The earliest land plants, similar to present-day liverworts, arose
at least 475 million years ago, suggest tiny fossilized fragments from
Oman. Up to 420,000 different plant species may be growing on Earth, of
which perhaps 80% have been found and named. The Index Kewensis, a species
record held at Britain's Royal Botanic Gardens in Kew, near London, lists
more than a million Linnaean titles : plants are going extinct before botanists
can record their existence
Web resources :
Until now, researchers believed that pitcher plants—studied since the 17th
century, Federle said—captured most insects using waxy crystals making
slippery inner walls. However, when Federle's team studied Nepenthes bicalcarata—one
of the few species of pitcher plants that have no slippery waxy inner walls
but are nevertheless able to capture insects—after a rainfall
cellulose : a b(1-4)
D-glucose
homopolysaccharide, is the most abundant carbohydrate polymer in nature.
Although abundant, it is extremely difficult to degrade, as it is insoluble
and is present as hydrogen-bonded crystalline fibres. Anaerobic microorganisms
(symbiont in ruminant guts) have evolved a system to break down plant cell
walls that involves the formation of a large extracellular enzyme complex
called the cellulosome
(also in some Protozoa (symbiont in termite gut) and some Fungi
?)
hemicellulose
xilans : b(1->4) heteropolysaccharides
of D-Xil
glucomannans : b(1->4) Glc- and Man-
containing heteropolysaccharides)
It arises from a cellular plate during mitosis.
phragmoplast = the developing cell wall between the nuclei of a
vegetal cell in telophase
protoplast = a vegetal cell deprived (by lisozime) of its cell wall
in an isotonic environment
median lamella = a pectin structure between adjacent cell walls
plasmodesm = cytoplasmic channel between cells (20-30 nm diameter)
whose lumen is occupied by a central desmotubule arose from smooth
endoplasmic reticulum
glyoxisome = the vegetal equivalent of animal peroxisome
tonoplast = the membrane of the vacuole
plastids = vegetal organelles
chloroplasts
leukoplasts
modification : a mantainance methylase creates N5-methylC
in CpNpGp box in both strands during chromosome replication using SAM as
donor
plant cuticular lipid export : up until now, we knew that plants
produce this waxy coating on their cuticle, which is essential for water
conservation, and for their ecology in general, but no one knew how these
highly hydrophobic molecules that are made in the cells get out of the
cells. Plants export wax from epidermal cells to the surface of their aerial
parts through CER5, a lipid transporter similar to ABC transporters present
in mammalian cells. This is the first component of the plant lipid export
system to be characterized functionally. Traditionally, wax precursors
were thought to be exported by a vesicular pathway from their site of synthesis
to their destination at the plant surface. The identification of the CER5
transporter does not absolutely rule out the vesicular hypothesis. Because
of the limited resolution of fluorescence imaging, it remains possible
that CER5 is localized in a compartment involved in secretion. The simplest
hypothesis, advanced by the authors, is that the transporter located in
the plasma membrane has a pore that goes from the inside to the outside
through which lipids go out. It could also have a side pore, similar to
the bacterial MsbA ABC transporter, through which the lipids enter or exit
the transporter. A third possibility is that the transporter is not a pore
but a flippase that flip-flops fatty acids from the inner to the outer
leaflet of the plant cell plasma membrane
a cellular-automaton model (simple, discrete 'particles' programmed to
switch between different states depending on the states of their neighbours)
can explain the way that plants regulate their uptake of CO2,
which they use for photosynthesis, and their loss of water vapour. Leaves
have openings called stomata that open wide to let CO2 in, but
close up to prevent precious water vapour from escaping. Plants attempt
to regulate their stomata to take in as much CO2 as possible
while losing the least amount of water. But they are limited in how well
they can do this: leaves are often divided into patches where the stomata
are either open or closed, which reduces the efficiency of CO2
uptake. Patches of open or closed stomata in leaves of the cocklebur plan
sometimes move around a leaf at constant speed, for example
stoma : any minute pore, orifice, or opening on a free surface
pistil /gynecium : the female part of a flower
stigma : the uppermost part of a pistil, which secretes a moist,
sticky substance to trap and hold the pollen that reaches it
leaf : a flattened structure of vascular plants, attached to the
plant by a stem and usually green in color, that is the primary site of
photosynthesis and transpiration
root : the lowermost part of a plant or other structure
invading plant species, such as the Centaurea, establish monocultures
in novel habitats by displacing the indigenous plant communities. It is
thought that the absence of "natural enemies" and/or the release of phytotoxins
from the invading plants by allelopathy promote this process. The European
spotted knapweed (Centaurea
maculosa) releases racemic catechin; the antimicrobial (+)-catechin
and the phytotoxin (-)-catechin that inhibits germination and growth of
a number of nature plants (including Arabidopsis
thaliana and Centaurea
diffusa) by altering gene expression, resulting in rapid reactive
oxygen species wave, similar to that observed for root cell death, but
proceeding cell death by 5-10'. This increase in ROSs induced Ca2+-dependent
triggering of cell death. Gene expression analysis of A. thaliana
showed that 10 genes were upregulated 10' after treatment, with 956 genes
being upregulated 50' later. Many of the 956 gene products are linked to
oxidative stress and the phenylpropanoid and terpenoid pathways. At 12
hours, many of these genes were repressed, possibly as a result of the
onset of cell death. Allelopathy challenges the conventional ecological
perspective that a species' invasiveness is mainly due to enhanced resource
competition after escape from natural enemies and highlights the role for
the biochemical potential of the plant as an important determinant of invasive
success
the world's biggest-ever bloom, at more than 2.7 metres tall, the Titan
Arum flowered in the University of Bonn Botanical Garden on May 23, 2003.
It beats the previous record - set 70 years ago - by 7 centimetres. More
than 2,000 people have so far rushed to witness the event, as the spadix,
the blossom's fleshy central column, is expected to collapse on Saturday
afternoon. The growth, smell and warm temperature of the spadix were closely
studied in 4 flowers between 1987 and 1989. Amorphophallus
titanum, the blue whale of botany comes from the rainforests of
western Sumatra, Indonesia. It was discovered in 1878 by the Florentine
botanist Odoardo Beccari. He sent the seeds to Kew Royal Botanical Gardens
in London, where the first cultivated specimen flowered in 1889. Famously,
3 blooms appeared at Kew last year. Hothouse Titan Arums rarely flower,
but when they do, they are hard to ignore. The colossal lily-shaped blooms
smell of rotting flesh - hence the plant's nickname 'the corpse flower'.
By mimicking a carcass in decay, the brownish flowers attract insects that
deposit their eggs inside the plant, spreading its pollen in the process.
most flowering plants arrange their leaves and petals in spirals around
their stems. And in most species, the angle between successive elements
is close to the so-called golden angle, 137.5°, a number derived from
mathematic theory that correlates to artistic aesthetics and biological
patterning. This convergence has puzzled researchers for 250 years : the
arrangement minimizes the shadow each leaf casts on those below it, maximizing
the plant's light-gathering ability. Once built an optimality model of
light capture, the angle between leaves tends towards 137.5° as leaves
became thinner. The model's predictions matched results from an earlier
study on geometry and light-capture efficiency of the forest-dwelling daisy
Adenocaulon
bicolor. But there are many examples where the leaf spiral doesn't
match the golden angle, and some cases where it does but the plant is not
oriented to gather maximum light
trees grow tall where resources are abundant, stresses are minor, and competition
for light places a premium on height growth. The height to which trees
can grow and the biophysical determinants of maximum height are poorly
understood. Some models predict heights of up to 120 m in the absence of
mechanical damage, but there are historical accounts of taller trees. Current
hypotheses of height limitation focus on increasing water transport constraints
in taller trees and the resulting reductions in leaf photosynthesis. The
tallest known tree on Earth (112.7 m) is a redwood (Sequoia
sempervirens) in wet temperate forests of northern California.
