyden, C. 1983. Problems and control of
Alternaria leaf spot on strawberries. Med. Fac. Landbouww. Rijksuniv. Gent
48:637-646.
Cho, J.T. & Moon, B.J. 1980. Occurrence of strawberry black leaf spot caused by
Altenaria alternata (Fr.) Keissler in Korea. Korean J. Plant Prot. 19:221-227.
Dingley, J.M. 1970. Records of fungi parasitic on plants in New Zealand, 1966-68
N.Z.J. Agric. Res. 1 3:325-337.
Howard, C.M. & Albregts, E.E. 1973. A strawberry fruit rot caused by Alternaria
tenuissima. Phytopathology 63:938-939.
Maas, J.L. 1984. Alternaria leaf spot. pp. 53-54. In: Compendium of Strawberry
Diseases. Ed. J.L. Maas. APS Press, St. Paul.
Roudeillac, P. & Veschambre, D. 1987. La Fraise: Techniques de Production. Centre
Technique Interprofessionnel des Fruits et Legumes, Paris.
Yamamoto, M., Namiki, F., Nishimura, S. & Kohmoto, K. 1985. Studies on host-
specific AF-toxins produced by Alternaria alternata strawberry pathotype
causing Alternaria black spot of strawberry. 3. Use of toxin for determining
inheritance of disease reaction in strawberry cultivar Morioka-16. Ann.
Phytopathol. Soc. Japan 51:530-535.
39
2. Anthracnose
Cause
Col l et ot ri chum spp.; C. fragariae A. N. Brooks, C. acutatum Si mmonds, C .
gloeosporioides Penz. [Glomerella cingulata (Ston.) Spauld. & Schrenk].
Symptoms
Symptoms range from fruit rot to stolon, petiole, and leaf lesions and crown rot.
Fruit rot begins as light to dark brown, slightly depressed lesions on unripe or ripe
fruits with pink to buff masses of spores (conidia) on the lesion surface. Fruit
lesions are firm and dry. Lesions on petioles and fruit trusses are dark, elongate,
slightly depressed, and often develop into a canker that kills the petiole or fruit
truss. Blossoms of highly susceptible cultivars may be attacked and killed.
Anthracnose black leaf spots developing on young expanding leaves are round and
3 mm or less in diameter. Strawberry plants affected by crown rot develop a
reddish brown, firm rot or streaking in interiors of crowns of wilting plants.
Infected plants generally wilt suddenly (collapse) and die.
Host range
In addition to strawberry, Cassia obtusifolia for C. fragariae; C acutatum and C.
gloeosporioides each have a large host range of other fruit, vegetable, and non-
food plants.
Geographical distribution
Almost worldwide.
40
Biology and transmission
Spores from infected plants are blown or carried by splashing water or insects to
healthy plants. Ground cover (plastic, straw, etc.) greatly affects spore dispersal
from fruit infections. High moisture and temperature favour disease development.
The fungi are able to over-season on some alternative hosts and in infected plant
debris in soil. The disease may be carried to healthy fields with nursery plants if
their stolons or petioles are infected.
References
Eastburn, D.M. & Gubler, W.D. 1990. Strawberry anthracnose: Detection and
survival of Colletotrichum acutatum in soil. Plant Dis. 74:161-163.
Howard: C.M. & Albregts, E.E. 1984. Anthracnose. pp. 85-87 In: Compendium of
Strawberry Diseases. Ed. J.L. Maas. APS Press, St. Paul.
Howard, C.M., Maas, J.L., Chandler, C.K. & Albregts, E.E. 1992. Anthracnose of
strawberry caused by the Colletotrichum complex in Florida. Plant Dis.
76:976-981.
Wilson, L.L., Madden, L.V. & Ellis, M.A. 1990. Influence of temperature and
wetness duration on infection of immature and mature strawberry fruit by
Colletotrichum acutatum. Phytopathology 80:111-116.
3. Fusarium wilt
Cause
Fusarium oxysporum f.sp. fragariae Winks & Williams.
Symptoms
Symptom development of this systemic disease
temperature, which cause leaves of infected plants to wilt and die rapidly. Sudden
plant collapse is similar to that caused by some other wilt diseases. Leaf chlorosis
may or may not develop. Crowns show distinct
as the disease advances, the lower crown tissues may decay completely.
in strawberry is favoured by high
reddish brown discoloration, and
Host range
Cultivated strawberries.
Geographical distribution
Australia, Japan, Korea.
41
Biology and transmission
Fusarium wilt is a soil-borne disease that begins as infection of roots and crowns
and becomes systemic. The fungus may be isolated from petioles of infected plants.
The fungus can survive in soil in infected strawberry plant debris, but it does not
infect other crop or cover plants in rotation with strawberry. The disease is
favoured by high temperature and plant stress during fruiting. Infection by F.
oxysporum f.sp. fragariae should not be confused with other Fusarium spp. that
also infect strawberry roots or fruit. Cultivars differ in susceptibility to Fusarium
wi l t , t hus i t i s possi bl e t hat t he pat hogen may be carri ed syst emi cal l y i n
symptomless and apparently healthy plant material of resistant cultivars.
Reference
Wilhelm, S. 1984. Fusarium wilt (yellows). pp. 97-98. In: Compendi um of
Strawberry Diseases. Ed. J.L. Maas. APS Press, St. Paul.
4. Phytophthora crown rot
Cause
Phytophthora cactorum (Lebert & Cohn) Schröt. Strawberry crown rot is induced
by specific strains of P. cactorum pathogenic to strawberry and not to apple or
other crops. Not to be confused with strawberry fruit rot, also caused by P .
cactorum strains that occur in temperate regions.
Symptoms
The youngest leaves wilt suddenly and often turn blush-green. Wilting quickly
spreads to include all leaves, typically within a few days. Crowns show necrosis
and intensive browning of the vascular tissue. Generally, roots are unaffected until
the entire crown is destroyed.
Host range
Cultivated strawberries.
Geographical distribution
Europe, Australia and USA.
Biology and transmission
The fungus is a common soil-inhabitant in temperate regions, however, apparently
only certain strains infect strawberry crowns while most strains infect strawberry
fruit. Strawberry isolates apparently are not pathogenic to other crop hosts or
42
weed species. War m, wet weat her f avour s i nf ect i on and hi gh t emper at ur e
enhances disease development. Stress conditions and short day-length promote
sympt om devel opment . Speci f i ci t y of condi t i ons necessar y f or sympt om
development is important, otherwise infections may remain latent in plants.
References
Seemüller, E. 1984. Crown rot (vascular collapse). pp. 83-85. In: Compendium of
Strawberry Diseases. Ed. J.L. Maas. APS Press, St. Paul,
Seemüller, E. & Schmidle, A. 1979. Einfluss der Herkunft von Phyt opht hora
cactorum-Isolaten auf ihre Virulenz an Apfelrinde, Erdbeerrhizomen und
Erdbeerfrüchten. Phytopathol. Z. 9 4:218-225.
5. Strawberry black root rot
Cause
Black root rot is a collective descriptive term for a complex of diseases having
more than one possible causal agent. Symptoms may be brought on by injurious
environmental conditions such as freezing or water logging of the soil, by
pathogenic fungi or nematodes, or most likely, by a combination of these factors.
The fungi Rhizoctonia spp., Pythium spp. and many others have been associated
with black root rot, as have Pratylenchus spp. nematodes.
Symptoms
Symptoms on roots generally are apparent when infections of lateral and main
roots occur. Dark lesions enlarge and girdle roots, eventually infecting the entire
root system. Cortex tissues are rotted, while steles of roots remain white. Quite
often, cortical tissues of roots can be pulled away from steles.
Fig. 15. Strawberry black root rot. (Dr.
J.L. Maas, USDA-ARS Fruit Laboratory,
Beltsville)
43
Geographical distribution
Black root rot occurs world-wide, however specific biotic causes may be localized.
Biology
The disease is generally associated with certain soil types, especially those with
high clay contents. The disease is not of a systemic nature.
Reference
Wilhelm, S. 1984. Black root rot. p. 90 In: Compendium of Strawberry Diseases. Ed.
J.L. Maas. APS Press, St. Paul.
6. Strawberry red stele (red core)
Cause
Phytophthora fragariae var. fragariae Hickman.
Symptoms
Young roots rot first at the tip, and when the root is cut open lengthwise, the stele
above the rot is red. As the rot progresses, lateral roots are quickly destroyed,
giving the main roots a ‘rat-tail’ appearance. The red discoloration of the stele often
progresses to the crowns of susceptible plants. Only roots are infected. The red
stele disease ranges in extent from sporadic infection of root tips in strawberry
cultivars with the highest resistance to total root destruction in those with the
lowest resistance. Infected plants in the field may occur in irregular patches rather
than in rows. Diseased susceptible plants become stunted, produce small or no
fruit, and eventually die.
Host Range
Species of Dryas, Geum, Potentilla, and Rubus have been infected experimentally
and Rubus spp. may become infected naturally in infested areas, posing potential
risks to strawberry plantings if they are transferred as planting material from
infested soil to clean soil that may be later used for strawberry production. This
pat hogen i s not t o be conf used wi t h P. f ragari ae var . rubi , t he cause of
Phytophthora root rot of Rubus (see Rubus diseases).
Geographical distribution
Temperate strawberry growing regions.
44
Biology and transmission
At least 15 physiologic races of P. fragariae are known worldwide, and strawberry
cultivars differ in susceptibility to the races. Spores of the fungus (zoospores) are
released in soil during wet, cool periods. These spores germinate on tips of main or
lateral roots and infection proceeds toward the stele of the main root. Roots begin
to rot from the tip a few days after infection and eventually, rotted roots
containing zoospores become incorporated into the soil. The zoospores may
germinate to produce more zoospores, or they may remain inactive in soil for
many years before germinating. The fungus may be moved to new areas in
infected roots of susceptible or resistant plants, plant debris, or in infested soil
adhering to plant roots. High rainfall, poor soil drainage, and low temperature
favour the disease.
References
Montgomerie, I. G. 1984. Red stele root rot. pp. 79-83. In: Co mp e n d i u m o f
Strawberry Diseases. Ed. J.L. Maas. APS Press, St. Paul.
Pepi n, H. S. 1967. Suscept i bi l i t y of members of t he Rosaceae t o races of
Phytophthora fragariae. Phytopathology 57:782-784.
7. Verticillium wilt
Cause
Verticillium albo-atrum Reinke & Berth. and/or V. dahliae Kleb.
Symptoms
Outer leaves of the strawberry plant show marginal and interveinal browning and
eventually collapse. Inner leaves are stunted, but tend to remain green and turgid
until the plants die. The wilting symptom generally distinguishes Verticillium wilt
from other root and crown diseases that cause wilting of all leaves at the same
time. First-year strawberry plantings are affected most severely.
Host range
A large number of crop and weed species.
Geographical distribution
Throughout temperate zones of the world.
Biology and transmission
Pathogens can over-season in infected plant debris as small, dormant structures
(microsclerotia). Infection occurs in the soil through spores (conidia) or hyphae in
45
contact with plant roots. Infections destroy roots, causing plants to wilt and die.
The disease is systemic; Verticillium can be readily isolated from petioles of
infected plants. Verticillium wilt is often most prevalent and severe in arid or
semiarid, irrigated areas and is favoured by periods of environmental stress, such
as high temperature and drought. Disease Spread from plant to plant is negligible.
Verticillium may be disseminated to new locations by water, wind, on infected
planting stock, in crop or weed debris, or in soil. Strawberry cultivars differ in
susceptibility to this wilt and isolates of Verticillium differ in pathogenicity.
References
Maas, J.L. & Galletta, G.J. 1989. Germplasm evaluation for resistance to fungus-
incited diseases. Acta Hortic. 265:461-472.
Maas, J.L., Galletta, G.J. & Draper, A.D. 1989. Resistance in strawberry to races of
Phytophthora fragariae and to isolates of Verticillium from North America.
Acta Hortic. 265:521-526.
Wilhelm, S. 1984. Verticillium wilt. pp. 87-90. In: Compendium of Strawberry
Diseases. Ed. J.L. Maas. APS Press, St. Paul.
Ribes spp. (currant, gooseberry)
Viruses
1. Alfalfa mosaic virus (AMV)
Virus particles are bacilliform and of different lengths; the longest usually about 60
nm. All particles are approximately 16 nm wide.
Fig. 16. Spring symptoms of interveinal
white mosaic in
alfalfa mosaic virus. (Dr. R.H. Converse,
Horticultural Crops Research
red currant, caused by
Laboratory, Corvallis)
46
Symptoms
Interveinal white mosaic. Leaves of affected plants show yellow or white patches
which often occur between the main veins. Leaves produced later in the season
may show only yellow or white flecking on the outer margins.
Host range
Although AMV has a wide natural host range extending over several genera, Ribes
seems to be infected only rarely.
Geographical distribution
AMV occurs worldwide, but is reported in Ribes only from Europe.
Transmission
AMV is transmitted in nature by many species of aphids in a non-persistent
manner and also through the seed of some hosts. Experimentally, AMV is
transmitted by mechanical inoculation of sap to herbaceous test plants and by
graft-inoculation.
Therapy
No specific information for Ribes.
Indexing
Mechanical inoculation of sap extracted in 2% nicotine alkaloid solution to
Chenopodium quinoa (see underlined note of caution on p. 10), which develops
both local lesions and systemic mosaic. The development of systemic symptoms in
C. quinoa distinguishes these isolates from cucumber mosaic and tobacco rattle
viruses which do not infect this host systemically. The presence of AMV should be
confirmed serologically to distinguish it from other possible viruses.
References
Jaspers, E.M.J. & Bos, L. 1980. Alfalfa mosaic virus. CMI/AAB Descriptions of
Plant Viruses No. 229. Commonwealth Agricultural Bureaux, Slough.
van der Meer, F.A. Interveinal white mosaic. pp. 153-155. In: Virus Diseases of
Small Fruits. Ed. R.H. Converse. United States Department of Agriculture,
Agriculture Handbook No. 631, Washington, D.C.
2. Cucumber mosaic virus (CMV)
Virus particles are isometric, about 30 nm in diameter.
4 7
Fig. 17. Green mottle disease in red
currant, caused by cucumber mosaic
virus. (Dr. R.H. Converse,
Horticultural Crops Research
Laboratory, Corvallis)
Symptoms
Green mottle disease in Ribes. Symptoms are variable, depending on the Ribes
species and cultivar infected as well as time of infection and environmental
conditions. Symptoms in sensitive material are chlorotic line-patterns, often
associated with leaf veins, or mottling; they are most obvious in rapidly growing
plants in spring and in fully expanded leaves.
Host range
CMV has a very wide host range covering several genera. Ribes seems to be
infected only occasionally.
Geographical distribution
World-wide in many crop species. Has been found in Europe in Ribes.
Transmission
Transmitted in a non-persistent manner by many species of aphids, including those
that colonize Ribes spp., and through the seed of some host plants. Transmitted
experimentally by grafting and by mechanical inoculation of sap extracts to
herbaceous plants.
Therapy
Eradicated by thermotherapy at 36°C for 3 weeks, followed by apical tip
propagation.
48
Indexing
Detected by mechanical inoculation of sap in 2% nicotine alkaloid solution to many
herbaceous test plants (see underlined note of caution on p. 10). Chenopudi um
quinoa is sensitive to infection producing local necrotic lesions a few days after
inoculation; it is not infected systemically. Serological tests are necessary to
identify and distinguish CMV from other possible viruses. Also detectable by
ELISA or other serological tests, but several serotypes of the virus are known and
these may not react with some antisera in certain kinds of tests.
References
Adams, A.N. & Thresh, J.M. 1987. Green mottle of black currant. pp. 136-137. In:
Virus Diseases of Small Fruits. Ed. R.H. Converse. United States Department
of Agriculture, Agriculture Handbook No. 631, Washington, D.C.
Francki, R.I.B., Mossop, D. W. & Hat t a, T. 1979. Cucumber mosai c vi rus.
CMI / AAB Des cr i pt i ons of Pl ant Vi r us es No. 213. Commonweal t h
Agricultural Bureaux, Slough.
van der Meer, F.A. 1987. Green mottle of red currant. pp. 145-146. In: Vi r us
Diseases of Small Fruits. Ed. R.H. Converse. United States Department of
Agriculture, Agriculture Handbook No. 631, Washington, D.C.
3. Gooseberry vein banding virus (GVBV)
Possibly a member of the badnavirus group; in infected plants small unenveloped
bacilliform particles of about 30 x 130 nm were found.
Symptoms
Chlorotic banding along the main veins of leaves which may be distorted in
severely affected plants. Symptoms are most evident in early spring growth and
become less obvious later in the season. Symptom expression is also greatly
influenced by cultivar and species.