Regression analyses of height gradients in leaf functional characteristics
estimate a maximum tree height of 122–130 m barring mechanical damage,
similar to the tallest recorded trees of the past. As trees grow taller,
increasing leaf water stress due to gravity and path length resistance
may ultimately limit leaf expansion and photosynthesis for further height
growth, even with ample soil moistureref.
plant mitochondrial genes are transmitted horizontally across mating barriers
with surprising frequency, but the mechanism of transfer is unclear. Horizontal
gene transfer from parasitic flowering plants to their host flowering plants
occurs as a result of direct physical contact between the 2. Genes can
also be transferred in the opposite direction, from host to parasite plantref.
The unicellular conifer tracheid should have greater flow resistance per
length (resistivity) than the multicellular angiosperm vessel, because
its high-resistance end-walls are closer together. However, tracheids and
vessels had comparable resistivities for the same diameter, despite tracheids
being over 10 times shorter. End-wall pits of tracheids averaged 59 times
lower flow resistance on an area basis than vessel pits, owing to the unique
torus-margo structure of the conifer pit membrane. The evolution of this
membrane was as hydraulically important as that of vessels. Without their
specialized pits, conifers would have 38 times the flow resistance, making
conifer-dominated ecosystems improbable in an angiosperm worldref
When plants experience drought or cold, they cannot get themselves a glass
of water or move to a warmer place. Instead, their ability to survive lack
of water, extreme temperatures and such stresses as high salt levels relies
heavily on a plant hormone called abscisic acid (ABA). Binding of 2 proteins,
FCA and FY, to one another results in a decrease in expression levels of
Flowering Locus C (FLC), causing a transition from vegetative growth to
flowering. The FCA–FY complex also causes synthesis of a truncated, non-functional
FCA messenger RNA in a negative feedback loop that results in fewer full-length
FCA mRNA transcripts and less FCA protein. Binding of abscisic acid
(ABA) to FCA abolishes the interaction of FCA with FY, leading to an
increase in full-length FCA transcripts and — through increased FLC activity
— a delay in flowering. Red lines depict negative regulationref
schematic
of the structures of jasmonate and its precursors
The Arabidopsis Information Resource (TAIR)
by the Carnegie Institution of Washington Department of Plant Biology and
the National Center for Genome Resources (NCGR)
canola (oil) - there are 2 types
of canola, the short-growing season Polish type (Brassica
rapa and Brassica
campestris) and the longer-season Argentine type (Brassica
napus). Canola is produced extensively in Europe, Canada, Asia,
Australia, and to a limited extent in the United States.
maize - Zea
mays (721 379 361 metric tonnes, 2004). The people of Mesoamerica
are largely responsible for the golden corn we grow today, having domesticated
tough teosinte grass thousands of years ago and bred it into modern maize.
A mutant maize that was found in South America in the 1920s is unable to
grow branches or flowers, and happens to resemble a particular rice mutant
in this respect. Because the sequence of the gene that causes the effect
is known for rice, the sequence in maize was pinned down and called barren
stalk1 : the normal version of barren stalk1 regulates how the maize plants
branch and is also located within one of five regions that maize researchers
have identified as targets of domestication. So, was it one of the genes
that the Mesoamericans unknowingly selected for as they tamed teosinte
(Zea
mexicana)? To investigate further, the researchers compared the
number of variants of the barren stalk1 gene in teosinte, which still grows
wild in Mexico's Sierra Madre, with the number in modern maize. In teosinte,
there are about 12 common variants of the gene, all of which probably produced
subtly different branching patterns in the plants. It is common for this
number of variants to be present in a particular species of plant. But
in modern maize, only one variant exists, suggesting that the others must
have been eliminated by rigorous selective breeding. Why did the Mesoamericans
plump so strongly for one branching pattern rather than another? Presumably
there was something about the branching of maize with that particular variant
that was useful. In combination with other genes it probably had some impact
on the architecture that was important to the Mesoamericans, perhaps bigger
seeds. The next step will be to paste all the variants of the barren stalk
that exist in teosinte into modern maize : once you see what the differences
are in maize, it will be easier to guess why a particular variant was chosen.
Teosinte grass (left) compared to "reconstructed" primitive maize, created
by crossing teosinte with Argentine pop corn :
The most critical step in maize (Zea mays ssp. mays)
domestication was the liberation of the kernel from the hardened, protective
casing that envelops the kernel in the maize progenitor, teosinte. This
evolutionary step exposed the kernel on the surface of the ear, such that
it could readily be used by humans as a food source. This key event in
maize domestication is controlled by a single gene (teosinte glume architecture
or tga1), belonging to the SBP-domain family of transcriptional regulators.
The factor controlling the phenotypic difference between maize and teosinte
maps to a 1-kilobase region, within which maize and teosinte show only
seven fixed differences in their DNA sequences. One of these differences
encodes a non-conservative amino acid substitution and may affect protein
function, and the other 6 differences potentially affect gene regulation.
Molecular evolution analyses show that this region was the target of selection
during maize domestication. Modest genetic changes in single genes can
induce dramatic changes in phenotype during domestication and evolutionref.
Common bread wheat/spring wheat is typically planted in Florida in late
November to early December and harvested in late April to May, predominantly
in the panhandle counties. Wheat occupied ca. 10 000 acres in the 2003
growing season. The annual growth rate in wheat production in India dropped
from a healthy 3.57% in the 1980s to 2.11% in the 1990s and below 1% in
the current decade. After hitting a peak of 76 million tons in 2000, wheat
harvest has been hovering around 72 to 74 million tons, according to the
Food Corporation of India (FCI). In fact, the erosion of FCI's stock need
not be viewed with concern, as it has been the result of a deliberate move
to shed burdensome inventories through subsidized exports and liberal use
of grains in welfare and food-for-work programs. The relatively lower wheat
procurement also should not be a cause for much concern. It only reflects
higher purchases by private trade and withholding of some stocks by big
farmers in anticipation of better prices in lean seasons. These stocks
have to, sooner or later, come out in the market. However, the below-anticipation
wheat harvest for the 5th successive year should be a matter of real discomfiture
and should make wheat scientists and policy makers sit up. The agriculture
ministry, which had earlier reckoned the wheat harvest to be around 74.05
million tons, has scaled it down to 73.5 million tons. Wheat experts, who
were hoping to bag a harvest of around 75 million tons, now feel that the
production would be just around 73 million tons. The wheat trade, on the
other hand, is projecting a still lower output of around 71 to 72 million
tons. Some causes for a low wheat yield have, of course, been identified.