Host range
Repor t ed onl y f r om Ri bes spp. More research is required to determine the
properties of isolates in the three cultivated Ribes spp.
Geographical distribution
Common in Europe and in countries of the former Soviet Union. Found in North
America and New Zealand probably as a result of importing infected material.
4 9
Fig. 18. Symptoms of gooseberry vein
banding virus infection in red currant.
(Dr. J. Postman, USDA-ARS-NCGR,
Corvallis)
Transmission
Transmitted in a semi-persistent manner by several species of aphids, including
Aphis grossulariae, A. schneideri Cryptomyzus ribis, Hyperomyzus lactucae,
Myzus persicae and Nasonova ribisnigri Transmitted experimentally by grafting
and, with great difficulty, by mechanical inoculation of sap to some herbaceous
plants.
Therapy
Eradicated from red currant by thermotherapy at 38°C for 3 weeks followed by
shoot-tip propagation. Gooseberry is heat sensitive, so that thermotherapy of
infected plants is more difficult. The virus has been eradicated from plants by
meristem tip culture alone, and a combination of thermotherapy at a lower
temperature, followed by meristem tip culture.
Indexing
Graft-inoculation to sensitive gooseberry indicator cultivars or clones such as
‘Leveller’ or B1385/81.
References
Adams, A.N. & Posnette, A,F. 1987. Gooseberry vein banding. pp. 129-130. In:
Virus Diseases of SmalI Fruits. Ed. R.H. Converse. United States Department
of Agriculture, Agriculture Handbook No. 631, Washington, D.C.
5 0
Adams, A.N. & Thresh, J.M. 1987. Vein clearing and vein net disease of black
currant. pp. 137-138. In: Virus Diseases of Small Fruits. Ed. R.H. Converse.
United States Department of Agriculture, Agriculture Handbook No. 631,
Washington, DC.
Jones, A.T., McGavin, W.J. & Watkins, C.A. 1992. Recent studies in Scotland on the
aetiology of virus and virus-like diseases of small fruit crops. Acta Hortic.
308:31-35.
van der Meer, F.A. 1987. Red currant vein banding. pp. 143-145. In: Virus Diseases
of Small Fruits. Ed. R.H. Converse. United States Department of Agriculture,
Agriculture Handbook No. 631, Washington, D.C.
Wood, G.A. 1991. Three graft-transmissible diseases and a variegation disorder of
small fruit in New Zealand. N.Z.J. Crop Hortic. Sci. 1 9:313-323.
4. Nepoviruses
Virus particles are isometric, about 30 nm in diameter with a angular outlines; a
proportion of the particles are penetrated by negative stains.
Symptoms
Symptoms vary depending on the cultivar, virus and environmental conditions.
Sympt oms may range from chl orot i c mot t l i ng or l i ne-pat t ern t o mosai c;
symptomless infection also occurs. Symptoms are most obvious in early spring
growth and are often less noticeable as the season progresses.
Host range
Nepoviruses infect a wide range of hosts covering many genera, including several
weed species.
Fig. 19. Chlorotic mottling in red
currant, caused by tomato ringspot
virus. (Dr. J. Postman, USDA-ARS-
NCGR, Corvallis)
51
Geographical distribution
Nepoviruses occur worldwide, but infection in Ribes is not common. Arabis
mosaic virus (ArMV), strawberry latent ringspot virus (SLRSV), raspberry ringspot
virus (RRSV) and tomato black ring virus (TBRV) are reported in Ribes in Europe.
Tomato ringspot virus (ToRSV) occurs in North America.
Transmission
Transmitted in nature through soil by nematodes of the genus Longidorus (RRSV,
TBRV) and Xiphinema (ArMV, SLRSV, ToRSV) and through seed of some hosts.
Transmitted experimentally by grafting and by mechanical inoculation of sap
extracts to herbaceous test plants.
Therapy
ToRSV was eradicated from red currant by thermotherapy for three weeks at 38°C
followed by apical tip propagation. No information available for the other
nepoviruses in Ribes.
Indexing
Detected by mechanical inoculation of sap extracted in 2% nicotine alkaloid
solution to herbaceous test plants (see underlined note of caution on p. 10).
Chenopodium quinoa produces chlorotic or necrotic local lesions followed by
systemic necrosis. However, serological tests are necessary to identify and
distinguish nepoviruses from one another and from other viruses. ELISA alone is
not recommended for the detection of RRSV, TBRV and ToRSV as a range of
serological variants exist that may not react with certain antisera.
References
Sections on nepoviruses in: Virus Diseases of Small Fruits. Ed. R.H. Converse.
United States Department of Agriculture, Agriculture Handbook No. 631,
Washington, D.C.
5. Tobacco rattle virus (TRV)
TRV has straight tubular particles of two predominant lengths; the longer are
about 190 nm and the shorter 50-115 nm, depending on the virus isolate. Particle
width is approximately 23 nm.
Symptoms
Reported only from red currant and R. sanguineum in which the virus induces
chlorotic or yellow mosaic and line-pattern symptoms. Symptoms are restricted to
only a few branches and usually only in the first-formed leaves of these branches.
52
Fig. 20. Yellow mosaic and line-pattern symptoms in Ribes
sanguineum. (Dr. R.H. Converse, Horticultural
Crops Research Laboratory, Corvallis)
Host range
TRV infects a wide range of host plants that extends over several genera, but
infects Ribes only rarely.
Geographical distribution
Reported in Ribes only from the Netherlands and Germany, but the virus probably
occurs world-wide.
Transmission
The virus is transmitted through soil by nematodes in the genera Paratrichodorus
and Tr i chodor us and al so t hr ough t he seed of some host s. Tr ansmi ssi bl e
experimentally by grafting and by inoculation of sap extracts to herbaceous test
plants.
Therapy
None reported for Ribes as plants are infected only rarely.
Indexing
Detected by mechanical inoculation of sap, extracted from symptom-bearing leaves
of Ribes in 2% nicotine alkaloid solution, to Chenopodium amaranticolor or C.
quinoa in which TRV induces spreading necrotic local lesions within a few days;
most virus isolates do not become systemic. See underlined note of caution on p.
10. Serological tests and/or electron microscopy of infected test plants are
necessary to identify and distinguish TRV from other possible viruses. The virus
cannot be detected reliably by ELISA with the available antisera because of the
wide range of serological variants that exist in nature.
5 3
References
Robinson, D.J. & Harrison, B.D. 1989. Tobacco rattle virus. AAB Descriptions of
Plant Viruses No. 346. Association of Applied Biologists, Wellesbourne.
van der Meer, F.A. 1987. Leaf pattern of red currant. pp. 150-152. In: Vi r us
Diseases of Small Fruits. Ed. R.H. Converse. United States Department of
Agriculture, Agriculture Handbook No. 631, Washington, D.C.
Diseases of unknown etiology
1. Black currant yellows
Cause
Unknown.
Symptoms
Symptoms are noticeable in early spring as chlorotic or yellow flecks in newly
expanding leaves. These flecks and spots increase in number and may merge to
produce an overall yellowing of the leaf. Leaves emerging during the more rapid
phase of summer growth are often symptomless.
Host range
Reported only in Ribes.
Fig. 21. Black currant yellows in
‘Baldwin’. (Scottish Crop Research
institute, Invergowrie)
54
Geographical distribution
Reported only in Britain, but similar symptoms have been observed in black
currant plants in Europe and New Zealand.
Transmission
No vector has been identified. Natural spread in the field is slow. Experimentally,
the agent is transmissible by grafting, but not by mechanical inoculation of sap
extracts to herbaceous plants.
Therapy
Attempts to eradicate the agent from infected plants by thermotherapy were not
successful.
Indexing
Graft-inoculation to the sensitive black currant cultivars ‘Baldwin’ or ‘Amos Black’.
Reference
Thresh, J.M. 1987. Black currant yellows. pp. 140-141. In: Virus Diseases of Small
Fruits. Ed. R.H. Converse. United States Department of Agriculture,
Agriculture Handbook No. 631, Washington, D.C.
2. Reversion of red and black currant
Cause
Unknown. Reports that the causal agent is potato virus Y or a mycoplasma-like
organism have not been confirmed bv other workers.
Fig. 22. Reversion disease of black currant, symptoms of
infection with strain E. Infected plants are characterized by the
absence of downy hairs and the-brighter colour of flower buds
(left) compared to the healthy plant (right). (Scottish Crop
Research Institute, invergowrie)
55
Symptoms
Symptoms do not usually appear until at least one year (sometimes longer) after
infection and then often in only a few branches. Full systemic infection may take
up to three to five years. At least two strains are recognized: the common
European strain (E), and a more virulent strain (R) present in Scandinavia, eastern
and central Europe, and countries of the former Soviet Union. Flower bud
symptoms induced by these strains are quite distinct. In black currant, infection
with strain E results in decreased hairiness of the sepals of the unopened buds so
t hat t hey appear more bri ght l y col oured compared wi t h t he grey, downy
appearance of normal buds. In addition to these symptoms, infection with strain R
also results in much darker pigmentation of the sepals and, most characteristically,
sepal division to form 10 instead of the usual 5 sepals (‘double’ flowers). Symptoms
in leaves are much less diagnostic, being influenced greatly by cultivar and season.
Some sensitive black currant cultivars show a transient chlorotic line-pattern
usually associated with the main veins. Other leaf symptoms include decreased
marginal serrations and number of main veins, and a smaller basal sinus. Flower
bud and leaf symptoms are much less obvious in red currant.
Host range
Only reported from Ribes spp.
Geographical distribution
Common in Europe, countries of the former Soviet Union, New Zealand; not
reported from the Americas.
Fig. 23. Reversion disease of black
currant, symptoms of infection with
strain R. Infected plants are
characterized by darker pigmentation
of the sepals and ‘double’ flowers, as
well as reverted leaves (left) compared
to the healthy plant (right). (Scottish
Crop Research Institute, Invergowrie)
56
Transmission
late spring and early summer and their feeding
Transmitted in nature by the black currant gall mite, Cecidophyopsis ribis. These
mites colonize young buds in
induces the formation of distinctive galling of the buds. Tens of thousands of mites
may be found in a single galled bud. Plants affected with reversion are more
susceptible to infestation by mites than healthy plants. Experimentally, the
reversion agent is transmitted by grafting, but not by mechanical inoculation of sap
to herbaceous plants.
Therapy
Reversion-free plants have been obtained from infected ones by thermotherapy of
plants and tip grafting the heat-treated shoots to healthy black currant seedlings.
Indexing
In black currant, flower bud symptoms are the most reliable for diagnosis; some
cultivars also show obvious leaf symptoms. In red currant, symptoms are much
less ‘noticeable than in black currant. Because of the slow development of
symptoms and the erratic distribution of the agent in infected plants, they should
be observed for two flowering seasons. For uncertain material and for red currant,
graft-inoculation to reversion-sensitive black currant cultivars such as ‘Baldwin’,
‘Ojebyn’ and ‘Silver Gieters’ is necessary. Because of the erratic distribution of the
reversion agent in plants, scions for grafting should be selected from three separate
branches of each plant to be tested. Grafted plants should be observed for
symptoms for two flowering seasons.
References
Adams, A.N. & Thresh, J.M. 1987. Reversion of black currant. pp. 133-136. In:
Virus Diseases of Small Fruits. Ed. R.H. Converse. United States Department
of Agriculture, Agriculture Handbook No. 631, Washington, D.C.
Campbell, A.I. 1965. The inactivation of black currant reversion by heat therapy.
pp. 89-92. Long Ashton Res. Stn. Report for 1964.
Wood, GA. 1991. Three graft-transmissible diseases and a variegation disorder of
small fruit in New Zealand. N.Z.J Crop Hortic. Sci. 19: 313-323.
3. Wildfire of black currant
Cause
Unknown.
57
Symptoms
Symptoms occur in spring as chlorotic spotting of the leaves; spots may coalesce to
form large chlorotic areas along and between the main veins. Sometimes chlorosis
takes the form of rings or streaks. Tissues in the centre of chlorotic areas become
thin and translucent. In severely affected plants leaves are deformed and small.
Symptoms become less intense in leaves produced during hot summer conditions.
Host range
Reported only in Ribes.
Geographical distribution
Reported only from Siberia and the Far East of the former Soviet Union.
Transmission
Transmi t t ed i n nat ure by t he aphi d Aphi s gr os s ul ar i ae, but t he mode of
transmission is not known. Experimentally, the agent of the disease is readily
transmitted between Ribes plants by grafting, but not by mechanical inoculation of
sap to herbaceous plants.
Therapy
Prolonged thermotherapy of entire plants or, for shorter periods, shoot tips, is
reported to free plants from infection.
Indexing
Observations of characteristic symptoms in infected plants or in graft-inoculated
pl ant s of t he sensi t i ve Russian black currant cultivar ‘Lisavenko’s Black’.
Symptoms appear 3-5 weeks after graft-inoculation.
Reference
Kalinitchenko, A.N. & Gladkych, V.I. 1976. Wildfire of black currants. Acta Hortic.
66:85-89.
4. Yellow leaf spot of currant
Cause
Unknown.
Symptoms
Red currant plants may show chlorotic or yellow spotting, often more noticeable at
the outer leaf margins, but also found scattered over the whole leaf. Symptom
expression is very dependent on the cultivar and growing season. Black currant
seems to be symptomlessly infected.
58
Host range
Reported only from red currant.
Geographical distribution
Reported only from Europe.
Transmission
No information on natural spread, but the agent is graft-transmissible.
Therapy
No information.
Indexing
Detected only by symptoms in plants or by graft-inoculation to the sensitive red
currant cultivars ‘Laxton No.1’ or ‘Fay’s Prolific’. However, mechanical inoculation
of sap to Chenopodium quinoa should be attempted to determine the presence of
alfalfa mosaic virus which can induce symptoms in red currant similar to yellow
leaf spot.
Reference
van der Meer, F.A. 1987. Yellow leaf spot of red currant. pp. 152-153. In: Virus
Diseases of Small Fruits. Ed. R.H. Converse. United States Department of
Agriculture, Agriculture Handbook No. 631, Washington, D.C.
Prokaryotic disease
Full blossom of currant
Cause
The causal agent appears to be a non-cultivable mollicute, often referred to as a
mycoplasma-like organism (MLO).
Symptoms
Flower malformations are most typical and include some of the following: absence
of stamens, presence of more than one style, petals with sepal-like appearance,
leaf-like development of petals or sepals, and misshapen berries.
Host range
Reported only in Ribes.
59
Geographical distribution
Reported only from Czechoslovakia.
Transmission
No information on natural spread. Experimentally, the causal agent can be
transmitted by graft-inoculation.
Therapy
No information.
Indexing
Detected by symptoms on flowering plants or in graft-inoculated plants of the red
currant cultivar ‘Houghton Castle’.
References
Rakus, D., Kralik, O. & Brack, J. 1974. Mycoplazma V. Ribes houghtonianum Jancz.
nakazene ‘plnokvetosti’. Sborni k Ust av Vedeckot echmckych Inf ormaci
Ochrana Rostlin 10:307-309.
van der Meer, F.A. 1987. Full blossom of red currant. pp. 155-157. In: Vi r us
Diseases of Small Fruits. Ed. R.H. Converse. United States Department of
Agriculture, Agriculture Handbook No. 631, Washington, D.C.
Fungal diseases
1. American powdery mildew
Caus e
Sphaerotheca mars-uvae (Schwein.) Berk. & Curt.
Fig. 24. American powdery mildew
(Sphaerotheca mors-uvae) on black
currant. (Dr. P.R. Bristow, Washington
State University, Puyallup)
60
Symptoms
The lower portion of plants usually show the first symptoms. Tips of young shoots
are attacked and may become distorted. Leaves are covered on both sides with a
white mycelium which turns rusty-brown with age. Leaves and berries in all stages
are attacked. Infected berries may be dwarfed, roughened and cracked. Severe
infection reduces shoot growth, thus having an adverse impact on the crop in the
following year.
Host range
Chiefly on gooseberry (Ribes grossularia and R. hordeolum), but also on currants
(R. sativum, R. rubrum and R. nigrum).
Geographical distribution
Asia, Europe, North America, Australia and New Zealand.
Biology and transmission
The disease is favoured by cool, humid and rainy periods during spring and early
summer. The main source of infection in the spring is ascospores released from
overwintering cleistothecia. Cleistothecia form on living and on fallen leaves. On
gooseberries the pathogen normally overwinters as mycelium in dormant buds.
Wind-borne conidia formed on infected plant parts cause secondary infections.
Reference
Purnell, T.J. & Sivanesan, A. 1970. Sphaerotheca mors-uvae. CMI Descriptions of
Pathogenic Fungi and Bacteria No. 254. Commonwealth Agricultural
Bureaux, Slough.
2. Anthracnose (leaf spot)
Cause
Drepanopezlia ribis (Kleb.) Höhn.
(anamorph: Gloeosporidiella ribis (Lib.) Petr.).
Symptoms
The disease is a leaf spot or anthracnose of currants and gooseberries. The primary
symptom is small, circular or irregular spots on both leaf surfaces. Spots are dark
brown and coalesce when numerous. Minute, grey acervuli develop in lesions.
61
Fig. 25. Anthracnose (Drepanopeziza
ribis) on black currant. (Dr. P.R.
Bristow, Washington State University,
Puyallup)
Leaves become chlorotic and drop prematurely. Yellowing of leaves is more
pronounced on gooseberries. All succulent plant parts including petioles,
peduncles and fruit are susceptible, but leaf spotting is the most pronounced
symptom. On fruit the spots resemble flyspecks. Severely infected berries crack
open and drop.
Host range
Ribes spp. , including currants (R. rubrum, R. nigrum) and gooseberries ( R.
grossularia, R. hirtellum).
Geographical distribution
Australia, Europe, Japan, New Zealand and North America.
Biology and transmission
Primary inoculum are ascospores produced in apothecia on overwintering leaves
beneath plants. Ascospores are air-borne. Conidia produced in acervuli on leaf
lesions are waterborne. Conidia are inoculum for the repeating secondary cycle.
References
Blodgett, E. C. 1936. The anthracnose of currant and gooseberry caused by
Pseudopeziza ribis. Phytopathology 26:115-152.
Boot h, C. & Waller, J.M. 1979. Drepanopezi za ri bi s. CMI Descri pt i ons of
Pathogenic Fungi and Bacteria No. 638. Commonwealth Agricultural
Bureaux, Slough.
62
Rubus spp. (blackberry, raspberry)
Viruses
1. Blackberry calico virus (BCV) (see also wineberry latent virus)
A carlavirus with flexuous, rod-shaped particles about 15 x 627 nm in length. Very
similar to, and possibly the same as wineberry latent virus.
Symptoms
Yellow spots, blotchy chlorosis and ring-and-line patterns appear first on floricane
leaves. Similar symptoms develop on primocane leaves in hot weather. In some
cases, red pigmentation of the chlorotic areas also occurs. Infected plants may be
symptomless in cool weather.
Host range
Wild and cultivated Rubus ursinus, blackberry x raspberry hybrids such as
boysenberry and loganberry.
Geographical distribution
North America and possibly through imported material in Europe.
Fig. 26. Blackberry calico disease in
‘Marion’ blackberry. (Dr. R.H.
Converse, Horticultural Crops
Research Laboratory, Corvallis)
63
Transmission
The virus spreads very slowly in the field by unknown means. Experimentally,
BCV is graft-transmissible to other Rubus plants and is mechanically transmitted
with great difficulty to Nicotiana occidentalis accession Pl-c.
Therapy
Thermotherapy for 35 days at 37°C.
Indexing
Serological detection of BCV by ELISA is probably the fastest and most sensitive
technique currently available. BCV is very irregularly distributed within naturally
infected Rubus plants. Therefore, multiple sampling is needed for virus detection
in a given plant. BCV can be detected by grafting onto loganberry seedlings which
should then be grown out of doors through two complete growing seasons to
permit symptom expression.
References
Converse, R.H. 1987. Blackberry calico. pp. 245-246. In: Virus Diseases of Small
Fruits. Ed. R.H. Converse. United States Department of Agriculture,
Agriculture Handbook No. 631, Washington, D.C.
Jones, A.T., Mitchell, M.J., McGavin, W.J. & Roberts, I.M. 1990. Further properties
of wineberry latent virus and evidence for its possible involvement in calico
disease. Ann. Appl. Biol. 117:571-581.
van der Meer, F.A. 1989. Nicotiana occidentalis, a suitable test plant in research on
viruses of small fruit crops. Acta Hortic. 236:27-35.
2. Black raspberry necrosis virus (BRNV)
Virus particles are isometric, about 25-30 nm in diameter and many are penetrated
by negative stains.
Host range
Rubus spp. and a few herbaceous test species.
in most Symptomless
Symptoms
Induces severe tip necrosis and mosaic in black raspberry.
red raspberry and blackberry cultivars, but some may show a veinal chlorotic
mottle or line-pattern during early growth.
64
Fig. 27. Veinal chlorotic mottle caused
by black raspberry necrosis virus. (Dr.
R.H. Converse, Horticultural Crops
Research Laboratory, Corvallis)
Geographical distribution
Probably occurs wherever Rubus is grown. Usually occurs as a complex infection
with one or more of the following viruses: raspberry leaf mottle, raspberry leaf
spot, and Rubus yellow net to cause diseases known as veinbanding mosaic
disease or raspberry mosaic. In Australasia, where the main vector aphid species
are absent, little or no spread occurs apart from propagation of infected material.
Transmission
Transmitted in nature in a semi-persistent manner by the aphids Amphorophora
idaei in Europe and A. agathonica in North America. Possibly other Rubus -
infesting aphids are also able to act as vectors. Transmitted experimentally by
grafting and, with great difficulty, by mechanical inoculation of sap extracts in 2%
nicotine alkaloid solution to herbaceous indicator plants (see underlined note of
caution on p. 10).
Therapy
Eradicated from infected plants by thermotherapy although a heat-stable isolate
was reported in Canada.
Indexing
Detected by transmission to R. occidentalis (black raspberry) or R. henryi which
develop apical tip necrosis and mosaic. However, identification is dependent on
distinguishing it from raspberry leaf mottle and raspberry leaf spot viruses which
react similarly on these indicators. BRNV is symptomless in the red raspberry
indicators of the other two viruses. Mechanical inoculation is difficult to achieve
because of low virus concentration in raspberry plants, but sap extracts in 2%
nicotine alkaloid solution when inoculated to Chenopodium quinoa somet i mes
65
induce necrotic local lesions followed by systemic chlorotic flecks or mottle. See
underlined note of caution on p. 10.
Reference
Stace-Smith, R. & Jones, A.T. 1987. Black raspberry necrosis. pp. 178-183. In: Virus
Diseases of Small Fruits. Ed. R.H. Converse. United States Department of
Agriculture, Agriculture Handbook No. 631, Washington, DC.
3. Bramble yellow mosaic virus (BrYMV)
A probable potyvirus with flexuous particles of about 15 x 730 nm.
Symptoms
Pronounced yellow mosaic and line-pattern in R. rigidus that persists through the
growing season.
Host range
Rubus spp.
Geographical distribution
Reported only from South Africa.
Transmission
Natural mode of spread is not known. Transmitted experimentally by grafting and
by mechanical inoculation of sap extracts to herbaceous plants.
Therapy
No information.
Indexing
Readily transmitted from Rubus by mechanical inoculation of sap extracts in 2%
nicotine alkaloid solution to several herbaceous species (see underlined note of
caution on p. 10). Chenopodium morale is sensitive to infection and develops large
local chlorotic or yellow lesions that are irregular in size and later become necrotic,
and systemic chlorotic or yellow rings.
Graft-inoculated R. henryi develop a
transient chlorotic mottle. No antiserum is available to the virus.
Reference
Engelbrecht, D.J. 1987. Bramble yellow mosaic. pp. 243-244. In: Virus Diseases of
Small Fruits. Ed. R.H. Converse. United States Department of Agriculture,
Agriculture Handbook No. 631, Washington, D.C.
66
4. Cucumber mosaic virus (CMV)
Virus particles are isometric and about 30 nm in diameter.
Symptoms
Severe chlorotic blotching and line-pattern, leaf deformation, decreased vigour and
plant death in wineberry (R. phoenicolasius), chlorotic mottling and blotching in
some raspberry cultivars and symptomless infection in blackberry.
Host range
Rubus spp.
Geographical distribution
The virus occurs worldwide in many plant species. Reported in Rubus only from
Britain and Eastern Russia.
Transmission
Transmitted in nature in a non-persistent manner by many species of aphids,
including those that colonize Rubus; seed-transmitted in many hosts but not
detected in Rubus. Also transmitted experimentally by grafting and by mechanical
inoculation of plant sap to herbaceous plants.
Therapy
No information for Rubus.
Indexing
Readily detected by mechanical inoculation of sap in 2% nicotine alkaloid solution
to many herbaceous test plants (see underlined note of caution on p. 10).
Chenopodium quinoa is sensitive to infection producing local necrotic lesions; it is
not infected systemically. Serological tests are necessary to identifv and distinguish
CMV from other possible viruses. Several serotypes are known and these may not
react with some antisera in certain kinds of tests.
References
Francki, R.I.B., Mossop, D. W. & Hat t a, T. 1979. Cucumber mosai c vi rus.
CMI/AAB Descriptions Plant Viruses No. 213. Commonwealth Agricultural
Bureaux, Slough.
Jones, A.T. 1987. Cucumber mosaic virus in raspberry. pp. 191-192. In: Virus
Diseases of Small Fruits. Ed. R.H. Converse. United States Department of
Agriculture, Agriculture Handbook No. 631, Washington, D.C.
67
5. Ilarviruses
At least two ilarviruses have been reported in Rubus, namely apple mosaic virus
(ApMV) and tobacco streak virus (TSV) and its serological relatives. Ilarvirus
particles are quasi-isometric and range in diameter from 23-35 nm.
Symptoms
Ilarvirus infection appears to be symptomless in Rubus. However, in Germany
ApMV infection of some red raspberry cultivars was associated with conspicuous
yellow spots and line-pattern.
Host range
Ilarviruses infect a wide range of plant species. ApMV is especially common in
woody perennials, including Malus, Prunus, Rosa and Humulus as well as Rubus
species. TSV infects in addition to Rubus several herbaceous species including
Fragaria.
Geographical distribution
The viruses are reported worldwide in various crops. In Rubus, TSV is reported
only from Australia and North America and ApMV only from Germany and North
America.
Transmission
Transmi t t ed t hrough seed and possi bl y t hrough pol l en. Thri ps have been
implicated in pollen transmission of some isolates in experiments using herbaceous
plants.
Therapy
No i nf or mat i on f or Rubus . ApMV has been el i mi nat ed from Rosaceae by
thermotherapy.
Indexing
Readily detected in young leaf tissue in early spring by mechanical inoculation of
sap in 2% nicotine solution to many herbaceous plants (see underlined note of
caution on p. 10). While the response of test plants varies with the virus isolate,
Chenopodium quinoa is sensitive to infection with most isolates. The symptoms
are local chlorotic or necrotic lesions, followed by systemic necrosis or ‘chlorotic
rings and line-patterns. Serological tests are necessary to identify and distinguish
ApMV and TSV isolates from other possible viruses. Several serotypes of these two
viruses are known, which may not react with some antisera in certain kinds of
tests.
68
References
Baumann, G., Casper, R. & Converse, R.H. 1987. Apple mosaic virus in Rubus. pp.
246-248. In: Virus Diseases of Small Fruits. Ed. R.H. Converse. United States
Department of Agriculture, Agriculture Handbook No. 631, Washington,
D.C.
Jones, A.T. & Mayo, M.A. 1975. Further properties of black raspberry latent virus,
and evidence for its relationship to tobacco streak virus. Ann. Appl. Biol.
79:297-306.
Stace-Smith, R. 1987. Tobacco streak virus in Rubus. pp. 235-239. In: Virus Diseases
of Small Fruits. Ed. R.H. Converse. United States Department of Agriculture,
Agriculture Handbook No. 631, Washington, D.C.
6. Nepoviruses
Virus particles are isometric and about 30 run in diameter, with angular outlines; a
proportion on the particles are penetrated by negative stains. The following
nepoviruses have been reported in Rubus: arabis mosaic virus (ArMV), cherry leaf
roll virus (CLRV), strawberry latent ringspot virus (SLRSV), raspberry ringspot
virus (RRSV), tomato black ring virus (TBRV), cherry rasp leaf virus (CRLV),
tobacco ringspot virus (TRSV), tomato ringspot virus (ToRSV) and Rubus Chinese
seed-borne virus (RCSbV).
Symptoms
Symptoms vary depending on the cultivar, virus and environmental conditions.
Symptoms may range from chlorotic mottling, line-pattern, mosaic, vein yellowing
to leaf curling; symptomless infection also occurs. There is usually a progressive
decline in vigour and plants become stunted. Some cultivars are prone to develop
‘crumbly’ fruit following infection with some nepoviruses. Symptoms are most
obvious in early spring growth and are often less noticeable as the season
progresses.
Host range
Nepoviruses infect a wide range of plants in many genera, including many weed
species.
Geographical distribution
Nepoviruses occur worldwide, but are most common in Europe and North
America. ArMV, CLRV, SLRSV, EtRSV and TBRV are reported in Rubus f r om
Europe; CRLV and TRSV from North America; ToRSV from North America and
Chile. CLRV has also been detected in red raspberry in New Zealand. RCSbV was
detected in Rubus seed imported into England from China.
69
Fig. 28. Chlorotic mottling in red raspberry infected with
cherry leaf roll virus. (Dr. AT. Jones, Scottish Crop
Research Institute, Invergowrie)
Transmission
With the exception of RCSbV, for which little information exists, and of CLRV,
nepoviruses are transmitted in nature through soil by nematodes of the genus
Longidorus (RRSV, TBRV) and Xiphinema (ArMV, SLRSV, TRSV, ToRSV). CLRV
was not transmitted experimentally by nematodes; evidence exists for its pollen
transmission in some host species. All are transmitted, often to a high frequency,
through the seed of some hosts. Nepoviruses can be transmitted experimentally by
grafting and by mechanical inoculation of sap extracts to herbaceous test plants.
Therapy
No information available for nepoviruses in Rubus, but see the Nepovirus item in
the strawberry section.
Indexing
Detected by mechanical inoculation of sap extracted in 2% nicotine alkaloid solution to
herbaceous test plants (see underlined note of caution on p. 10). Chenopedium quinoa
is sensitive to infection, producing chlorotic or necrotic local lesions followed by
systemic mosaic or necrosis. However, serological tests are necessary to identify and
distinguish nepoviruses from one another and from other possible viruses. ELISA alone
is not recommended for detecting CLRV, RRSV, TBRV and ToRSV as a range of
serological variants exist that may not react with certain antisera.
70
References
Barbara, D.J., Ashby, S.C. & McNamara, D.G. 1985. Host range, purification and
some properties of Rubus Chinese seed-borne virus. Ann. Appl. Biol. 107:45-55.
Jones, A.T. 1985. Cherry leaf roll virus. AAB Descriptions of Plant Viruses No. 306.
Association of Applied Biologists, Wellesbourne.
Jones, A.T., McElroy, F.D. & Brown, D.J.F. 2981. Tests for transmission of cherry
leaf roll virus using Longidorus, Paralongidorus and Xiphinema nematodes.
Ann. Appl. Biol. 9 9:143-150.
Jones, A.T., Mitchell, M.J. & Brown, D.J.F. 1989. Infectibility of some new raspberry
cultivars with arabis mosaic and raspberry ringspot viruses and further
evidence for variation in British isolates’ of these two nepoviruses. Ann.
Appl. Biol. 115:5769.
Murant, A.F. 1970. Arabis mosaic virus. CMI/AAB Descriptions of Plant Viruses
No. 16. Commonwealth Agricultural Bureaux, Slough.
Murant, A.F. 1970. Tomato black ring virus. CMI/AAB Descriptions of Plant
Viruses No. 16. Commonwealth Agricultural Bureaux, Slough.
Murant, A.F. 1974. Strawberry latent ringspot virus. CMI/AAB Descriptions of
Plant Viruses No. 126. Commonwealth Agricultural Bureaux, Slough.
Murant, A.F. 1978. Raspberry ringspot virus. CMI/AAB Descriptions of Plant
Viruses No. 198. Commonwealth Agricultural Bureaux, Slough.
St at e-Smi t h, R. & Hansen, A. J. 1976. Cherry rasp l eaf vi rus. CMI/ AAB
Descriptions of Pl ant Vi r uses No. 159. Commonweal t h Agr i cul t ur al
Bureaux, Slough.
7. Raspberry bushy dwarf virus (RBDV)
Virus particles are quasi-isometric and about 33 nm in diameter. They are
disrupted in phosphotungstate, but stable in uranyl acetate and uranyl formate
negative stains.
Symptoms
Often symptomless in Rubus plants. However, in sensitive raspberry cultivars and
under ill-defined environmental conditions, it is the cause of yellows disease,
characterized by yellowing of interveinal areas of leaves. These areas can merge to
form rings or line-patterns or complete yellowing of the leaf. In mixed infections
with aphid-borne viruses in raspberry it causes degeneration in vigour. In some
cultivars it is the cause of ‘crumbly’ fruit.
Host range
Rubus spp.