Noted wheat expert and Indian Agriculture Research Institute (IARI) director
S. Nagarajan believes that the unexpected emergence of 2 diseases so close
to ripening of the crop is responsible for yield drop. Black rust, a dreaded
plant disease, resurfaced after over 10 years, affecting the predominant
cultivar PBW-343 in Punjab and adjoining areas when the crop was heading
towards maturity. Another relatively lesser-known disease, called head
scab, struck the durum wheat (hard wheat used for making noodles and pasta
products) around the same time to cause yield loss. This disease is endemic
to North America and has not been reported in India in the recent past.
Poor wheat yields in earlier years of this decade had been caused largely
by unfavorable climatic factors, such as untimely rains or temperature
rise. Moreover, 2 dreaded weeds, Phalaris minor and wild oats, had
posed a formidable danger to wheat cultivation. But fortunately, their
control was discovered through pesticides and agronomic management. More
recently, rust diseases -- yellow, brown and black rusts -- spread like
an epidemic throughout the northwestern wheat belt. Fortunately, they were
tamed by breeding rust-resistant varieties and breaking the disease cycle
by saturating the wheat-growing southern hilly region with rust-immune
varieties. That was the region where the rust pathogen used to survive
in summer when the crop was not being grown in the plains. Wheat, being
a non-monsoon-dependent winter season cereal, is critical for the country's
food security, and any deceleration in its production growth is unwarranted.
Wheat output needs to grow annually by at least 2.5% to keep pace with
the rise in demand. The major wheat-producing countries of northern Asia
are India, Pakistan, Nepal, Bangladesh and Myanmar in order of importance.
Most of the wheat is produced in the Ganges and Nurmada basins of India
and the Indus River Valley of Pakistan. Much of the wheat in India and
Pakistan is irrigated, while in Nepal and Bangladesh it is mostly rain
fed. White grain cultivars are preferred and are primarily of spring habit,
but are usually sown in November and December and harvested in April and
May. Consumption is highest in Pakistan at 141 kg/caput and lowest in Myanmar
at 3 kg/caput. World production as of 2004 is 624 093 306 metric tons.
India is one of the largest wheat producers in the world, with about 25
million a [1 hectare= 10,000 square meters] under production and averaging
almost 60 million tons in recent years. > 90% of the area is sown to bread
wheat, which is grown throughout the country. Durum or macaroni wheat accounts
for around 8% of the area. The crop is grown in most parts of the country,
but nearly 70% lies in the northern plains and 20% in central India. A
rice-wheat rotation is the dominant cropping sequence. Crops other than
rice that precede wheat are also used, particularly in the central and
southern regions. In the large wheat research and development program in
India, much germplasm is screened for important biotic and abiotic stresses.
Important biotic pests include the rusts, Karnal bunt, foliar blight, powdery
mildew, common bunt, flag smut and nematode and insect pests. Salt, heat
and drought are the major abiotic stresses. Large amounts of NPK fertilizers
are used to produce the wheat crop in India. Over the past 3 decades, increased
agricultural productivity in Pakistan occurred largely due to the deployment
of high-yielding cultivars, increased fertilizer use and greater availability
of irrigation water. By the mid-1980s, semidwarf wheat cultivars had been
adopted on almost all irrigated land, and over 100 kg/ha on average of
fertilizer was being applied to wheat. Pakistan production averaged 16.1
million tons on 8.2 million ha each year during the period 1993-1995. Rice-wheat,
berseem-wheat and cotton-wheat are major systems of intense cropping in
Pakistan. Wheat scab (also known as Fusarium head blight) is caused
by the fungus Fusarium graminearum. It is a common problem in Europe,
Asia, South Africa, and the Midwestern and Eastern U.S.A. Scab severity
is very erratic and depends heavily on wet weather conditions. Scab often
causes reduction in test weight, sometimes down to near 50 lb/bu. In addition,
scabby kernels count as "damaged" in the grading process. Although scabby
wheat is often very good, it may contain the mycotoxins DON (vomitoxin)
and zearalenone (an estrogen analog). Swine are most sensitive to scabby
wheat mycotoxins, and as little as one ppm of DON can significantly reduce
daily weight gains in pigs. Higher concentrations result in feed refusal
and vomiting. Swine reproduction is also sensitive to disruption by the
zearalenone mycotoxin. Non-breeding cattle and poultry seem to tolerate
both toxins better than swineref1,
ref2,
ref3,
ref4 There are 3 main rust diseases of the cereal crop plant wheat. These
are wheat stem rust (Puccinia
graminis f.sp. tritici), wheat leaf rust (P.
triticina aka P. recondita f. sp. tritici) and wheat
stripe rust (P.
striiformis f. sp. tritici), all caused by species of the
fungus Puccinia. Severe losses that can occur due to wheat stem
rust have been abated in the USA since the 1960's by effective resistance
breeding, though the knowledge of resistance breaking strains of the pathogen,
such as Ug99 in Uganda, is a concern [note "see also"]. Severe losses are
still a possibility with leaf rust. As recently as 1993, leaf rust destroyed
over 40 million bushels of wheat in Kansas and Nebraska. In 1985, Texas
and Oklahoma lost 95 million bushels of wheat to leaf rust. The USDA Cereal
Disease Laboratory St. Paul, MN publishes regular reports on cereal rusts
in the USA during the crop season. 10 were published between March and
September 2005. Each report gives detailed state-by-state information,
including a summary map, all in pdf file format. Wheat is not doing well
in early 2006 in southern states because of drought, e.g. in Texas and
Oklahoma. This condition is also not conducive for leaf rust, which
partly explains the low levels of incidence reported so far March in 2006.
In Central Asia, yellow rust (Puccinia
triticina)ref,
tan
spot (Pyrenophora triticirepentis),
common
bunt (Tilletia caries), and
Tilletia
laevis are major foliar diseases of spring wheat, although Septoria
leaf blotch (Mycosphaerella graminicola
and Phaeosphaeria nodorum),
leaf
rust (Puccinia recondita f. sp.
tritici), and cereal
cyst nematode (Heterodera latipons) also occur in some areas.
Yellow rust and leaf rust are also very important in the Caucasian countries.
As researchers develop new varieties resistant to these diseases, progress
is tested through a step-by-step evaluation at different locations in the
region. In the first step, resistance to yellow rust, leaf rust, stem rust,
Septoria leaf blotch, cereal cyst nematode, and common bunt is evaluated
at Tel Hadya, ICARDA's headquarters, where wheat nurseries are artificially
inoculated with these diseases. In the 2nd phase, varieties identified
as resistant are further screened for resistance to different diseases
in heavily infected areas in different countries in Central and West Asia
and North Africa (CWANA) in collaboration with local scientists at 3 to
5 sites per country. It is difficult to assess disease loss given the information
available. The fact that about 350 000 ha. were treated with fungicides
indicates that farmers needed to try to control the diseases affecting
their cropsref.
Web resources : Wheat
Food Council
citrus (108 535 488 metric tonnes, 2004) : on a worldwide
basis, there are at least 6 citrus viroids: Citrus
exocortis viroid (CEVd), Citrus
bent leaf viroid (CBLVd), Hop stunt
viroid (HSVd), Citrus viroid III (CVd-III),
Citrus
viroid IV and Citrus viroid OS (CVd-OS).