71
Fig. 29. Leaves on the right show
yellowing caused by raspberry bushy
dwarf virus. (Dr. G. Wood,
Horticulture and Food Research
Institute of New Zealand, Auckland)
Geographical distribution
Worldwide. One strain, termed RB, seems restricted to central Europe, Russia and
Siberia and to isolated areas in England and some parts of western Europe.
Transmission
In nature, RBDV is transmitted through seed of Rubus hosts and also through
infected pollen to the plant pollinated. Transmitted experimentally by grafting and
by mechanical inoculation of sap extracts to herbaceous plants.
Therapy
Not readily eradicated by thermotherapy alone. However, thermotherapy for
several weeks at 36°C followed by propagating from shoot tips or apical meristems
has been successful in eradicating the virus from plants.
Fig. 30. Crumbly fruit caused by
raspberry bushy dwarf virus,
compared to healthy (left). (Dr. G.
Wood, Horticulture and Food
Research Institute of New Zealand,
Auckland)
7 2
Indexing
Readily transmitted from Rubus by mechanical inoculation of sap extracts in 2%
nicotine alkaloid solution to several herbaceous species (see underlined note of
caution on p. 10). Chenopodium quinoa is sensitive to infection and develops
occasional local chlorotic or necrotic lesions and systemic chlorotic spots and line-
patterns. Serological tests are necessary to identify and distinguish RBDV from
other possible viruses. ELISA readily detects RBDV and is more reliable then
bioassay for detecting black raspberry isolates which appear to have a low specific
infectivity.
References
Barbara, D.J., Jones, A.T., Henderson, S.J., Wilson, S.C. & Knight, V.H. 1984.
Isolates of raspberry bushy dwarf virus differing in Rubus host range. Ann.
Appl. Biol. 105:49-54.
Murant, A.F. 1987. Raspberry bushy dwarf. pp. 229-234. In: Virus Diseases of Small
Fruits. Ed. R.H. Converse. United States Department of Agriculture,
Agriculture Handbook No. 631, Washington, D.C.
8. Raspberry leaf mottle virus (RLMV)
No information on morphology and taxonomy.
Symptoms
Induces severe tip necrosis and mosaic in black raspberry. Most red raspberry and
blackberry cultivars are infected symptomlessly or show only a transient chlorotic
mottle or line-pattern in early spring growth. However, a few red raspberry
cultivars show sharply defined angular chlorotic or yellow spots randomly
distributed over the leaf to give a mosaic appearance. Leaves of affected plants are
often smaller in size and deformed. Symptoms are usually more severe on leaves
of fruiting canes than of primocanes and affected plants die within 3-5 years of
infection. In mixed infections with rubus yellow net virus in sensitive red
raspberry cultivars, it causes veinbanding mosaic disease, characterized by
chlorosis of the lamina adjacent to the main veins; in severely affected plants leaves
become puckered and distorted.
Host range
Rubus spp.
Geographical distribution
Common in Europe and detected in Australia and New Zealand probably as a
result of importing infected material. Circumstantial evidence suggests it also
73
occurs in North America. Usually occurs as a complex infection with one or more
of the following viruses: black raspberry necrosis, raspberry leaf spot, and Rubus
yellow net to cause diseases known as veinbanding mosaic disease or raspberry
mosaic.
Transmission
Transmitted in nature in a non-persistent manner by the aphid Amphor ophor a
i daei and possi bl y by ot her aphi ds f eedi ng on Ru b u s s pp. Tr a ns mi t t e d
experimentally by grafting, but not by mechanical inoculation of sap extracts to
herbaceous plants.
Therapy
Eradicated from plants by thermotherapy.
Indexing
Graft-inoculation to cultivars ‘Mailing Delight’, ‘Mailing Landmark’, ‘St. Walfried’
and ‘Veten’. The commonly used virus indicators, R. henryi and R. occidentalis
develop severe tip necrosis followed by mosaic when infected, but they react
similarly to infection with some other aphid-borne viruses of Rubus.
References
Guy, G.L., McGechan, J., Sampson, P.Y. & Stace-Smith, R. 1982. Occurrence of
viruses in Rubus cultivars and species in Australia. Acta Hortic. 129:31-39.
Jones, A.T. 1987. Raspberry leaf mottle and raspberry leaf spot. pp. 183-187. In:
Virus Diseases of Small Fruits. Ed. R.H. Converse. United States Department
of Agriculture, Agriculture Handbook No. 631, Washington, D.C.
Jones, A.T. 1991. Rubus host range of rubus yellow net virus and its involvement
with other aphid-borne latent viruses in inducing raspberry veinbanding
mosaic disease. Ann. Appl. Biol. 118 :331-338.
9. Raspberry leaf spot virus (RLSV)
No information on morphology and taxonomy.
Symptoms
Induces severe tip necrosis and mosaic in black raspberry. Most red raspberry and
blackberry cultivars are infected symptomlessly or show only a transient chlorotic
mottle or line-pattern in early spring growth. However, a few red raspberry
cultivars show sharply defined angular chlorotic or yellow spots randomly
distributed over the leaf to give a mosaic appearance. Affected leaves are often
smaller in size and deformed, and plants die within 3-5 years of infection
Symptoms are usually more severe on leaves of fruiting canes than of primocanes.
74
Fig. 31. Angular chlorotic spots caused
by raspberry leaf spot virus. Left leaf
from infected primocane, right from
infected fruiting cane. (Dr. R.H.
Converse, Horticultural Crops Research
Laboratory, Corvallis)
Host range
Rubus spp.
Geographical distribution
Common in Europe and detected in Australia and New Zealand probably as a
result of importing infected material. Probably of limited distribution in Australia.
Circumstantial evidence suggests it also occurs in North America. Usually occurs
as a complex infection with one or more of the following viruses: black raspberry
necrosis, raspberry leaf mottle and Rubus yellow
veinbanding mosaic disease or raspberry mosaic.
net to cause diseases known as
Transmission
Transmitted in nature in a non-persistent manner by the aphid Amphor ophor a
i daei and pos s i bl y by ot her aphi ds f eedi ng on Ru b u s s pp. Tr a ns mi t t e d
experimentally by grafting, but not by mechanical inoculation of sap extracts to
herbaceous plants.
Therapy
Eradicated from plants by thermotherapy.
Indexing
Identified only by symptoms in sensitive red raspberry cultivars, or by graft-
inoculation to such cultivars. Indicator cultivars include ‘Burnetholm’, ‘Glen Clova’,
‘Norfolk Giant’ and ‘Phyllis King’. The commonly used virus indicators R. henryi
and R. occidentalis develop severe tip necrosis followed by mosaic when infected,
but they react similarly to infection with some other aphid-borne viruses of Rubus.
Reference
Jones, A.T. 1987. Raspberry leaf mottle and raspberry leaf spot. pp. 183-187. In:
Virus Diseases of Small Fruits. Ed. R.H. Converse. United States Department
of Agriculture, Agriculture Handbook No. 631, Washington, D.C.
75
10. Raspberry vein chlorosis virus (RVCV)
Electron microscopy of ultrathin sections of infected leaves show large bacilliform
particles about 65-91 x 430-560 nm which are rounded at each end. Particles have a
densely staining nucleocapsid, about 50 x 70 nm in diameter, showing cross-
banding with a periodicity of 4-5 nm, and surrounded by an electron-lucent zone
and a unit membrane. No particles were observed in the nucleus of infected cells.
Symptoms
Symptoms are most noticeable on leaves of primocanes, appearing as a chlorosis of
the fine veins, either in patches or throughout the leaf. The extent and severity of
the symptoms depends on the cultivar and growing conditions.
Host range
Found only in red raspberry.
Geographical distribution
Canada, Europe, New Zealand.
Transmi ssion
Transmitted in nat ur e i n a persistent manner
by
t he aphi d Aphi s idaei.
Transmitted experimentally by grafting, but not by mechanical inoculation of sap
extracts or through seed of infected plants.
Therapy
Not eradicated from infected plants by thermotherapy alone, but plants free from
the virus were obtained when this treatment was followed bv rooting excised
,
shoot tips or by meristem tip culture.
Fig. 32. Chlorosis of the fine veins caused by raspberry vein
chlorosis virus. (Scottish Crop Research Institute,
Invergowrie)
76
Indexing
Graft-inoculation to indicator red raspberry cultivars such as ‘Malling Delight’,
‘Lloyd George’ or ‘Washington’.
References
Jones, A.T., Murant, A.F. & Stace-Smith, R. 1987. Raspberry vein chlorosis. pp. 194-
197 In: Virus Diseases of Small Fruits. Ed. R.H. Converse. United States
Department of Agriculture, Agriculture Handbook No. 631, Washington, D.C.
Jones, A.T. & Wood, G.A. 1979. The virus status of raspberries (Rubus idaeus L.) in
New Zealand. N.Z. J. Agric. Res. 22:173-182.
11. Raspberry yellow spot virus (RYSV)
No information on morphology and taxonomy.
Symptoms
Diffuse chlorotic or yellow spots of regular size randomly distributed over the leaf.
In the most severe instances the whole leaf may appear yellow. Affected leaves are
often smaller in size and deformed. Symptoms are usually more severe on leaves
of fruiting canes than of primocanes.
Host range
Only reported from ‘Malling Promise’ red raspberry.
Geographical distribution
Reported only from Poland, but similar symptoms have been observed in plants of
‘Malling Promise’ raspberry in Scotland.
Transmission
Reported to be transmitted in nature in a semi-persistent manner by the aphid
Amphorophora idaei. Transmitted experimentally by grafting.
Therapy
Eradicated from infected plants by thermotherapy.
Indexing
Graft-inoculation to ‘Malling Promise’ red raspberry.
Reference
Basak, W. 1974. Yellow spot - a virus disease of raspberry. Bull. Acad. Pol. Sci. Cl.
V. Ser. Sci. Biol. 22:47-51.
77
12. Rubus yellow net virus (RYNV)
Virus particles are bacilliform, rounded at both ends and measure 25-31 x 80-150
nm, with an electron-dense core about 17 nm in diameter; a possible member of the
‘badnavirus’ group.
Symptoms
Often symptomless when alone in raspberry; in sensitive cultivars it produces a
chlorosis of the fine veins to form a net appearance. Infected plants show no
obvious decrease in vigour. However, t he vi rus i s usual l y found i n mi xed
infections with other aphid-borne viruses. In combination with some of these in
sensitive raspberry cultivars it induces raspberry veinbanding mosaic disease
characterized by a chlorosis along the lamina adjacent to the main veins. Such
multiple infections greatly decrease plant vigour.
Host range
A few species in the genus Rubus.
Geographical distribution
Probably worldwide, wherever Rubus is grown. Usually occurs as a complex
infection with one or more of the following viruses: black raspberry necrosis,
raspberry leaf spot, and raspberry leaf mottle to cause diseases known as
veinbanding mosaic disease or raspberry mosaic.
Fig. 33. Chlorosis of the fine veins forming a net
appearance, caused by Rubus yellow net virus. (Dr.
R.H. Converse, Horticultural Crops Research
Laboratory, Corvallis)
78
Transmission
Transmitted by the raspberry aphids Amphorophora agathonica in North America
and A. rubi in Europe. Other Rubus-infesting aphids may also serve as vectors.
The vector transmits after an acquisition feed of 1 hour. There is no latent period in
the vector, and aphids lose the capacity to transmit the virus after feeding for 2-3
hours.
Therapy
RYNV is classified as a heat-stable virus, in that it survives in plants held for
several weeks at an air temperature of 37°C, near the maximum at which plants
can survive. Small shoot tips or meristems excised from heat-treated plants and
induced to root may be free of the virus.
Indexing
When on its own in plants, RYNV can be detected by graft-inoculation to R .
macraei in which the virus induces distinct interveinal clearing and yellowing.
Symptoms are less clear in graft-inoculated R. occidentalis. However, as RYNV is
usual l y found i n compl ex wi t h ot her aphi d-borne vi ruses, graft or aphi d
transmission to R. occidentalis will transmit the complex of viruses and some of
t hem wi l l i nduce necrot i c sympt oms t hat mask t hose i nduced by RYNV.
Thermotherapy of plants infected with the virus complex will inactivate most other
viruses, leaving RYNV free from contaminating viruses.
References
Jones, A.T. 1991. Rubus host range of Rubus yellow net virus and its involvement
with other aphid-borne latent viruses in inducing raspberry veinbanding
mosaic disease. Ann. Appl. Biol. 118 :331-338.
Stace-Smith, R. & Jones, A. T. 1978. Rubus yel l ow net vi r us. CMI / AAB
Descriptions of Plant Viruses No. 188. Commonweal t h Agr i cul t ur al
Bureaux, Slough.
Stace-Smith, R. & Jones, A.T. 1987. Rubus yellow net. pp. 175-178. In: Virus
Diseases of Small Fruits. Ed. R.H. Converse. United States Department of
Agriculture, Agriculture Handbook No. 631, Washington, D.C.
13. Wineberry latent virus (WLV) (see also blackberry calico
virus (BCV))
Virus particles are flexuous filaments about 12 x 620 nm which showed no
serological relationship to viruses with particles of similar size. However, it shows
several similarities to blackberry calico carlavirus.
Fig. 34. Necrotic local lesions in
Chenopodium amaranticolor 20 days
after inoculation with wineberry latent
virus. (Scottish Crop Research Institute,
Invergowrie)
79
9
Symptoms
In mixed infections with raspberry bushy dwarf virus (RBDV) WLV induced
pronounced veinal chlorotic line-pattern and/or chlorotic blotches, symptoms
typical of calico disease.
Host range
Reported only in Rubus spp.
Geographical distribution
Detected in Scotland in wineberry (R. phoenicolasius) originally imported from
USA.
Transmission
No information on natural transmission. Not seed transmitted in wineberry.
Transmitted experimentally by grafting and by mechanical inoculation of sap
extracts to herbaceous plants.
Therapy
No information.
Indexing
WLV from wineberry, co-infected with RBDV, was readily transmitted from Rubus
in 2% nicotine alkaloid solution to herbaceous plants (see underlined note of
caution on p. 10). However, a Dutch culture of a virus that may be similar to WLV,
but free from RBDV, was transmitted in this way only with great difficulty. In
Chenopodium quinoa and C. amaranticolor, WLV induces necrotic local lesions
that gradually expand in size; it is only weakly systemic in these species. Electron
microscopy and/or serological tests are necessary to identify and distinguish WLV
from other possible viruses. WLV was not detected by ELISA in Rubus.
80
References
Converse, R.H. 1987. Blackberry calico. pp. 245-246. In: Virus Diseases of Small
Fruits. Ed. R.H. Converse. United States Department of Agriculture,
Agriculture Handbook No. 631, Washington, D.C.
Jones, A.T. 1987. Wineberry latent virus. pp. 239-241. In: Virus Diseases of Small
Fruits. Ed. R.H. Converse. United States Department of Agriculture,
Agriculture Handbook No. 631, Washington, D.C.
Jones, A.T., Mitchell, M.J., McGavin, W.J. & Roberts, I.M. 1990. Further properties
of wineberry latent virus and evidence for its possible involvement in calico
disease. Ann. Appl. Biol. 117 :571-581.
Prokaryotic diseases - ‘MLOs’
1. Boysenberry decline
Cause
Unknown, possibly a non-cultivable mollicute, often referred to as mycoplasma-
like organism (MLO).
Fig. 35. Symptoms of boysenberry decline in
flowers (top) and fruits (bottom) of
boysenberry. Flower symptoms are shortened
stamens, with styles and stigmas enlarged;
fruitlets from infected plants have the
appearance of a hard green cone. (Dr. G. Wood,
Horticulture and Food Research Institute of
New Zealand, Auckland)
81
Fig. 36. Fruiting canes of plants
affected by boysenberry decline,
showing proliferating shoot growth and
red down-curled leaves (right),
compared to shoot growth of a healthy
plant on the left. (Dr. G. Wood,
Horticulture and Food Research
Institute of New Zealand, Auckland)
Symptoms
Abnormally large flowers with crinkled petals, and large distorted sepals. Stamens
are shortened, styles and stigmas enlarged, giving the young fruitlet formed in the
flowers the appearance of a hard green cone. Large, sharp spines develop on
flower stems. Fruits fail to develop and remain as small, hard, hairy cones. Shoot
growth proliferates on the fruiting canes, growing to a metre or more in length,
and develops small down-curled leaves which become distinctly red in colour.
Symptoms do not occur on the primocanes.
Host range
Confined to boysenberry, but suspected symptoms have been found on loganberry
and several blackberry cultivars following graft-inoculation.
Geographical distribution
Found only in New Zealand.
Transmission
Transmitted by grafting. Suspected to be transmitted by the bramble leaf hopper
Ribautiana tenerrima, but this has not been confirmed.
Therapy
No information available.
Indexing
Grafting to boysenberry,
Reference
Wood, G.A. 1991. Three
small fruit in New
graft-transmissible diseases and a variegation disorder of
Zealand. N.Z.J. Crop Hortic. Sci. 1 9:313-323.
82
2. Rubus stunt
Cause
The causal agent is believed to be a non-cultivable mollicute, often referred to as
mycoplasma-like organism (MLO).
Symptoms
The disease is characterized by thin, spindly canes showing excessive lateral
branching, to form a witches-broom appearance, proliferation of flowers and
phyllody.
Host range
All raspberry and blackberry cultivars as well as raspberry x blackberry hybrids
seem infectible.
Geographical distribution
Reported only from Southern Britain, Europe and Russia.
Transmission
Transmitted in nature in a persistent manner by leafhoppers, mainly in the genus
Mac r ops i s . The mai n vect or i n Europe i s M. f us cul a. Al s o t r a ns mi t t e d
experimentally by froghoppers (spittle bugs) and by graft-inoculation to Rubus and
plants of other genera.
Fig. 37. Floricane of blackberry showing witches’
broom symptoms typically of Rubus stunt disease. (Dr.
R.H. Converse, Horticultural Crops Research
Laboratory, Corvallis)
83
Therapy
Eradicated from plants by thermotherapy in hot water (45°C) for 2-3 hours.
Indexing
Graft-inoculation to sensitive cultivars such as ‘Malling Landmark’ raspberry or
‘Thornless Evergreen’ blackberry.
References
Murant, A.F. & Roberts, I.M. 1971. Mycoplasma-like bodies associated with Rubus
stunt disease. Ann. Appl. Biol. 6 7:389-393.
van der Meer, F.A. 1987. Rubus stunt. pp. 197-203. In: Virus Diseases of Small
Fruits. Ed. R.H. Converse. United States Department of Agriculture,
Agriculture Handbook No. 631, Washington, D.C.
Prokaryotic diseases - bacteria
1. Crown and cane gall
Cause
Two species of Agrobacterium are associated with the crown gall syndrome on
Rubus: A. tumefaciens (E.F. Smith & Towns.) Conn and A. rubi (Hildebr.) Starr &
Weiss. The latter is associated with galls on canes.
Symptoms
Galls typically form in the crown area or on roots. They may also form at pruning
wounds or natural splits in canes. Initially galls are soft and become hard with age.
Severely infected canes exhibit a number of symptoms including stunting, foliar
chlorosis, small and seedy fruit, wilting and at times death. Galls blacken and die
during winter. New galls erupt the following spring in the vicinity of old galls.
With time plants become progressively less vigorous.
Host range
Broad, including all species of Rubus.
Geographical distribution
Worldwide.
8 4
Biology and transmission
Infection occurs through wounds. Wounds can result from natural causes (lateral
root formation, leaf scars) or mechanical damage (pruning, training practices,
cultivation, harvesting, insect feeding, frost, etc.). Infection results in the
uncontrolled synthesis of plant hormones stimulating host cells to abnormally
multiply. Temperatures below 15°C delay symptom development leading to latent
infections. Symptoms develop at 20°C. Infection is inhibited above 32°C. Once the
pathogen‘s DNA becomes incorporated into the genome of the host, new galls
develop even though the pathogen dies during winter
Reference
Moore, L.N. 1991. Crown and cane gall. pp. 39-40. In: Compendium of Raspberry
and Blackberry Diseases and Insects. Eds. M.A. Ellis, R.H. Converse, R.N.
Williams & B. Williamson. APS Press, St. Paul.
2. Fireblight
Cause
Erwinia amylovora (Burr.) Winslow et al.
Symptoms
Charact eri st i c wat er-soaked l esi ons t hat produce abundant bact eri al ooze.
Diseased parts of canes become necrotic and purplish black. Infected berries do not
mature; they become dry, brown, and very hard.
Host range
Fireblight is a common and very serious disease of many rosaceous plants, but on
Rubus cane fruits it is relatively uncommon and rarely of economic importance.
Geographical distribution
Fireblight on Rubus has occasionally been reported from eastern USA.
Biology and transmission
The initial inoculum source is probably from overwintering cankers on Rubus.
Isolates from Rubus infect only Rubus, those from apples and pears are not
pathogenic on Rubus. Warm temperature and light rain favour infections.
Reference
Ries, S. M. 1991. Fireblight. pp. 40-41. In: Compendi um of Raspberry and
Blackberry Diseases and Insects. Eds. M.A. Ellis, R.H. Converse, R.N.
Williams & B. Williamson. APS Press, St. Paul.
85
3. Hairy root
Cause
Agrobacterium rhizogenes (Riker et al.) Conn.
Symptoms
Infected parts develop abnormally fibrous roots.
Host range
Rubus spp., Malus spp. and Rosa spp.
Geographical distribution
Unknown.
Biology and transmission
The bacterium is exclusively a wound pathogen and soil-borne and may be readily
transmitted with nursery stock.
Reference
Ellis, MA. 1991. Hairy root. p. 42 In: Compendium of Raspberry and Blackberry
Diseases and Insects. Eds. M.A. Ellis, R.H. Converse, R.N. Williams & B.
Williamson. APS Press, St. Paul.
Fungal diseases
1. Blackberry rust
Cause
Phragmidium violaceum (C.F. Schultz) Winter, a macrocyclic autoecious rust
fungus.
Symptoms
The disease affects most plant parts including leaves, leaf veins, petioles, flowers
and fruit. Symptoms on leaves are the most common. On the upper surface of
leaves, symptoms first appear as yellowish-red blotches and develop in about ten
days into purple or red circular spots (up to 4 mm in diameter). These spots often
have yellow to brown centers. On the lower leaf surface beneath the spots, golden
yellow powdery pustules (uredinia) appear. When the disease is severe, leaf edges
may curl, the entire leaf may turn chlorotic and drop prematurely. Uredinia
eventually turn black as telia develop. Pustules are larger on susceptible genotypes
than on resistant ones.
86
Host range
European blackberry (Rubus fruticosus) and some cultivated blackberries.
Geographical distribution
Common in Europe and the Middle East. The disease also occurs in Australia,
Chile and New Zealand.
Biology and transmission
The pathogen most likely overwinters as teliospores on old leaves. One report
indicates that the pathogen overwinters as a perennial mycelium on stems and
produces urediniospores directly in the spring,
Reference
Washington, W.S. 1991. Blackberry rust. pp. 32-33. In: Compendium of Raspberry
and Blackberry Diseases and Insects. Eds. M.A. Ellis, R.H. Converse, R.N.
Williams & B. Williamson. APS Press, St. Paul.
2. Cane and leaf rust
Cause
Kuehneola uredinis (Link) Arthur, a macrocyclic autoecious rust fungus.
Symptoms
Large, lemon yellow pustules of powdery urediniospores split the bark in late
spring on infected floricanes. In early summer, small yellow uredinia develop on
the lower surfaces of the leaves of these floricanes. Severe infection causes
premature defoliation. Only rarely are rust symptoms observed on fruit.
Host range
This rust attacks blackberry and blackberry hybrids. It occurs only rarely on red
and black raspberries.
Geographical distribution
North America and Australia.
Biology and transmission
The fungus probably overwinters on canes as mycelium or latent uredinia.
Urediniospores infect leaves on the same or other floricanes during the growing
season. Telia develop on leaves in late fall and basidiospores from germinating
teliospores infect adjacent leaves of primocanes. Disease development is favoured.
87
by wet conditions. Cane and leaf rust is not systemic and care should be taken not
t o conf us e i t s i dent i f i cat i on wi t h t he s ys t emi c or ange r us t s caus ed by
Arthuriomyces peckianus and Gymnoconia nitens.
Reference
Ellis, M.A. 1991. Cane and leaf rust p. 28. In: Compendium of Raspberry and
Blackberry Diseases and Insects. Eds. M.A. Ellis, R.H. Converse, R.N.
Williams & B. Williamson. APS Press, St. Paul.
3. Downy mildew
Cause
Peronospora sparsa Berk.
Symptoms
Angular lesions occur on upper surfaces of leaves, first yellow, later turning red to
purple. On lower leaf surfaces opposite these lesions, pink to tan spots appear on
which spore masses may be borne. Systemically infected plants may produce
distorted leaves with a mosaic pattern of small, reddish lesions, later becoming
necrotic with chlorotic margins. Suckers and infected canes from such plants may
be stunted with reddish blotches on leaves and canes. Infected fruit is dull, without
sheen. Berries infected early turn red prematurely, shrivel and harden, while those
infected late may split in two and become shriveled. Pedicels may become infected,
turning red.
Host range
Rubus and Rosa species.
Geographical distribution
Worldwide on Rubus, except in South America.
Biology and transmission
Air-borne spores of this obligate parasite are produced on infected plants during
cool, wet nights and are wind-disseminated. These spores can infect foliage,
blossoms and berries. Cool, moist conditions favour infection. In some areas,
oospores develop in early summer in infected leaves and sepals. Systemic
infections may occur, especially in blackberry-raspberry hybrids, like boysenberry,
in which intercellular mycelium may spread throughout the plant. Inoculum from
Rubus and Rosa species is cross-infective.
88
Reference
Gubler, W.D. 1991. Downy Mildew. pp. 15-16. In: Compendium of Raspberry and
Blackberry Diseases and Insects. Eds. M.A. Ellis, R.H. Converse, R.N.
Williams & B. Williamson. APS Press, St. Paul.
4. Late leaf rust
Cause
Pucciniastrum americanum (Farl.) Arthur.
Symptoms
This rust disease is not systemic. On mature leaves many small spots develop and
turn yellow and eventually brown before the leaves die in autumn. Small uredinia
filled with powdery yellow spores are formed on the underside of infected leaves.
Badly infected leaves drop prematurely, and the canes of highly susceptible
cultivars may be bare by early autumn. Flower calyces, petioles, and fruit at all
stages of development are also attacked. On fruit, uredinia develop on individual
drupelets, producing yellow masses of urediniospores.
Host range
Many cultivated red and purple raspberries and some wild red raspberries.
Geographical distribution
Canada, USA.
Biology and transmission
The causal organism is heteroecious and macrocyclic. It produces spermagonia and
aecia on white spruce (Picea glauca) and uredinia and telia on Rubus spp. White
spruce is the most common host for the aecial stage. The main uredinial hosts are
red and purple raspberries.
Reference
Ellis, M.A. 1991. Late leaf rust. pp. 30-31. In: Compendium of Raspberry and
Blackberry Diseases and Insects. Eds. M.A. Ellis, R.H. Converse, R.N.
Williams & B. Williamson. APS Press, St. Paul.
5. Orange rus t
Cause
Art huri omyces pecki anus (Howe) Cummins & Y. Hirats. (demicyclic) and
Gymnoconia nitens (Schwein.) F. Kern & Thurst. (endocyclic); both rust fungi are
autoecious.
89
Fig. 38. Orange rust caused by
Gymnoconia nitens native North
American blackberry Rubus alumnus.
(Dr. J. Postman, USDA-ARS-NCGR,
Corvallis)
Symptoms
Fi r s t s ympt oms i n s pr i ng ar e t he s pi ndl y and cl us t er ed young s hoot s .
Characteristic are the bright orange aecia on the lower leaf surface. Plants infected
with the demicyclic form Arthuriomyces peckianus develop dark telia. Plants
become systemically infected, although primocanes and floricanes may appear
healthy.
Host range
The demicyclic form attacks mostly black raspberries, whereas the endocyclic form
predominates on blackberries. Red raspberries are immune.
Geographical distribution
Asia, Australia, Europe and North America.
Biology and transmission
The fungi overwinter as systemic, perennial mycelium. Gymnoconia nitens ma y
also overwinter as teliospores. Disease development is favoured by cool and wet
conditions. Orange rust is easily confused with the non-systemic cane and leaf rust
caused by Kuehneola uredinis.
Reference
Kleiner, W.C. & Travis, J.W. 1991. Orange rust pp. 26-28. In: Compendi um of
Raspberry and Blackberry Diseases and Insects. Eds. M.A. Ellis, R.H.
Converse, R.N. Williams & B. Williamson. APS Press, St. Paul.
90
6. Phytophthora root rot
Cause
Six different Phytophthora species have been reported on roots of Rubus.
Species Location
P. fragariae Hickman var. rubi Wilcox & Duncan
P. cactorum (Lebert & Cohn) Schröt.
P. citricola Sawada
P. cryptogea Pethybr. & Laff.
P. drechsleri Tucker
P. cambivora (Petri) Buisman
Eastern N. America*
Western N. America**
UK and Europe***
USA and UK
USA, UK and Poland
USA and Australia
UK
UK
* formerly P. fragariae Hickman
** formerly P. erythroseptica Pethybr.
*** formerly P. megasperma (type 2) Drechsler
Symptoms
Both primocanes and floricanes may exhibit symptoms. Infected primocanes may
rapidly wilt and collapse. Collapse can occur at any time during the spring. On
succulent young primocanes dark, water-soaked lesions form at the base. Wilting
usually begins at the tip of primocanes progressing downward. Primocanes which
survive may die during the winter. Affected floricanes typically produce weak
lateral shoots. Leaves turn yellow, wilt or scorch along the margins or between the
veins. Severely affected floricanes may wilt and die during flowering or before
harvest . Scrapi ng t he epi dermi s f r om r oot s of i nf ect ed pl ant s r eveal s a
characteristic reddish brown discoloration. A distinct margin is usually evident at
the interface of diseased and healthy root tissues. Extension of necrosis into the
crown is common.
Host range
Red raspberry (Rubus idaeus) and some of its hybrids. Black raspberry ( R.
occidentalis) may also be infected.
91
Geographical distribution
Worldwide. Serious outbreaks have occurred in Australia, Europe, North America
and the UK. For distribution of species, see above.
Biology and transmission
Once present, Phytophthora spp. persist primarily as mycelium in recently infected
tissues or as dormant oospores that are released into soil as infected tissues die and
decompose. Oospores may remain viable for a number of years in soil in the
absence of a host. Oospores are insensitive to environmental extremes and
chemicals (fungicides and f umi gant s ) appl i ed t o s oi l . The s oi l moi s t ur e
requirement for germination of oospores is high.
References
Bristow, P.R., Daubeny, H.A., Sjulin, T.M., Pepin, H.S., Nestby, R. & Windom, G.
1988. Evaluation of Rubus germplasm for reaction to root rot caused by
Phytophthora erythroseptica. J. Am. Soc. Hortic. Sci. 113:588-591.
Duncan, J.M. & Kennedy, D.M. 1989. The effect of waterlogging on Phytophthora
root rot on red raspberry. Plant Pathol. 38:161-168.
Wilcox, W.F. 1991. Phytophthora root rot. pp. 34-36. In: Compendium of Raspberry
and Blackberry Diseases and Insects. Eds. M.A. Ellis, R.H. Converse, R.N.
Williams & B. Williamson. APS Press, St. Paul.
Wilcox, W.F., Scott, P.H., Hamm, P.B., Kennedy, D.M., Duncan, J.M., Brasier, C.M.
& Hansen, E.M. 1993. Identity of a Phytophthora species attacking red
raspberry in Europe and North America. Mycol. Res. 97:817-831.
7. Verticillium wilt (bluestem or bluestripe wilt)
Cause
Verticillium albo-atrum Reinke & Berth. and/or V. dahliae Kleb.
Symptoms
On black and purple raspberry, leaves of infected fruiting canes may turn yellow
and then wilt and die. Infected canes are often stunted and may turn entirely blue
or blue on one side before they die. Infected vessels generally have a red
coloration. Symptoms on red raspberry are usually less severe than on black
raspberry. Leaflets on infected plants often fall before the petioles drop. Cane
discoloration is not as evident as on black raspberry. Plants may survive for years,
but are stunted and suckering is reduced. On blackberries the infected canes wilt,
92
leaves turn yellow and become brown and necrotic, Cool weather in the autumn
may lead to a disappearance of symptoms. Canes do not turn blue, as they do in
infected black raspberry. Infected fruiting canes may survive the winter, leaf out
and set fruit, but as the fruits ripen during the summer, the canes usually collapse.
Host range
Black, purple and red raspberry and blackberry.
Geographical distribution
Northern part of the USA and along the Pacific Coast, particularly in California.
Biology and transmission
The fungus survives as microsclerotia or as melanized hyphal fragments bound
within plant debris or free in the soil. Hyphae from these structures penetrate root
hairs or the root cortex directly and enter xylem vessels. The fungi can also
penetrate through breaks or wounds in the roots. Movement within the host occurs
by growth of the hyphae through the vessels and by movement of conidia in the
transpiration stream. Upon death of infected plant parts, new fungal survival
structures are formed and returned to the soil where they survive for up to 14
years.