CEVd causes the bark-scaling citrus exocortis disease on trifoliate orange
(Poncirus trifoliata) [Pt] root stocks, and some HSVd variants cause
citrus cachexia disease in sensitive hosts such as mandarins (Citrus
reticulata). CEVd, HSVd, and CVd -III are predominately found
in introduced cultivars such as lemons and oranges, while CVd-OS, HSVd,
and CVd-III are frequently found in the domestic cultivar 'Shiranui'. Other
viroids induce different degrees of stunting. Since commercial citrus trees
are commonly infected with viroid mixtures, only limited information is
available on their effects in species other than Etrog citron. In general,
yield reduction was associated mainly with loss of production of large
fruits. Bark-cracking of Pt may be caused by CEVd, CVd-IV, and HSVd, but
not by CBLV d or CVd-III. The International Committee on Taxonomy of Viruses
(ICTV) has proposed the name Citrus dwarfing viroid (CDVd) as a replacement
for CVd-III. Disease management depends upon sterilizing pruning
shears with bleach before moving to the next tree. Modern techniques for
detection of viroids in citrus are required as well, because viroid-infected
plants are often symptomlessref1,
ref2.
A multiplex RT-PCR has been developed to detect 6 citrus viroids (Citrus
exocortis viroid (CEVd), Citrus
bent leaf viroid (CBLVd), Hop stunt
viroid (HSVd), Citrus viroid III (CVd-III),
Citrus
viroid IV and Citrus viroid OS (CVd-OS))
and Apple stem grooving virus (ASGV,
synonym: Citrus tatter leaf
virus (CTLV)) from citrus plants. The multiplex RT-PCR was also designed
to distinguish CVd-I-LSS (a distinct variant of CBLVd) from CBLVd. By the
multiplex RT-PCR, 1-8 fragments specific to the pathogens were simultaneously
amplified from 1 sample and identified by their specific molecular sizes
in 6% PAGE. The results of the multiplex RT-PCR were consistent with those
of other diagnoses, such as uniplex RT-PCR, to detect each of the pathogens.
The multiplex RT-PCR provides a simple and rapid method for detecting various
viroids and ASGV in citrus plants, which will help diagnose many citrus
plants at a timeref1,
ref2
potato - Solanum
tuberosum (327 624 417 metric tonnes, 2004). Sprouting is one of
the biggest problems when storing potatoes. Untreated potatoes start to
sprout after 60 days. Lower temperatures reduce sprouting, but they also
increase the sugar content of the potato. When deep-fried, this sugar caramelizes,
giving fries a nasty brown colour that turns consumers off. A quick dose
of low-energy electrons stops potatoes sprouting for up to four months,
even if they are stored at room temperature. The researchers used a Van
der Graaf generator to deliver a beam of electrons to potatoes moving along
a conveyor belt. The electron beam works by preventing cell division within
the sprout bud tissue, similar to the way that radiotherapy stops cancer
cells multiplying. The method could replace the potentially harmful chemical
sprays such as chloropropham (also known as CIPC, whose residues can linger
on a potato's skin, worrying consumers and regulatory bodies alike) and
expensive g-radiation treatments that are currently
used to stem the surging sprouts (a special facility in Hikkedo, Japan,
treats > 100,000 tons of potatoes annually. But the process is expensive
and requires hefty shielding to protect workers). Camote is a type of sweet
potato having somewhat dry, bland, yellowish to white flesh, used as a
staple food in many tropical countries, and is also called boniato or batata
tomato - Lycopersicon
esculentum originated in South America, were introduced into Europe
in the 16th century, and are now a popular food worldwide. The Roma tomato
was developed in the mid-1950s as a firmer and more disease-resistant varietyref.
Uncooked tomatoes have become an integral and nutritious component of the
daily diet. Approximately 5 billion pounds of fresh market tomatoes are
eaten annually in the USA (120 384 017 metric tonnes, 2004)
banana -
Musa
x paridasiaca L., Musa
acuminata is the 4th most important global food crop after rice,
wheat and maize in terms of gross value of production. Total world Musa
production is currently about 97 million tones annually (FAOSTAT, 2003),
of which bananas cultivated for export account for only 10%. Hence, they
are important for food security in the humid tropics and provide income
to farmers. It is a major staple food, supplying up to 25% of the carbohydrates
for approximately 70 million people in Africa's humid forest and mid-altitude
regions. The East and Central Africa sub-region alone produces nearly 20
million tons of bananas annually (71 343 413 metric tonnes, 2004)
cassava - Manihot
esculenta - is a hardy, drought-resistant tuber with an edible
root that grows in tropical and sub-tropical areas of the world. It provides
an important source of energy for millions of people in Africa. (202 648
218 metric tonnes, 2004). Cassava is among the most common crops in sub-Saharan
Africa, accounting for > 50% of world production with over 90 million tons
of fresh product, more than any other crop in Africa. Cassava is vital
to the livelihood of over 200 million people and plays a key food security
role for rapidly expanding rural and urban populations and has huge potential
for commercialization, income generation, and poverty reduction
grapevine - Vitis
labrusca, Vitis
vinifera (66 569 761 metric tonnes, 2004). Wine enchants because
of its complexity, but that very trait makes it difficult to regulate.
That bottle full of aromatic red liquid with hints of cherry may be genuine
Pinot Noir from the California coast, or it may be a New Jersey Merlot,
diluted with water and tarted up with sugar or sophisticated synthetic
flavourings. In the arms race between the adulterators and the regulators,
detection systems have become ever more sophisticated, as have the cheaters.
But at least one common ruse - claiming that the wine is one variety, when
it is actually entirely or partly another - may come to a sudden stop if
DNA can be successfully extracted from wine on the shelf.
stable isotope analysis. Carbon, hydrogen and oxygen atoms all occasionally
show up in versions with slightly different mass. The amounts of such isotopes
vary from region to region, so when they are incorporated into grapes,
they tell a tale about where the wine was made. The snag is that they also
vary with local weather conditions, so samples of wine from each region
have to be taken each year for comparison and entered in the European Wine
Data Bank. For example, 2003 wines were collected before the late rains,
so there were values for oxygen that were more like Southern Italy.
chromatography creates a graph showing which wavelengths of light are absorbed,
and software types wines according to absorption pattern with decent accuracy.
Things fall apart a bit, however, with blends. In Germany, the world's
largest wine importer, regulators often compare the ratios of two forms
of anthocyanin, the molecules that make wine red. This ratio is determined
by the genes of the vine, and was thought to be an unalterable marker that
could tell you what variety of wine you were drinking. But some processing
techniques can change this ratio quite significantly. Techniques can involve
long fermentation, high temperatures and adding enzymes. Many producers
of Cabernet Sauvignon have had their wine unfairly rejected by the German
government and been forced to sell it at half price. More kinds of anthocyanins
should be used to type wine.
extraction and purification of grape-skin DNA from bottles of wine, confident
that if forensic scientists can get DNA from ancient skeletons, he can
do the same for a bottle of Pinot Gris. Researchers are also working to
identify a set of genetic markers to differentiate the 2,500 or so varieties
of grape in existence. Short sections that repeat a different numbers of
times in different varieties seem like a good bet.