Reference
Ellis, M.A. 1991. Verticillium wilt. pp. 36-37. In: Compendium of Raspberry and
Blackberry Diseases and Insects. Eds. M.A. Ellis, R.H. Converse, R.N.
Williams & B. Williamson. APS Press, St. Paul.
8. White root rot
Cause
Vararia spp. (Lachnocladiaceae), various basidiomyceteous fungi.
Symptoms
These pathogens cause a root rot, dieback and death of plants. Vararia spp. induce
yellowing, wilting and dieback of canes which is especially rapid in young plants.
Roots and crowns are also rotted and characteristically covered by a white
mycelial mat. White rhizomorphs may develop on the surface of these parts.
Similar symptoms have been obs er ved i n New Zeal and, but unr el at ed
basidiomyceteous fungi have been reported.
93
Host range
This disease has been reported on field-infected raspberry, on loganberry and once
on plum. Other rosaceous plants have been artificially inoculated.
Geographical distribution
Australia, New Zealand.
Biology and transmission
Vararia can probably survive in soil for several years on infected roots or canes. It
spreads within a planting via root contact and less often by the spread of infected
roots and canes through cultivation. Disease severity is greatest when the soil
moisture is low and soil temperatures are high.
References
Pascoe, I.G., Washington, W.S. & Guy, G. 1984. White root rot of raspberry in
Victoria is caused by a Vararia species. Trans. Br. Mycol. Soc. 82:723-726.
Washington, W.S. 1991. White root rot. pp. 38-39. In: Compendium of Raspberry
and Blackberry Diseases and Insects. Eds. M.A. Ellis, R.H. Converse, R.N.
Williams & B. Williamson. APS Press, St. Paul.
Vaccinium spp. (blueberry, cranberry)
Viruses
1. Blueberry red ringspot virus (BRRV)
A caulimovirus with isometric of particles of about 42-46 nm in diameter.
Fig. 39. Symptoms of blueberry red
ringspot virus on highbush blueberry:
red rings enclosing green leaf tissue.
(Dr. J. Postman, USDA-ARS-NCCR,
Corvallis
94
Symptoms
Infected plants are usually symptomless until fruit is formed. Then red rings or
reddish spots 2-6 mm in diameter may develop on the upper sides of leaves. The
rings often enclose green leaf tissue. Similar spots and rings form on the epidermis
of canes. Occasionally rings form on the fruit of some cultivars. Leaves often
develop reddish autumn coloration several weeks before those of healthy plants.
Host range
Vaccinium corymbosum and V. australe.
Geographical distribution
USA.
Transmission
BRRV spreads in New Jersey but not in Michigan or in Oregon. The vector is
suspected, but not proven, to be a mealybug (Dysmicoccus spp.). The virus is not
mechanically transmitted.
Therapy
BRRV is difficult to eliminate by propagating from new growth following extended
thermotherapy.
Indexing
Chronic infections of BRRV are not known to be latent when leaf symptoms reach
their height after harvest and before normal autumn foliar coloration develops. At
other times of the year BRRV is difficult to detect by symptomatology. Identity can
be confirmed by ELISA in symptomatic leaves.
References
Hepp, R.F. & Converse, R.H. 1987. Blueberry red ringspot virus detection in crude
sap of highbush blueberry plants. Plant Dis. 71:536-539.
Ramsdell, D.C., Kim, K.S. & Fulton, J.P. 1987. Red ringspot of blueberry. pp. 121-
123. In: Virus Diseases of Small Fruits. Ed. R.H. Converse. United States
Department of Agriculture, Agriculture Handbook No. 631, Washington,
D.C.
Ramsdell, D.C. 1994. Red ringspot. In: Compendium of Blueberry and Cranberry
Diseases. Eds. F.L. Caruso & D.C. Ramsdell. APS Press (in press).
95
2. Blueberry scorch virus (BBScV)
A flexuous, rod-shaped carlavirus, about 610-700 nm in length. Virus particles
contain a positive sense, single-stranded RNA genome. Sheep Pen Hill disease
(SPHD) in New Jersey, USA is caused by a closely related virus.
Symptoms
Some cultivars react with complete necrosis of flowers and leaves that eventually
leads to bush death, others do not seem to be adversely affected by infection. Some
cultivars show a flower necrosis combined with a marginal leaf chlorosis.
Sympt oms us ual l y appear on one or a f ew br anches t he f i r s t year and
progressively spread to affect the entire bush in subsequent years.
Ho s t r a n g e
Highbush blueberry (Vaccinium corymbosum).
Ge ogr aphi c al di s t r i but i on
USA.
Tr ans mi s s i on
BBScV has been experimentally transmitted by the blueberry aphid Fimbriaphis
fimbriata. Field studies involving placement of healthy ‘trap’ bushes in commercial
plantings with scorch disease have shown that transmission is directly correlated
wi t h t he col oni zat i on of t rap pl ant s by bl ueberry aphi ds. BBScV i s graft -
transmissible.
Fig. 40. Complete necrosis of flowers
and leaves of highbush blueberry
caused by blueberry scorch virus. (Dr. J.
Postman, USDA-ARS-NCGR, Corvallis)
96
Therapy
No information is available about the elimination of BBScV from Vaccinium.
Indexing
ELISA detects BBScV and SPHD-related virus in blueberry.
References
MacDonald, S.G., Martin, R.R. & Bristow, P.R. 1989. Viruses capable of causing a
scorch disease of highbush blueberry. Acta Hortic. 241 :295-300.
Martin, R.R. & Bristow, P.R. 1988. A carlavirus associated with blueberry scorch
disease. Phytopathology 7 8: 1636- 1640.
Martin, R.R. & Bristow, P.R. 1994. Blueberry scorch. In: Compendium of Blueberry
and Cranberry Diseases. Eds. F.L. Caruso & D.C. Ramsdell. APS Press (in
press).
Podleckis, E.V. & Davis, R.F. 1989. Infection of highbush blueberries with a
putative carlavirus. Acta Hortic. 241:337-342.
3. Blueberry shock ilarvirus (BSIV)
A virus with quasi-isometric particles 26-29 nm in diameter.
Symptoms
Affected young leaves wilt and have blackened veins and black streaks down the
petiole, or they blight to an orange colour. Both blighted blossoms and leaves drop,
so by early summer the affected bushes can be completely defoliated. As the
season progresses the bushes appear to recover as a second flush of leaves is
produced. By late summer, these plants appear normal except there is little fruit
produced. On occasi on, t he affect ed bushes are st unt ed, especi al l y when
symptoms persist for 3 or 4 years.
Host range
Highbush blueberry
(Vaccinium corymbosum).
Geographical distribution
Northwest USA.
Fig. 41. Blighted blossoms and leaves in
highbush blueberry infected with
blueberry shock ilarvirus. (Dr. P.R.
Bristow, Washington State University,
Puyallup)
97
Transmission
BSIV is graft-transmissible. It can be transmitted mechanically to Ni cot i ana
clevelandii from blossoms of infected bushes. It has not been possible to transmit
the virus mechanically from other blueberry tissues. The virus can be transmitted
to a number of species of Nicotiana and maintained in these plants in a glasshouse
at temperatures below 22°C, but not at higher temperatures. Also pollen-borne in
blueberry. Natural infection only occurs during the bloom period. There is a one
year latent period between infection and symptom development.
Therapy
No information is available about the elimination of BSIV from Vaccinium.
Indexing
ELISA is reliable for the detection of BSIV in blueberry tissues. Graft-inoculation to
‘Berkeley’.
References
MacDonald, S.G., Martin, R.R. & Bristow, P.R. 1991. Characterization of an
i l ar vi r us as s oci at ed wi t h a necr ot i c s hock r eact i on i n bl ueber r y.
Phytopathology 81:210-214.
Martin, R.R. & Bristow, P.R. 1994. Blueberry shock. In: Compendium of Blueberry
and Cranberry Diseases. Eds. F.L. Caruso & D.C. Ramsdell. APS Press (in
press).
4. Blueberry shoestring virus (BSSV)
An isometric virus, about 28 nm in diameter.
Symptoms
The most prominent symptoms consist of elongated reddish streaks approximately
0.4 x 1.25 to 2.5 cm on current year and l-year-old stems. Blossoms may have a
pinkish cast on infected bushes. Infected leaves are often strap-shaped or may be
crescent shaped. Some leaves may show a reddish oak-leaf pattern on the lamina.
Ripe fruit on infected bushes usually has a reddish to purplish cast rather than a
deep blue colour. The terminal one third of stems may be crooked on infected
bushes. There is a 4-year latent period between infection and onset of symptoms.
Host range
Host range of BSSV is limited to some cultivars of highbush blueberry (Vaccinium
corymbosum).
98
Fig. 42. Strap-shaped leaves infected
with blueberry shoestring virus (in
foreground left) compared to normal
leaves. (Dr. J. Postman, USDA-ARS-
NCGR, Corvallis)
Geographical distribution
Northeast USA.
Transmission
BSSV is transmitted by the blueberry aphid Illinoia pepperi. The virus is not
mechanically transmissible.
Therapy
No information.
Indexing
Indexing by ELISA is routinely used to detect BSSV in suspect plants. Polyclonal
antisera work extremely well. Commercial ELISA kits are available in the USA.
References
Morimoto, K.M., Ramsdell, D.C., Gillett, J.M. & Chaney, W.G. 1985. Acquisition
and transmission of blueberry shoestring virus by its aphid vector Illinoia
pepperi. Phytopathology 75:709-712.
Ramsdell, D.C. 1987. Blueberry shoestring. pp. 103-405. In: Virus Diseases of Small
Fruits. Ed. R.H. Converse. United States Department of Agriculture,
Agriculture Handbook No. 631, Washington, D.C.
Ramsdell, D.C. 1994. Shoestring. In: Compendium of Blueberry and Cranberry
Diseases. Eds. F.L. Caruso & D.C. Ramsdell. APS Press (in press).
5. Nepoviruses
Four nepoviruses have been reported from blueberry, namely tobacco ringspot
virus (TRSV), tomato ringspot virus (ToRSV), blueberry leaf mottle virus (BLMV),
and peach rosette mosaic virus (PRMV). Virus particles are isometric, about 30 nm
in diameter with angular profiles.
99
Symptoms
Symptoms vary with the individual virus, cultivar and time of the year. Symptoms
are usually more conspicuous in spring, when new growth may show chlorotic
and necrotic spots. Stem dieback and stunting frequently occur when susceptible
cultivars are infected.
Host range
Within Vaccinium, the viruses have only been found in the highbush blueberry (V.
corymbosum). Nepoviruses that have been isolated from blueberry have a wide
natural host range.
Geographical distribution
In highbush blueberry, the viruses are confined to the USA. ToRSV occurs in the
northern states, TRSV in the eastern states, BLMV and PRMV in Michigan.
Transmission
In nature, transmitted by vectors belonging to the Dorylaimidae. Natural spread of
TRSV, ToRSV and PRMY is thought to be by Xiphinema americanum. Natural
transmission of BLMV is by honey bees (Apis mellifera). Pollen contains a high
level of virus.
Therapy
No information available for Vaccinium.
Indexing
Serological procedures (usually ELISA) may be used to identify nepoviruses either
directly from blueberry or from herbaceous test plants. Nepoviruses can be
mechani cal l y t ransmi t t ed from bl ueberry t o herbaceous host s, whi ch are
satisfactory for detection, but not for identification.
References
Boylan-Pett, W., Ramsdell, D.C., Hoopingarner, R.A. & Hancock, J.F. 1991.
Honeybee foraging behavior, in-hive survival of infectious, pollen-borne
blueberry leaf mottle virus and transmission of the virus in highbush
blueberry. Phytopathology 8 1:1407-1412.
and sections on nepoviruses in: Compendi um of Bl ueberry and Cranberry
Diseases. Eds. F.L. Caruso & D.C. Ramsdell. APS Press (in press).
100
6. Ringspot of cranberry
The causal agent has not been positively identified, but is probably a caulimovirus.
Virus-like particles and inclusion bodies have been observed in diseased leaf
tissue.
Symptoms
Fruit on affected plants is often misshapen with pale or whitish rings when ripe.
There is necrosis at the blossom end of many berries and in severe cases whole
berries are necrotic. Ringspot symptoms are also produced on the leaves. Rings
become visible in the autumn when leaves turn colour; the rings stay green as the
remainder of the leaf turns reddish. The disease appears to be systemic. It
adversely affects the keeping quality of fruit.
Host range
American cranberry (Vaccinium macrocarporn). There is no information on
experimental hosts.
Geographical distribution
Eastern USA.
Fig. 43. Ringspot of cranberry: fruits with
whitish rings (top) and ringspot symptoms on
leaves (bottom). (Dr. P.R. Bristow, Washington
State University, Puyallup)
101
Transmission
At present there is no information on either natural or experimental transmission.
Therapy
No information available.
Indexing
No information available.
Reference
Boone, D.M. 1994. Ringspot. In: Compendi um of Bl ueberry and Cranberry
Diseases. Eds. F.L. Caruso & D.C. Ramsdell. APS Press (in press).
Stretch, A.W. 1987. Ringspot disease of cranberry. pp. 123-124. In: Virus Diseases
of Small Fruits. Ed. R.H. Converse. United States Department of Agriculture,
Agriculture Handbook No. 631, Washington, D.C.
Disease of unknown etiology
Blueberry mosaic
Cause
Unknown.
Symptoms
Patterns of yellow, light green or white mottle and mosaic that vary in intensity.
Pink areas sometimes appear in the mosaic or mottled tissues. Symptoms may be
uneven on an infected bush, infecting all or only a few branches. Over several
years, symptoms may appear, disappear, and reappear on the same bush. Fruit
yield and quality are reduced. The light and dark green mosaic pattern on leaves of
the cultivar ‘Coville’ may be of genetic origin.
Host range
Vaccinium corymbosum and V. vacillans.
Geographical distribution
Canada and USA.
Transmission
Blueberry mosaic disease is not sap-transmitted or dodder-transmitted. It spreads
slowly in the field by unknown means, and is graft-transmissible.
1 0 2
Fig. 44. Blueberry mosaic
J. Postman, USDA-
disease. (Dr.
ARS-NCGR,
Corvallis)
Therapy
No information.
Indexing
The cultivars ‘Rubel’ and ‘Bluecrop’, chip-bud graft-inoculated at bud-break, can be
used as indicators. True latency of blueberry mosaic disease in highbush blueberry
cultivars is not known to occur. However, because of the irregular timing of the
appearance of symptoms, a bush being used to obtain softwood or hardwood
cuttings for propagation should be observed for several years before being
declared free from this disease.
Reference
Ramsdell, D.C. & Stretch, A.W. 1987. Blueberry mosaic. pp. 119-120. In: Virus
Diseases of Small Fruits. Ed. R.H. Converse. United States Department of
Agriculture, Agriculture Handbook No. 631, Washington, D.C.
Prokaryotic diseases - ‘MLOs’
1. Blueberry stunt (BBS)
Cause
A phloem-limited non-cultivable mollicute, often referred to as mycoplasma-like
organism (MLO), with a diameter ranging from 160 to 700 nm.
103
Symptoms
On highbush blueberry, overall dwarfing of the bush is the primary symptom,
hence the name stunt. Symptomatic leaves may be spoon-shaped ‘rather than
lanceolate; they are usually cupped slightly downward, and exhibit chlorosis of the
margins. Chlorosis of the leaves may occur between lateral veins. The midribs and
lateral veins usually retain normal green coloration. Chlorotic areas often turn a
brilliant red in the late summer and early autumn. Stem internodes become
shortened, and growth of normally dormant buds causes twiggy branching.
Host range
All cultivars of highbush blueberry are susceptible. ‘Rancocas’ is the only cultivar
with a high degree of resistance. V. australe, V. vacillans, V. atrocuccum, V.
stamineum and V. myrtilloides are also susceptible to natural infection. Graft
transmission to V. amoenum, V. altomontanum, V. elliottii and V. ashei has been
achieved. Dodder (Cuscuta campestris and C. subinclusa) has been successfully
used to transmit the causal organism to periwinkle (Catharanthus roseus).
Geographical distribution
St unt di s eas e has been r epor t ed f r om
eas t er n Canada, and eas t er n and
southeastern USA.
Transmission
The leafhoppers Scaphytopius magdalensis, S. acutus and S. frontalis have been
shown experimentally to be vectors. The causal organism is not mechanically
transmitted.
Therapy
Thermotherapy is effective in eradicating infected blueberry of the causal
organism.
Indexing
Indexing on cultivar ‘Cabot’.
References
Chen, T.A. 1971. Mycoplasma-like organisms in sieve tube elements of plants
infected with blueberry stunt and cranberry false blossom. Phytopathology
61:233-236.
104
Maramorosch, K. 1955. Transmission of blueberry stunt virus by Scaphytopius
magdalensis. J. Econ. Entom. 48:106.
Ramsdell, D.C. 1987. Blueberry stunt. pp. 106-108. In: Virus Diseases of Small
Fruits. Ed. R.H. Converse. United States Department of Agriculture,
Agriculture Handbook No. 631, Washington, D.C.
Tomlinson, W.E. Jr., Marucci, P.E., & Doehlert, C.A. 1950. Leafhopper transmission
of blueberry stunt disease. J. Econ. Entom. 43:658-662.
Tozzi, D.C.M., Ramsdell, D.C., Taboada, O., Lee, I.M., & Davis, R.E. 1993.
Epidemiological studies on the stunt disease of highbush blueberry. Ann.
Appl. Biol. 123:579-599.
2. Cranberry false blossom
Cause
The causal agent appears to be a non-cultivable mollicute, often referred to as a
mycoplasma-like organism (MLO).
Symptoms
This disease is most easily recognized at bloom. Flowers on infected plants are
upright because the pedicels are straight rather than arched. The petals of diseased
flowers are short and streaked with green and red. The lobes of the calyx are
enlarged compared to those on a healthy flower. Diseased flowers are usually
sterile as both-the stamens and pistil are abnormal. Axillary buds which normally
remain dormant are stimulated to produce branches giving a witches’-broom effect
to infected uprights. Leaves on these branches are usually closely appressed to the
stem. In autumn infected branches prematurely redden. Terminal flower buds on
infected uprights are enlarged.
Host range
In nature restricted to American cranberry ( Vacci ni um macr ocar pon) a n d
European cranberry (V. oxycoccus), which reflects vector feeding preference.
Geographical distribution
Appears to be indigenous in Wisconsin, USA and was probably distributed to
other production areas in North America.
Transmission
Natural transmission is by the blunt-nosed leafhopper Scleroracus vaccinii. This
insect is the only known vector.
105
Fig. 45. Cranberry false blossom: upright flowers with
straight pedicels and short petals (right) compared to
normal flowers (left). (Dr. R.H. Converse, Horticultural
Crops Research Laboratory, Corvallis)
Therapy
Hold potted plants at 42-43°C for 8 days. Treat a large number of plants as about
one-third will be killed by the treatment. High temperatures for periods up to 10
days caused less injury ‘than treatments at somewhat lower temperatures for
longer periods. The pathogen is eliminated from the vines but it is unknown if the
roots are pathogen-free following thermotherapy.
Indexing
Transmission to tomato or periwinkle by dodder or by grafting.
References
Chen, T.A. 1971. Mycoplasmalike organisms in sieve tube elements of plants
infected with blueberry stunt and cranberry false blossom. Phytopathology
61:233-236.
Dobroscky, I.D. 1929. Cranberry false blossom spread by a leafhopper. Science
70:635.
Kunkel, L.O. 1945. Studies of cranberry false blossom. Phytopathology 35:805-821.
Stretch, A.W. 1987. Cranberry false blossom. pp. 110-111. In: Virus Diseases of
Small Fruits. Ed. R.H. Converse. United States Department of Agriculture,
Agriculture Handbook No. 631, Washington, DC.
106
3. Witches’-broom
Cause
Electron microscopy of ultra-thin sections has revealed polymorphous cell-wall-
less non-cultivable mollicutes, often referred to as mycoplasma-like organisms
(MLO), in phloem sieve tubes. No dimensions of the causal agent are reported.
Symptoms
Infected V. myrtillus plants show a very dense, bushy growth. This is due to the
erect position of the excessively formed new branches. This phenomenon is
associated with a striking reduction in size of branches and leaves. Branches of
plants affected in a later stage of growth have only an erect position instead of the
plagiotropic position of normal, healthy plants. Plants affected earlier in their
development remain small, are heavi l y branched and have smal l er l eaves.
Diseased plants drop their leaves later in autumn than healthy plants. Sometimes
leaves on infected plants show some reddening due to increased anthocyanin
formation. Diseased plants do not flower at all.
Host range
Vaccinium myrtillus, V. vitis-idaea, V. uliginosum and V. oxycoccus.
Geographical distribution
Czechoslovakia, France, Germany, The Netherlands, Scotland and Yugoslavia.
Transmission
The leafhopper Idiodunus cruentatus can transmit the disease to V. myrtillus,
however, t he di sease al so occurs where I. cruentatus has not been f ound.
Experiments have indicated that the leafhoppers Empoasca solani, Neophilaenus
exclamationis, Aphrodes bicinctus, Euscelis spp., and Macropsis fuscula do not
transmit the disease.
Fig. 46. Symptoms of witches’ broom
(right) compared to healthy Vaccinium
myrtillus (left). (Dr. R.H. Converse,
Horticultural Crops Research
Laboratory, Corvallis)
107
Indexing
The disease may be detected by graft or vector transmission to V. myrtillus, V.
vitis-idaea, V. uliginosum or V. oxycoccus.
References
deLeeuw, G.T.N. 1987. Witches’-broom of Vaccinium. pp. 108-110. In: Virus
Diseases of Small Fruits. Ed. R.H. Converse. United Sates Department of
Agriculture, Agriculture Handbook No. 631, Washington, DC.
Prokaryotic disease - bacteria
Crown gall
Cause
The soil-borne bacterium Agrobacterium tumefaciens (E.F. Smith & Towns.) Conn,
belonging to the family Rhizobiaceae. The causal agent of the disease in eastern
Nor t h Amer i ca was at t r i but ed t o Agr obac t e r i um t ume f ac i e ns var . r u b i
(Hildebrand) Starr & Weiss, a pathogen initially isolated from galls on floricanes of
Rubus spp.
Symptoms
Galls are most common at the base of canes or on the major roots but rarely on the
smaller roots. Occasionally galls form on branches higher in the bush, especially
after flooding. Young galls are cream-coloured to light brown while mature galls
are dark brown to black. Older galls are rough and hard. Galls may be elongate as
a result of several smaller adjacent galls coalescing, but are usually spherical. They
vary in size, with a few becoming large (1 to 16 cm in diameter). Infected bushes
may be stunted or weak compared to healthy ones. When older bushes (2 to 5
years) are affected the foliage discolours prematurely in the summer. Initially the
foliage on an affected branch or bush takes on a reddish hue and then becomes
yellowish-brown as the disease worsens.
Host range
Isolates of A. tumefaciens from other crops, including apple, dahlia, hop and
peach; did not induce gall formation on blueberry. Similarly, isolates from
blueberry were unable to infect apple and peach.
Geographical distribution
Crown gall is present in all blueberry growing areas of North America. The disease
has also been seen in Chile, but it may have come in on planting stocks from North
America.
108
Biology and transmission
The pathogen requires a
can result from natural
wound
causes,
to enter the host and initiate infection. Wounds
i.e. lateral root formation or bud scale and leaf
scars, or from mechanical causes, i.e. pruning, cultivating,
feeding, root injury at planting, or frost damage. Wounds
harvesting, insect
generally remain
suscept i bl e f or 2 t o 4 days dur i ng t he war m t emper at ur es of summer ; at
temperatures below 13°C they can remain susceptible for weeks. During this
period infection is also influenced by soil moisture and population levels of the
pathogen.
References
Demaree, J. B. & Smi t h, N. R. 1952. Bl ueberry gal l s caused by a st rai n of
Agrobacterium tumefaciens. Phytopathology 42:88-90.
Moore, L.W. 1980. Controlling crown gall with biological antagonists. Amer .
Nurseryman 151 :40-44.
Fungal diseases
1. Botryosphaeria stem canker
Cause
Botryosphaeria corticis (Demaree & Wilcox) von Arx & Müll.
Symptoms
Symptoms first appear as small red lesions on succulent stems 7 days after
infection Lesions develop slowly, becoming swollen and broadly conical within 6
months in susceptible cultivars. Symptoms vary with the susceptibility of the plant.
Large swollen cankers with deep fissures and cracks develop on susceptible
cultivars after 2 to 3 years, while cankers are restricted in size on the more resistant
cultivars. On very susceptible cultivars, e.g. ‘Weymouth’ and ‘Wolcott’, cankers
enlarge and may girdle and kill the stem.
Host range
The causal fungus infects highbush blueberry ( Vacci ni um corymbosum) a n d
rabbit&ye blueberry (V. ashei).
Geographical distribution
Southeastern USA, including New Jersey.
109
Biology and transmission
Stem infection of current season’s growth occurs in late spring when ascospores
and conidia are released from perithecia and pycnidia, respectively, during rain
and are disseminated throughout the planting. Temperature influences the number
and type of lesions. The optimal temperature for fungal growth, sporulation and
spore germination is 25-28°C. Disease development is limited to small red flecks at
16°C. However, at optimal temperatures large cankers form and stems become
girdled and die.
Reference
Milholland, R.D. & Galletta, G. J., 1969. Pathogenic variation among isolates of
Botryosphaeria corticis. Phytopathology 59:1540-1543.
2. Cottonball (Hard rot, Tip blight)
Cause
Monilinia oxycocci (Woronin) Honey.
Symptoms
The tip blight stage of the disease is visible in late spring when tips of uprights
suddenly wilt. The stem curves over forming a crazier. Masses of greyish-white
powdery conidia cover the crazier. Conidia infect flowers via the stigma and style
but flowers remain symptomless. Infected fruit ripen abnormally; rarely showing
any red colour. Yellowish-brown bands appear lengthwise on infected berries and
they expand until the berry is uniformly yellowish-brown in colour. The interior of
the berry is filled with the cottony white mycelium of the pathogen. Sclerotia form
in infected fruit in the fall (hard rot stage of the disease).
Fig. 47. Tip blight stage of cottonball disease
caused by Monilinia oxycocci. (Dr. P.R. Bristow,
Washington State University, Puyallup)
110
Host range
American cranberry (Vaccinium macrocarpon) and possibly European cranberry
(V. oxycoccus).
Geographical distribution
North America.
Biology and transmission
The pathogen overwinters as sclerotia on fruits. New vegetative growth is infected
by ascospores during early spring. Conidia only infect flowers, leading to the hard
rot stage.
References
Boone, D.M. 1982. Hard rot and tip blight of cranberry. University of Wisconsin
Extension A 3194.
Sanderson, P.G. & Jeffers, S.N. 1992. Cranberry cottonball: Dispersal periods of
primary and secondary inocula of Monilinia oxycocci host susceptibility and
disease development. Phytopathology 82:384-392.
Sanderson, P.G. & Jeffers, S.N. 1994. Cottonball. In: Compendium of Blueberry and
Cranberry Diseases. Eds. F.L. Caruso & D.C. Ramsdell. APS Press (in press).
3. Fusicoccum Canker (Godronia canker)
Cause
Godronia cassandrae Peck (anamorph = Fusicoccum putrefaciens Shear).
Symptoms
Reddish-brown elliptical cankers 1 to 10 cm in length form on l- and 2-year-old
stems. These cankers are often covered with black pycnidia that are 1 to 2 mm in
diameter. Usually cankers are centered on a leaf scar. Most cankers are in the
bottom 1/3 of the bush or in the crown area. During the summer when a fruit load
is on the bush, the entire stem may wilt. Leaves turn a reddish-brown colour and
remain attached. On older wood (especially pruning stubs), apothecia may form.
They are 1 to 3 mm in diameter, hard, black and somewhat difficult to find.
Host range
Found on highbush blueberry (Vaccinium corymbosum), V. angustifolium, V.
caespitosum, and Chamaedaphne calyculata. The causal organism is similar to that
causing end rot of cranberry.
Geographical distribution
Canada, Finland, northern Germany, UK and northern USA.
111
Biology and transmission
The causal fungus is spread by rain-splashed conidia from pycnidia on the canker
surface during the growing season from bud break in spring until leaf drop in
autumn. Direct infection occurs on current year as well as l- and 2-year-old stems.
References
Lockhart, C.L. & Craig, D.L. 1962. Fusicoccum canker of highbush blueberry in
Nova Scotia, Canada. Plant Dis. Survey 47:17-20.
Lockhart, C.L. 1972. Occurrence and pathogenicity of Godronia cassandrae f .
vaccinii on lowbush blueberry in Nova Scotia, Canada. Plant Dis. Survey
52:49-121.
Parker, P.B. & Ramsdell, DC. 1977. Epidemiology and chemical control of
Godronia (Fusicoccum) canker of highbush blueberry. Phyt opat hol ogy
67 :1475-1480.
Weingartner, D. P. & Klos, E. J. 1975. Etiology and symptomatology of canker and
dieback diseases of highbush blueberries caused by Godronia (Fusicoccum)
cassandrae and Diaporthe (Phomopsis) vaccinii. Phytopathology 65:105-110.
4. Mummy berry disease
Cause
Monilinia vaccinii-corymbosi (Reade) Honey.
Symptoms
A shoot blight occurs in early spring when shoots are 4-10 cm long. Symptoms
appear about two weeks after ascosporic infection of newly emerging leaf buds.
Blighted shoots and blossom clusters turn brown. Tan-coloured sporulation forms
in tufts on infected leaves. Conidia infect the blossoms as they open. No symptoms
occur until fruit ripening, at which point the fruit turns soft and pinkish. The fruits
fall to the ground, become shriveled, brown, and resemble a miniature pumpkin.
Host range
Highbush (Vaccinium corymbosum), lowbush (Vaccinium angustifolium) a nd
rabbiteye (Vaccinium ashei) blueberry.
Geographical distribution
North America.
112
Fig. 48. Mummy berry disease caused by
Monilinia vaccinii-corymbosi: shoot blight
occurring in early spring (top) and pinkish
fruits (bottom). (Dr. D.C. Ramsdell,
Department of Botany and Plant Pathology,
Michigan State University, East Lansing)
Biology and transmission
The fungus overwinters in mummified fruits. With sufficient moisture, apothecia
are formed in spring, which liberate ascospores and infect the newly emerging
green tissue.
References
Ramsdell, D.C., Nelson, J.W. & Myers, R.L. 1974. An epidemiological study of
mummy berry disease of highbush blueberry. Phytopathology 64:222-228.
Ramsdell, D.C., Nelson, J.W. & Myers, R.L. 1975. Mummy berry disease of
highbush blueberry: Epidemiology and control. Phytopathology 65:229-232.
5. Phomopsis canker of blueberry (twig blight)
Cause
Phomopsis vaccinii Shear.
113
Symptoms
Cankers may be formed on 1, 2 and 3-year-old stems. They are usually found from
the soil-line up to 1 to 1.5 m above ground. Newly formed cankers become evident
in early to mid-summer. They are brownish and are on l-year-old stems with a
length. of 2 to 10 cm or more. A canker may encircle the entire stem. Cankers on
older stems turn a greyish colour and become somewhat flattened. The surface of
older cankers is ususally covered with pycnidia that are about 0.5 mm in diameter.
The cankers usually progress downward and become 10 to 20 cm long, covering
the whole shoot. During the summer when a load of fruit is on the bush, cankered
stems wilt. Leaves are reddish in colour and will remain on the stem. This
symptom is very similar to that associated with Fusicoccum canker.
Host range
Limited to highbush blueberry (Vaccinium corymbosum).
Geographical distribution
Northern Germany and northern USA.
Biology and transmission
The causal fungus is spread by conidia in pycnidia on cankers as the result of
splashing rain. Disease spread occurs from bud break in the spring until late
summer when inoculum is depleted. Infection of current yea-r and l-and 2-year-old
stems occurs through wounds caused by mechanical abrasion and frost injury.
References
Parker, P.E. & Ramsdell, D.G. 1977. Epidemiology and chemical control of
Phomopsis canker of highbush blueberry. Phytopathology 67:1481-1484.
Weingartner, D.P. & Klos, E.J. 1975. Etiology and symptomatology of canker and
dieback diseases on highbush blueberries caused by Godronia (Fusicoccum)
cassandrae and Diaporthe (Phomopsis) vaccinii. Phytopathology 65:105-110.
6. Phytophthora root rot
Cause
Phytophthora cinnamomi Rands.
Symptoms
Foliar symptoms depend on the extent of root damage. When severe, early spring
growth may wilt and die suddenly. Less severe root damage may result in stunting
114
of terminal growth, yellowing of leaves, and possibly defoliation. Leaves on canes
which die suddenly usually turn orange. The fine fibrous roots are destroyed.
Major roots and the crowns show a reddish-brown vascular discoloration when
infected.
Host range
Highbush blueberry (Vaccinium corymbosum). Rabbiteye blueberry (V. ashei) is
tolerant to the disease. Fungus reported on some 900 host plants.
Geographical distribution
Worldwide.