All this fuss stems not just from a passion for authentic tastes, but from
economic motives. What other food has such a big price range? It goes from
$2 to $200 for the same size bottle. > 50 different viruses and viroids
are known to infect grapevines worldwide, and undoubtedly many unknown
ones that have yet to be detected. Evolution of new viruses is a constant
threat to grapevine producers and their spread by manref1,
ref2,
ref3,
ref4,
ref5.
lettuce - Lactuca
spp.. Ruccola is the Italian word for arugula, a popular leafy lettuce
in the USA. In other parts of the world, it is referred to as raketsla,
roquette, notensla, or zwaardherik.
sugar beet - Beta
vulgaris (249 208 061 metric tonnes, 2004) is a globally important
crop producing 27% of world sucrose supplies. It is grown in Europe, North
America, Chile, Uruguay, China, the Middle East, North Africa, and countries
of the former Soviet Union.
sweet potato - Ipomoea
batatas (127 139 553 metric tonnes, 2004), ranked 7th in worldwide
food production (5th in developing countries). China is the biggest producer
in the world. The most harmful diseases in sweet potatoes are caused by
a complex of viruses of which the most common is the aphid-transmitted
potyvirus sweet potato
feathery mottle virus (SPFMV). When the whitefly-transmitted sweet
potato chlorotic stunt virus (SPCSV) is also present, it breaks down
resistance to other viruses in sweet potato cultivars, which results in
the severe sweet potato virus disease (SPVD) and high or complete
yield loss. SPCSV was tested for but not found in this Italian study, but
it is known in Spain. SPFMV alone can cause severe cracking and corking
of sweet potatoes before and after harvest. When infected roots are used
to produce slips for new plantings, then plants derived from the infected
root will also be diseased. Therefore, it is extremely important to use
virus-free seed piece stockref1,
ref2,
ref3,
ref4,
ref5.
grapevine
yellow speckle viroid (GYSVd) is an elusive disease whose outward expression
is conditioned by climatic and possibly varietal factors. Symptoms, when
shown, consist of a few to many minute chrome yellow spots or flecks scattered
over part or all of the leaf surface or gathering along the main veins
to give a vein banding pattern. GYSVd-induced vein banding is very similar,
if not identical, to the symptoms of a disease also known by the name of
vein banding, which has long been regarded as part of the fanleaf degeneration
complex. Although vein banding may show in GFLV-free vines, it is more
often associated with GFLV infections. In fact, it has been suggested that
the presence of GFLV enhances the expression of GYSVd in the form of vein
banding patterns. Similar enhancement may occur in vines concurrently infected
by grapevine chrome mosaic virus. Unlike GFLV-induced yellow discolorations,
the symptoms of yellow fleck appear in the height of summer on a limited
number of mature leaves, and they persist for the rest of the vegetating
season. Yellow speckle symptoms may also show concurrently with symptoms
of other diseases such as, for instance, leafroll. No vector for GYSVd
is known. Natural dissemination occurs by mechanical inoculation through
surface-contaminated cutting tools during management operations (pruning
and propagation); by graft transmission: and by distribution of infected
propagating material. The absence of symptoms in most European scion varieties
and all American rootstocks greatly facilitates inadvertent viroid dissemination,
making viroid dispersal virtually impossible to prevent. None of the grapevine
viroids is known to be seed-transmitted
coconut
cadang-cadang viroid (CCCVd) => cadang-cadang, which comes from
a Bicol term "gadan-gadan" meaning dead or dying, is a premature decline
and death of coconut and palm trees restricted to the Philippines, first
reported in 1937. CCCVd is the most serious of all known viroids because
of its lethality. It has killed over 40 million coconut palms and still
kills between 200 000 - 400 000 palms annually. It is spread by unknown
means, is seed-transmitted (1/320 seedlings), and also transmitted by pollen.
CCCVd contains 246 or 247 nucleotides and is the smallest known nucleic
acid-containing pathogen. Coconut palms less than 10 years old are rarely
affected, but disease incidence increases rapidly to about 40 years, remaining
constant thereafter. Disease management basically involves eradication
of infected palms when they become symptomatic. No resistance to CCCVd
has been identified. In the Philippines, the disease occurs in the central
region (southern Luzon, Samar, Masbate, and smaller islands within a zone
about 600 km x 300 km). Disease management requires use of sterilized pruning
tools to avoid spread of the viroid
coconut
tinangaja viroid (CTiVd) => Tinangaja,
first reported in 1917, shares about 65% overall sequence with CCCVd and
is confined to Guam, where it affected 30% of coconut plants and led to
the end of commercial production on the island following the death of 30
million trees in the period from 1950 to 1980. Incidence of the disease
is about 30%. There is some evidence that CTiVd is seed-transmitted at
very low levels.
hop latent viroid
CTiVd and CCCVd are the only viroids that infect monocotyledons. Both cause
lethal infections in coconut, causing death within 10 years of diagnosis.
Inasmuch as CCCVd and CTiVd occur separately in the Philippines and Guam,
respectively, it would be interesting to monitor differences in genomic
sequences between the 2 viroids over time.
hop
stunt viroid (HSVd) causes a severe disease in hop (Humulus
lupulus). The fruit crop plant plum, Prunus domestica, develops
dapple or no symptoms when infected by HSVd. HSVd consists of a 295-303
nucleotide circular single-stranded RNA. It has been found in a wide range
of herbaceous and woody hosts, where the infection seems to be latent (such
as grapevine, apricot, pear) or may induce specific disease symptoms such
as hop stunt, citrus cachexia, and dapple fruit of plum and peach. It has
also been reported in cucumber. HSVd is not difficult to find in plum in
China, despite this being the 1st report in that host. No symptoms have
been associated with these findings. The detection of HSVd in plum in China
is significant in part because this is the geographical origin of the species
and because of the threat this pathogen could have to the other crops it
infects. Like other viroids, HSVd is transmitted mechanically, by budding
and grafting, and by vegetative propagation. Note that HSVd has been reported
in grape and apricot in Chinaref1,
ref2.
Isolates of HSVd have been classified into 5 groups; 3 major types (plum,
hop and citrus) each containing isolates from only a limited number of
isolation hosts, and 2 minor ones (plum-citrus and plum-hop-citrus) presumably
derived from recombination between members of the main groups. HSVd apparently
has a wide host range, infecting hop, cucumber, grapevine, citrus, plum,
peach, pear, apricot, pomegranate and almond. It has been found latent
in a wide range of herbaceous and woody hosts (grapevine, apricot, pear)
and may induce peculiar symptoms such as hop stunt, dapple fruit of plum
and peach, and citrus cachexia. HSVd is very contagious and is found worldwide.
In the Czech Republic, HSVd incidence in grapevine planted in the vicinity
of hop gardens was found to be about 70%. Previous work has characterized
HSVd isolates from France, Italy, Japan, Spain and USA. Current studies
have revealed 16 new sequence variants from Cyprus, Greece, Morocco, and
Turkey, where HSVd had not been described previously. The origin and route
of the intrusion of HSVd into Canada remain unknown. Both PLMVd and HSVd
are also easily transmitted by grafting or by use of contaminated pruning
tools, but evidence of their transmission by vectors is apparently lacking
for HSVd. Viroid disease management depends upon sanitation; plant viroid-free
trees, sterilize shears after pruning each tree, and eradicate infected
treesref1,
ref2,
ref3,
ref4,
ref5,
ref6,
ref7,
ref8.
Transmission of grapevine yellow speckle viroid 1 and hop stunt viroid
via seeds has been confirmed in 11 seedlings of 8 grapevine Vitis vinifera
varieties using a combination of RT-PCR, dot-blot hybridization and northern
hybridization assays. This indicates that budwood stocks must be checked
for the presence of HSVd. At least 16 new sequence variants of HSVd have
been obtained from 4 Mediterranean countries (Cyprus, Greece, Morocco and
Turkey) where this viroid had not previously been described. At present
it appears that HSVd is limited to Japan. In some hosts, such as grapevine
and apricot, the infection appears to be latent but in other cases, specific
disorders such as hop stunt, dapple fruit of plum and peach and citrus
cachexia have been associated with HSVd infection. Phylogenetic analyses
revealed that sequence variants belonging to the 2 minor recombinant subgroups
are more frequent than previously though
citrus
cachexia viroid is a graft-transmissible viroid that causes phloem
deterioration and blockage in many mandarin, mandarin hybrids, Citrus
macrophylla Wester, Rangpur lime, and sweet lime. This disease causes
decline, stunting, and crop reduction. Sour orange is tolerant to the viroid.
There appears to be consensus among viroid specialists, based on molecular
genetic studies, that the viroid moved from grapevine to hop.
Mexican
papita viroid (MPVd), found in 1982 in symptomlessly infected Solanum
cardiophyllum in Aguascalientes state, suggest that MPVd may be
the putative ancestor of crop viroids. MPVd, present in symptomlessly infected
solanaceous plants, may have been transferred by chewing insects (aphids,
grasshoppers, flea beetles, tarnished plant bug, leaf beetle, and Colorado
potato beetle) to breeding plots and commercial potato crops.
potato
spindle tuber viroid (PSTVd) has been reported from Solanum
tuberosum (France) and tomato
(Lycopersicon esculentum)(Netherlands and UK). In tomatoes,
PSTVd symptoms develop slowly, often not becoming apparent until 4 or 5
weeks after infection. Infected plants become stunted and show "bunchy
top" symptoms (crowded foliage, due to shortening of internodes, and occasional
formation of spindly shoots). Leaf symptoms include yellowing and purpling
as well as considerable leaf distortion including downward curling of the
leaflets (epinasty), curling, and twisting (rugosity). Severe necrosis
along the veins develops later in the lower and middle leaves, which eventually
die. Younger leaves at the top of the plant remain but are reduced in size.
Flowers are often aborted, and fruit ripening is erratic. Fruits becomes
small and hard and can turn dark green. Overall yields can be significantly
reduced. Disease management basically depends on planting viroid-free transplants,
adherence to a strict phytosanitary regimen to prevent contamination and
subsequent spread of the viroid. Benches, tools, storage bins, and sacks
can be disinfected with 3% hypochloriteref.
Once PSTVd has been introduced onto a farm or nursery, it can be rapidly
spread from plant to plant through the use of contaminated cutting tools
and/or machinery, by handling, or simply by direct plant to plant contact.
PSTVd can also be transmitted via infected pollen. To prevent the spread
within growers' fields, good hygienic practices are necessary to prevent
contact with potentially infected plants, and, to avoid subsequent spread
of the viroid. Contaminated benches, tools, etc. should be disinfected.
2-3% hypochlorite has been shown to be effective. PSTVd can reduce yields
by as much as 65 and 50% in potato and tomato, respectively. Other natural
hosts include pepino (Solanum
muricatum), avocado (Persea
americana), and a range of solanaceous crops. PSTVd was reported
in the 1930's to be transmitted by chewing insects (aphids, grasshoppers,
flea beetles, tarnished plant bug, leaf beetle, and Colorado potato beetle)
and is a nasty pathogen
tomato
apical stunt viroid (TASVd)ref1,
ref2
was first found and characterized in Ivory Coast in 1980's, but no data
was given on its epidemiology or economic impact. Another strain was found
in Indonesia in 1980's, but again without data on potential economic impact.
Both cause significant crop loss. The genomes of the 2 viroids are very
similar (99.7% identity) despite their distant geographic origins. A third
strain, isolated from Solanum
pseudocapsicum [Jerusalem cherry], does not occur naturally in
tomato but can infect tomato by mechanical inoculation. First found in
Israel (on tomato (Lycopersicon
esculentum) grown under plastic houses in the coastal region) in
2003 for samples collected in 1999/2000; first found in Tunisia in 2006ref.
The RNA sequence of the Tunisian, Israeli and Indonesian strains are very
similar. Affected tomato plants in Israel showed shortened internodes (bushy
appearance), leaf deformation and yellowing, reduced fruit size, and pale
red discoloration of fruit. Up to 100% disease incidence could be observed
at single sites with heavy yield losses. The present article also noted
100% disease incidence once temperatures were high, which is a characteristic
of several diseases caused by viroids. TASVd can be transmitted from infected
to healthy tomato plants by grafting or mechanical inoculation (in experimental
conditions). No data is available on pollen or seed transmission, though
some viroids are known to be transmitted by these means. Introduction on
transplants is a strong possibility. Control of viroids is difficult in
practice, so it would be desirable to avoid any further spread of a potentially
serious disease of tomatoes. This new report from Tunisia acts as a warning
to other countries. Other viroids that have been detected in Tunisia are
noted in the archive belowref
These pathogens are ubiquitous, and unfortunately some induce ephemeral
symptoms that complicate their detection. PCR-based diagnostic detection
systems are now available for some of them. AGVd appears to be the result
of recombination between nucleotide sequences in PSTVd, CEVd, Apple
scar skin viroid (ASSVd), and GYySVD-1. Interestingly, Vein banding
disease in grapevine results from the synergistic interaction between grapevine
viroids and Grapevine
fanleaf nepovirus (GFLV). There is evidence that some viroids are seed-and
pollen-transmitted in grapevine. Disease management requires the planting
of viroid-free planting stock, sterilization of pruning tools, and eradication
of infected vines.
unclassified viroids
apple
fruit crinkle viroid (AFCVd), a graft-transmissible fruit and/or bark
disorder of apple, was first reported in Japan. I was unable to obtain
information about the viroid outside of Japan. Apple scar skin viroid (ASSVd)
has 37% sequence homology with GYYSVd. Both viroids share a common
sequence in the central region of the molecule, but lack the central conserved
sequence of viroids in the potato spindle tuber viroid group. Other homologous
residues also occur as blocks of base-paired residues in the secondary
structures of ASSVd and GYSVd. ASSVd viroid also has some homology with
members of the Potato spindle tuber viroid group but not with Avocado sunblotch
viroidref1,
ref2,
ref3,
ref4,
ref5,
ref6,
ref7,
ref8
Disease management is based on prevention of viroid transmission, especially
in nursery production of viroid-free planting material. Strict measures
must be in place to reduce infestation of cutting tools and implements
by using chemical compounds to inactivate viroids. Only viroid-free stock
should be planted. However, cold treatment can be effective, e.g. storage
at 4°C for > 6 months, followed by apical shoot-tip-culture grafting,
can be used to eliminate HLVd. Pre-inoculation with protective mild strains
of viroids has proved effective to control PSTVdref1,
ref2.