Biology and transmission
The fungus is a common soil inhabitant with a wide host range outside of
Vaccinium. The disease is favoured by warm soil temperatures combined with
high soil moisture. The pathogen may be introduced via irrigation water from
lakes and rivers. The fungus survives for a number of years in soil or decomposing
plant debris as spores, and for shorter periods as chlamydospores. Zoospores
released from germinating sporangia are attracted to roots.
References
Milholland, R. D. 1975. Pathogenicity and histopathology of Phyt opht hor a
cinnamomi on highbush and rabbiteye blueberry. Phytopathology 6 5:789-
793
Milholland, R.D. 1994. Phytophthora root rot. In: Compendium Of Blueberry and
Cranberry Diseases. Eds. F.L. Caruso & D.C. Ramsdell. APS Press, St. Paul
(in press).
7. Rose bloom
Cause
Exobasidium oxycocci Rostr. ex Shear.
Symptoms
Infected dormant axillary buds begin to grow in the early spring, producing fleshy
pink abnormal branches. Affected buds are usually on the previous year’s growth
(one year-old wood). Leaves on the abnormal branch are swollen and close
together. The branch looks like a miniature rose blossom, hence the common name
for the disease. Prior to bloom the entire surface of the abnormal branch becomes
115
covered with whitish masses of basidia and basidiospores. Basidiospores infect
axillary buds on the current year’s growth which give rise to the abnormal
branches the following spring. By late June the abnormal branches wither and turn
black.
Host range
American cranberry (Vaccinium macrocarpon), European cranberry (V. oxycoccus)
and V. palustris.
Geographical distribution
Primarily in Oregon, Washington and British Columbia, but also reported from
other cranberry growing regions of North America. Originally reported from
northern Europe.
Transmission
Primarily in infected buds of one-year old wood.
Reference
Bristow, P.R. 1994. Rose bloom. In: Compendium of Blueberry and Cranberry
Diseases. Eds. F.L. Caruso & D.C. Ramsdell. APS Press (in press).
Fig. 49. Rose bloom of cranberry caused by
Exobasidium oxycocti fleshy pink branches. (Dr. R.S.
Byther, Washington State University, Puyallup)
116
8. Twig blight
Cause
Lophodermium oxycocci (Fr.) P. Karst. and L. hypophyllum (Dearn. & House)
Shear.
Symptoms
Infection of new vine growth occurs during the summer but symptoms do not
appear until winter or more commonly the following spring. Hence, symptomless
dormant vines maybe infected. The fungus kills only 1-year-old wood and does not
progress into older wood. Leaves on 1-year-old wood first turn light brown but
fade to a bleached tan and eventually silvery grey. Infected leaves are dull.
Elliptical black apothecia form on the underside of infected leaves. Mature
apothecia open by a median slit to expose the hymenial layer.
Host range
Limited to the American cranberry (Vaccinium macrocarpon) and possibly the
European cranberry (V. oxycoccus) and Lingonberry (V. vitis-idaea).
Geographical distribution
Cranberry growing regions in North America, but primarily in the states of Oregon
and Washington and Province of British Columbia, as well as Northern Europe.
Biology and transmission
Transmitted by vegetative propagation material and ascospores.
Fig. 50. Apothecia of the twig blight
fungus Lophodermium oxycocci on
cranberry leaves. (Dr. P.R. Bristow,
Washington State University,
Puyallup)
117
References
Bristow, P.R. 1983. Lophodermium twig blight of cranberry; relationship between
i nocul um densi t y, per i od of s us cept i bi l i t y and di s eas e s ever i t y.
Phytopathology 73:957 (abstr.).
Bristow P.R. 1994. Twig blight. In: Compendium of Blueberry and Cranberry
Diseases. Eds. F.L. Caruso & D.C. Ramsdell. APS Press (in press).
9. Upright dieback (Phomopsis canker of cranberry)
Cause
Diaporthe vaccinii Shear
(anamorph: Phomopsis vaccinii Shear).
Symptoms
Diseased upright branches have a yellowish cast in early spring that later may
become orange or bronze. When the branch dies it turns brown. At first, individual
leaves may exhibit a yellow mottling. The pathogen infects fruits causing a berry
rot called “viscid rot”. Infected leaves are soft and pale in colour. The most
diagnostic symptom for viscid rot is the stringing out of a viscous substance when
a finger is touched to and then withdrawn from the cut surface of the rotted berry.
Host range
Amer i can cr anber r y ( Vacci ni um macr ocar pon) , Eur opean cr anber r y ( V.
oxycoccus).
Geographical distribution
North America.
Biology and transmission
The pathogen can be isolated from symptomless cranberry tissues, suggesting that
incipient disease exists. While little is known about the disease cycle, the disease
appears to be favoured by warm temperatures. The pathogen may overwinter in
infected berries left in beds. Both pseudothecia and pycnidia have been observed
on rotted berries. Both types of fruiting bodies are occasionally found on uprights
killed during the previous crop year.
Reference
Boone, D.M. 1982. Viscid rot and upright dieback of cranberry. University of
Wisconsin. Extension Bulletin 3195.
118
Pests of small fruit
Arthropods
Many insects and mites are associated with small fruit germplasm. Some vector
viruses, while others are economic pests in their own right. Since information is
incomplete with respect to the rather large number of arthropods that are found on
the plant material that could be transported for breeding purposes, the application
of sound phytosanitary procedures to prevent the movement of pests is necessary.
Arthropods that are feeding on the roots should be eliminated by propagating
runners or stem cuttings. If it is necessary to move whole plants, the soil must be
washed from the roots. Vegetative material should be treated with a fumigant that
has ovicidal activity, or dipped in an appropriate insecticide prior to potting in
sterilized media. Placement of a systemic insecticide (e.g. aldicarb or oxamyl) in
the root zone of the plant will kill the remaining insects and mites that are feeding
within the plant tissues. Since some arthropod pests may emerge from the plant
material during treatment, the plants should be isolated within a quarantine
facility for at least 10 months. Seed should be free of fruiting material, and
fumigated to eliminate stored products pests if observed or suspected. Pollen may
be contaminated with mites and insects. It may also carry fungi and bacteria that
cause diseases of bees. Although storage of pollen at -20 C will be lethal to many
arthropods, it may not kill all of them. There is no technique available to eliminate
fungi or bacteria that cause bee diseases without destroying the viability of the
pollen. Tissue culture is the best way of ensuring pest-free material.
Fig. 51. Damage of eriophyid mite on
Ribes curvatum. (Dr. J. Postman,
USDA-ARS-NCGR, Corvallis)
119
Er i ophyi d mi t es coul d pr esent speci al pr obl ems f or t he t r ansf er of Ri b e s
germplasm. In particular, the black currant gall mite Cecidophyopsis ribis is a
serious pest of black currant, inducing galls of buds. It is also a vector of currant
reversion disease, which occurs in Ribes worldwide with the exception of the
Americas. Gall mites can be eradicated from buds by immersing them in water at
46 C for 10-20 minutes. However, vegetative material should be treated with a
systemic insecticide that has proven acaricidal value, to eliminate any of the 14
known species of eriophyids on Ribes.
References
Alford, D.V. 1984. A Colour Atlas of Fruit Pests: Their Recognition, Biology and
Control. Wolfe, London.
Hill, D.S. 1987. Agricultural Insect Pests of Temperate Regions and their Control.
Cambridge University Press, Cambridge.
Jeppson, L.R., Keifer, H.H. & Baker, E.W. 1975. Mites Injurious to Economic Plants.
University of California Press, Berkeley.
Nematodes
Nematodes may be found associated with soil surrounding plant roots, within the
roots themselves, or within the above-ground plant tissues. Symptoms of infection
often go undetected and precautions should be taken to eliminate these organisms.
Nematodes that feed on the roots can be eliminated by propagating runners or
stem cuttings. If it is necessary to move whole plants, all soil must be washed from
the roots. All vegetative material should be potted in sterilized media and treated
with a systemic nematicide (e.g. aldicarb or fenamiphos) on a regular basis for at
least 10 months to kill the remaining nematodes. During this time, the plants
should be isolated in a quarantine facility. Seed and pollen may be moved without
concern for nematodes. Tissue culture is the best way of ensuring nematode-free
material.
Bud and leaf nematodes of the genera Aphel enchoi des and Di t yl enchus c a n
present a difficult problem for the transfer of germplasm. In particular, the
strawberry eelworm, Aphelenchoides fragariae, deserves special mention. It is a
serious pest in Europe, causing severely distorted strawberry leaves and reduction
of plant growth. The nematodes inhabit the folded young leaves of crowns and
runner shoots. Field populations normally increase in the early spring and autumn,
but pl ant damage i s not mani fest ed unt i l l at e spri ng and summer, when
populations have already declined. Under glasshouse conditions suitable for
120
runner production, they may survive in low numbers, causing no symptoms until
they are transferred to the field where they experience a period of increasing
temperatures. They also survive for long periods on plants maintained in vitro. No
combination of conventional treatments, nematicide, hot-water treatment (46 C for
10 min.) or meristem tip culture is capable of ensuring freedom from these
nematodes. However, nematode infestation can be entirely eliminated from high-
value strawberry plants (e.g. nuclear stock) by cutting away the upper part of the
crown containing the leaves, thus removing all green tissue from the plant, and
then allowing regeneration from previously dormant buds below.
References
Evans, K., Trudgill, D. & Webster, J.M. (eds.) 1993. Plant Parasitic Nematodes in
Temperate Agriculture. CAB International, Wallingford.
Luc, M., Sikora, R.A. & Bridge, J. (eds.) 1990. Plant Parasitic Nematodes in
Subtropical and Tropical Agriculture. CAB International, Wallingford.
McNamara, D.G. & Barradas, C.M.F. 1985. Aphelenchoides in strawberries. pp.
161-162. In: East Malling Research Station Report for 1984.
McNamara, D.G., Stickles, J.E. & Flegg, J.J.M. 1986. Control of leaf nematodes in
nuclear stock strawberries. pp. 217-219. In: British Crop Protection Council
Monograph No. 33. Symposium on Healthy Planting Material.
121
APPENDIX 1: INSTITUTIONS MAINTAINING SMALL FRUIT GERMPLASM ***
Centre de Recherches Agronomiques
Station des Cultures Fruitières et
Maraîchères
234 chaussee de Charleroi
B-5030 Gembloux
BELGIUM
Plant Gene Resources of Canada
Canadian Clonal Genebank
Agriculture Canada
P.O. Box 340
Trenton, Ontario K8V 5R5
CANADA
Agricultural Research Centre of Finland
Laukaa Research and Elite Plant Unit
Juntula
FIN-41340 Laukaa
FI NLAND
Centre Interrégional de Recherche et
d’Expérimentation de la Fraise
C.I.R.E.F.
Lanxade
24130 Prigonrieux
FRANCE
Centre Technique Interprofessionel des
Fruits et Légumes (C.T.I.F.L.)
B.P. 32
Centre de Balandran
30127 Bellegarde
FRANCE
G.E.V.E.S. (Dr. F. Boulineau)
49250 Brion
FRANCE
Fragaria, in-vitro
virus-tested
Fragaria and Rubus
some material is virus-tested;
also virus-tested tissue cultures
available
Fragaria, Ribes, Rubus, Vaccinium
also virus-tested tissue cultures
available
Fragaria
some
virus-tested;
also virus-tested tissue cultures
material is
available
Fragaria
some material is virus-tested;
also virus-tested tissue cultures
available
Fragaria
virus-tested
122
Institute for Fruit and Ornamentals Fragaria, Rubus, Ribes
Dept. of Fruit Breeding some material is virus-tested;
Fertod - H 9431 also virus-tested tissue cultures
HUNGARY available
Holt Research Station
P.O. Box 2502
N 9002 Tromso
NORWAY
Research Institute of Pomology and
Floriculture
P.O. Box 105
96100 Skiernievice
POLAND
N.I. Vavilov Institute of Plant Industry
Bolshaya Morskaya 4244
190000 St. Petersburg
RUSSIA
Rubus chamaemorus,
Ribes spicatum ‘Atlas’,
wild Ribes spicatum.
The material is not virus-tested.
Fragaria, virus-tested: Senga
Sengana’, ‘Cama’, ‘Dukat’
Rubus, virus-tested: ‘Veten’,
‘Norna’, ‘Canby’, ‘Mailing Seedling’,
‘Polana’, ‘Beskid’, ‘Malling Jewel’
Fragaria, Rubus, Ribes
part of the collection has undergone
meristem tip culture, but no virus
indexing has been conducted.
Accessions received from other
genebanks are supplied with
information on the virus status.
Centro de Investigation y Desarollo
Agrario
C.I.D.A.
Fragaria
some material is virus-tested
Finca Cortijo de la Cruz
29140 Churriana
Malaga
SPAIN
Horticulture Research International
East Malling
Kent, ME 196BJ
UNITED KINGDOM
Fragaria, in vitro
some material is virus-tested
Rubus
untested root cuttings
123
Scottish Crop Research Institute
Invergowrie
Dundee DD25DA
Scotland
UK
Prof. Dr. Donald C. Ramsdell
Dept. of Botany and Plant Pathology
166 Plant Biology Building
Michigan State University
East Lansing, MI 48824
USA
USDA-ARS
National Plant Germplasm Quarantine
Center
Building 508 BARC-E
Beltsville, MD 20705
USA
USDA-ARS-NCGR
33447 Peoria Road
Corvallis, OR 97333
USA
Fragaria, Ribes, Rubus. virus
indicator species
virus-tested highbush blueberry
Fragaria
seeds of virus indicator ‘Alpine’
Ribes, Rubus
cuttings of virus indicators ‘Lloyd
George’, ‘Norfolk Giant’, ‘Munger’,
‘Baldwin’, ‘Amos Black’
Fragaria, Ribes, Rubus, Vaccinium
Some accessions are untested or
virus-infected;
*** This is not an exhaustive list; it contains information given by the contributors to these guidelines. The
details given in the table were supplied by the institutions listed. FAO and IPGRI do not guarantee the
acccuracy of this information. Institutions and individuals wishing to import material on this list shouid
negotiate directly with the supplier. FAO and IPGRI cannot be held responsible for problems resulting
from the introduction of material from the sources listed here.
124
Previ ous l y publ i s hed FAO/ I BPGR Techni cal Gui del i nes f or t he Saf e
Movement of Germplasm
Cocoa
1989
Edible Aroids
1989
Musa
1989
Sweet Potato
1989
Yam
1989
Legumes
Cassava
Citrus
Grapevine
1991
Vanilla
Coconut
1990
1991
1991
1991
1993
Sugarcane
1993
FAO/IPGRI Technical Guidelines for the Safe Movement of Germplasm are published under
the joint auspices of the Plant Production and Protection Division of the Food and Agriculture
Organization of the United Nations (FAO) and the International Plant Genetic Resources In-
stitute (IPGRI).
The designations employed and the presentation of material in these
Guidelines, do not imply the expression of any opinion whatsoever
on the part of FAO, IPGRI or the CGIAR concerning the legal status
of any country, territory, city or area or its authorities, or concerning
the delimitation of its frontiers or boundaries. Similarly, the views
expressed are those of the authors and editors and do not necessar-
ily reflect the views of FAO, IPGRI or CGIAR. In addition, the men-
tion of specific companies or of their products or brand. names does
not imply any endorsement or recommendation on the part of FAO,
IPGRI or CGIAR.
The International Plant Genetic Resources Institute is an autonomous international scientific
organization operating under the aegis of the Consultative Group on International Agricul-
tural Research (CGIAR). IPGRI’s mandate is to advance the conservation and use of plant ge-
netic resources for the benefit of present and future generations. IPGRI works in partnership
with other organizations, undertaking research, training, and the provision of scientific and
technical advice and information. IPGRI retains the strong programme link of its predecessor,
the International Board for Plant Genetic Resources, with the Food and Agriculture Organiza-
tion of the United Nations. Financial support for the core programme of IPGRI is provided by
the Governments of Australia, Austria, Belgium, Canada, China, Denmark, France, Germany,
India, Italy, Japan, the Republic of Korea, the Netherlands, Norway, Spain, Sweden, Switzer-
land, the UK, the USA, and the World Bank.
Citation:
Diekmann, M., Frison, E.A. and Putter, T. (eds.) 1994. FAO/IPGRI Technical Guide-
lines for the Safe Movement of Small Fruit Germplasm. Food and Agriculture Orga-
nization of the United Nations, Rome/International Plant Genetic Resources Insti-
tute, Rome.
ISBN 92-9043-157-1
All rights reserved. No part of this publication may be reproduced, stored in a retrieval sys-
tem, or transmitted in any form or by any means, electronic, mechanical, photocopying or
otherwise, without the prior permission of the copyright owner. Applications for such per-
mission, with a statement of the purpose and extent of the reproduction, should be addressed
to the Publications Office, IPGRI Headquarters, Via delle Sette Chiese 142,00145 Rome, Italy.
© FAO/IPGRI 1994