Viruses
ssDNA viruses
Geminiviridae
=> geminivirus-like symptoms (stunting, reduced leaf size, and leaf
curling "chino")
Web resources : Gemini
Detective : Geminiviridae:Begomoviruses whitefly-transmitted geminiviruses
Begomovirus : plant virologists continue to report new begomoviruses, and
new ones will undoubtedly emerge. The combination of high temperatures,
presence of high populations of whiteflies, and suitable natural host plants
apparently results in a mix that is conducive to generating new begomovirus
strains in the region. The begomovirus-satellite disease complexes are
associated with economically important diseases and have been isolated
from vegetable and fiber crops, ornamental plants, and weeds throughout
Africa and Asia. Their widespread distribution and diversity, coupled to
the global movement of plant material and the dissemination of the whitefly
vector, suggests that these disease complexes pose a serious threat to
tropical and sub-tropical agro-ecosystems worldwide.
=> Ageratum yellow vein disease is caused by the whitefly-transmitted
monopartite begomovirus Ageratum yellow vein virus (AYVV) and a DNA beta
satellite component. Naturally occurring symptomatic plants also contain
an autonomously replicating nanovirus-like DNA 1 component that relies
on the begomovirus and DNA beta for systemic spread and whitefly transmission
but is not required for maintenance of the disease. Systemic movement of
DNA 1 occurs in Nicotiana benthamiana when co-inoculated with the
bipartite begomovirus Tomato golden mosaic virus and the curtovirus Beet
curly top virus (BCTV), but not with the mastrevirus Bean yellow dwarf
virus. BCTV also mediates systemic movement of DNA 1 in sugar beet, and
the nanovirus-like component is transmitted between plants by the BCTV
leafhopper vector Circulifer tenellus. A 2nd nanovirus-like component,
referred to as DNA 2, has only 47% nucleotide sequence identity with DNA
1. AYVV disease occurs throughout the Indian subcontinent (Nepal, India,
Pakistan), China and parts of Africa. The disease may be associated with
distinct virus species at these locations. Ageratum conyzoides,
a weed species widely distributed throughout southeast Asia, frequently
exhibits striking yellow vein symptoms associated with infection by AYVV
Geminiviridae (genus Begomovirus). The widespread presence of AYVV-infected
Ageratum
conyzoides constitutes a major inoculum source. Ageratum ranges from
Southeastern North America to Central America, but the center of origin
is in Central America and the Caribbean. Most taxa are found in Mexico,
Central America, the Caribbean, and Florida. Ageratum conyzoides
now is found in several countries in tropical and sub-tropical regions,
including Brazil. It is widely utilized in traditional medicine by various
cultures worldwideref1,
ref2,
ref3
There are at least 5 strains/isolates of CLCuV known, most of which
are reported from Pakistan and western India. Cotton leaf curl Gezira virus
is the more cosmopolitan strain, occurring in Egypt and Sudan, and is known
to be present in Central Africa, Chad, Nigeria, Togo and West Africa. Cotton
leaf curl disease (CLuCD) is a serious disease of cotton and several
other malvaceous plant species that is transmitted by the whitefly Bemisia
tabaci. Control of CLCuD is mainly based on insecticide treatments
against Bemisia
tabaci. Roguing, particularly of ratoon cotton from the previous
seasons crop, is recommended but appears to have little affect in reducing
disease incidence. Resistant cotton cultivars have been introduced that
were developed by conventional breeding and selection. However, recent
reports have suggested that the virus complex has overcome the resistanceref1,
ref2,
ref3,
ref4,ref5,
ref6,
ref7,
ref8,
ref9,
ref10,
ref11
cotton
leaf curl Multan virus (CLCuMV) causes cotton leaf curl disease
(CLCuD), a major constraint to cotton production on the Indian subcontinent.
It has been shown to be caused by a monopartite begomovirus and a novel
ssDNA satellite molecule termed CLCuD DNA-beta. The satellite molecule
is trans-replicated by CLCuMV but does not possess the iteron sequences
of this virus. Field surveys across all the cotton-growing regions of Pakistan
indicate that dual and multiple infections are the norm for CLCuD with
no evidence of synergism. Despite the diversity of begomoviruses associated
with CLCuD, only a single class of DNA-beta has been detected, suggesting
that this satellite has the capacity to be recruited by unrelated begomoviruses.
As of 2003, an 26 additional DNA beta molecules, associated with diverse
plant species obtained from different geographical locations, have been
cloned and sequenced. They were shown to be widespread in the Old World,
where monopartite begomoviruses are known to occur. Analysis of the sequences
revealed a highly conserved organization for DNA-beta molecules consisting
of a single conserved open reading frame, an adenine-rich region, and the
satellite conserved region (SCR). The SCR contains a potential hairpin
structure with the loop sequence TAA/GTATTAC, similar to the origins of
replication of geminiviruses and nanoviruses. 2 major groups of DNA-beta
satellites were resolved by phylogenetic analyses. One group originated
from hosts within the Malvaceae and the 2nd from a more diverse
group of plants within the Solanaceae and Compositae. Within
the 2 clusters, DNA-beta molecules showed relatedness based both on host
and geographic origin. These findings strongly support coadaptation of
DNA-beta molecules with their respective helper begomoviruses. The begomovirus-satellite
disease complexes are associated with economically important diseases and
have been isolated from vegetable and fiber crops, ornamental plants, and
weeds throughout Africa and Asia. Their widespread distribution and diversity,
coupled to the global movement of plant material and the dissemination
of the whitefly vector, suggests that these disease complexes pose a serious
threat to tropical and sub-tropical agro-ecosystems worldwide.
East
African cassava mosaic virus (EACMV) : cassava mosaic disease (CMD)
is the most important constraint to cassava
(Manihot esculenta) production in Africa. Since the 1990s, the
importance of the disease has been greatly increased by the spread through
East and Central Africa. The most likely means of spread of EACMV-UG into
Burundi would be via viruliferous whiteflies (Bemisia
tabaci) and movement of infected cassava cuttings. The fact that
EACMCV has reached epidemic status in Nigeria threatens the food security
of that country and is a setback to plant pathologists who have been contending
with control of CMD. The virus is present in many parts of Africa (Congo
Republic, Democratic Republic of Congo, Kenya, Malawi, Rwanda, Tanzania,
Uganda and possibly in Madagascar, Zimbabwe, Zambia and Mozambique). Disease
management strategies include cultural control (planting of virus-free
stocks and use of stem branches of moderately resistant and resistant genotypes
as sources of cuttings), development of resistant lines through crosses
between cassava and wild species (Manihot
glaziovii) to restore root quality and resistance to CMD, as well
as lines derived from Nigeria and local Nigerian genotypes. Moreover, breeding
for the specific needs of farmers in different regions of Nigeria should
be consideredref1,
ref2,
ref3.
Cassava production in Africa faces new challenges from CMD. Disease has
spread in recent years, bringing increased risk of food insecurity to millions
of rural and urban households, particularly in eastern Africa. Research
and extension programs have helped limit the geographic spread of CMD,
but the potential magnitude of the problem threatens to overwhelm these
efforts. CMD continues to be prevalent in all the main cassava-growing
areas in the ECA (Economic Commission for Africa) sub-region and is regarded
as the most important disease, causing 20-90% crop losses based on the
cultivar, viral strain and environmental factors. Deterioration in the
status of CMD is a fact in East Africa, Uganda, DR Congo, and Kenya. Plants
infected via white fly-transmission dominate affected areas. Lower leaves
of infected plants look apparently healthy, while leaves above the point
of 1st infection show severe symptom expression, drastic reduction in leaf
size with marked distortion. Plants harbor numerous adult white fly (Bemisia
tabaci (Bt)) populations on young shoots and large nymph populations
on the lower surface of the apparently healthy lower leaves. Lack of alternative
propagation stock in disease-infected areas leaves farmers no choice but
to use material from the previous harvest of infected plants as planting
stock for the next generation. Environmental factors favoring the development
and fecundity of Bt enhance disease spread, and spread of CMD is therefore
highly linked to the vector. To alleviate the situation, a number of African
countries (Kenya, Burundi, and Madagascar) have made significant progress
in selecting resistant/tolerant clones, which are being evaluated within
their different ecological zones. The research discussed in this piece
was completed in 2002, and normally I would not post a piece that took
almost 3 years to be published in "New Disease Reports, but I believe that
it is important to recognize new virus threats to the food security of
Sudan and other African countriesref1,
ref2,
ref3
mungbean
yellow mosaic India virus (MYIMV) : the interaction between MYIMV and
satellite DNA-beta results in more severe symptoms compared to plants inoculated
with MYINV alone. Similar results have been reported for other DNA-beta
molecules and viruses. DNA-beta molecules are symptom-modulating, ss-DNA
satellites associated with monopartite begomoviruses belonging to the Geminiviridaeref1,
ref2,
ref3,
ref4
pepper
golden mosaic virus (PepGMV), formerly designated as Serrano golden
mosaic virus (SGMV) and Texas pepper virus (TPV), is present
in Costa Rica, Guatemala, Honduras, Mexico (7 states), and USA (Texas),
and causes significant crop losses. Scientists in Mexico are attempting
to select tomato plants that appear to be asymptomatic following inoculation
with PepGMV, suggesting that they may be useful in developing resistant
cultivars. Part of the resistance mechanism appears to be the lack of virus
movement in infected plants. At least 2 closely related strains of PepGMV
(Tamaulipas and La Paz) are present in Mexico.
It is transmitted by 2 whitefly species -- the sweet potato whitefly Bemisia
tabaci and the silverleaf whitefly, Bemisia
argentifolii -- although some taxonomists suggest that these species
are really biotypes. Squash and watermelon
(Citrullus lanatus) are preferred hosts. Disease management
utilizes cultural control (eradication of infected plants, use of UV-absorbing
greenhouse plastic films, and aluminum plastic mulches) and biological
control (use of parasitoids such as Encarsia
spp. and Eretmocerus
spp.). Use of insecticides is not very efficacious because whiteflies
tend to congregate on the undersides of leaves. In most instances, the
incidence of SLCV-affected plants in Israel was close to 100% and was always
associated with high populations of the whitefly, Bemisia tabaci.
SCLV has been reported from USA (Arizona, Texas, and California) as well
as from Guatemala, Honduras, Sinaloa and Sonora states in Mexico, Nicaragua,
and Panama. Epidemic caused by a 'New World' geminivirus in the Eastern
Hemisphere has also been reported.
=> leaf curl in the crop plant sweet
potato, Ipomoea batatas. SLCV or sweet potato with leaf curl
symptoms has been detected or reported in Taiwan, Japan, Brazil, China,
Mexico, Puerto Rico, and the USA, and Kenya (2005). The causal agent is
the whitefly-transmitted SPLCV. Viral genomic ssDNA can be detected in
plant samples using PCR with SPLCV-specific primers. SPLCV-like isolates
cluster into 3 groups, and all of them might have evolved from the same
common ancestor possibly from the Old Worldref1,
ref2
=> leaf crumple disease in soybean
(Glycine max) in India. An incidence of > 80% was observed in
Lucknow. Diseased plants exhibited severe yellowing, crumpling and distortion
of leaves. Infected plants were stunted, and had a very low yield.
The virus is not uncommon in solanaceous crops like tomato in India, but
detection in soybean is a 1st report. The complexity of different
begomoviruses in India and neighboring countries that cause similar diseases
can be followed in the posts listed below. Diversity is driven by an abundant
active vector, the whitefly Bemisia
tabaci, many weed and crop reservoirs, and the capacity for this
group of ssDNA viruses to share/swap genetic information thereby creating
new viruses and strains. Their ability to cause severe disease is demonstrated
in this reportref1,
ref2,
ref3.
tomato
leaf curl Mayotte virus. The agricultural sector on Mayotte is divided
into subsistence farming and farming for export. Subsistence farming, which
provides the staples making up 75% of the islanders' diet, consists of
coconuts, cassava, bananas and rice. Small quantities of fish and meat
are also consumed. Mayotte is not self-sufficient and must import a large
portion of its food requirements, mainly from France. Exports are mainly
ylang-ylang (perfume essence), vanilla, copra, coconuts, coffee, and cinnamon
=> leaf curl disease in potato
(Solanum tuberosum), Nicotiana
benthamiana, tomato
(Lycopersicon esculentum), and watermelon
(Citrullus lanatus) crops in the Indian subcontinentref.
Chilli
pepper (Capsicum annuum), an important crop on the Indian subcontinent,
often shows symptoms similar to tomato leaf curl, such as yellowing, leaf
curling, reduction in leaf size and stunting. Since chilli and tomato crops
overlap in the field, chilli peppers may become infected with tomato begomoviruses.
Tomato-infecting begomoviruses are particularly damaging to solanaceous
crops. In the 1970's there were only 3 tomato-infecting begomoviruses in
the Americas, but at present there are at least 14 new ones, of which 7
are distinct ToLCNDV species. Recombination or pseudorecombination are
driving forces in the evolution of new viruses, especially in tropical
regions. Disease management of ToLCV depends in part on preventing movement
of Bt-infested plants (e.g.. tomato transplants) to virus-free areas, where
the virus can become established and implementation of phytosanitary procedures.
Various control options include removal of infected plants (roguing) and
removal or burial of infected crop residues and intercropping in combination
with chemical insecticides and use of available resistant cultivars. Use
of plastic UV-absorbing screening material to exclude Bt is another method.
Genetic resistance to begomoviruses has been reported in some wild Lycopersicon
species such as L. hirsutum and L. peruvianum which might
be transferred to tomato. In Pakistan, resistance to leaf curl virus has
been incorporated into tomato and chili cultivarsref1,
ref2,
ref3,
ref4.
A whitefly-transmitted begomovirus originating in sponge
gourd (Luffa cylindrica) in Northern India has been shown to
be closely related to ToLCV-NDe. What is interesting is that the new virus
is a relatively rare example of a sap-transmissible begomovirus. Based
on genome sequence analysis, it is closely related to ToLCV-NDe but less
closely related to other ToLCV isolates/strains. At least 3 other begomovirus
strains/isolates have been reported from Asia. The one associated with
cucumber yellow leaf curl disease in Thailand shares 95% nucleotide sequence
similarity with the DNA-A of ToLCV-NDe, and pumpkin yellow vein mosaic
virus is most closely related to the same virus.
In June 2003, symptoms of stunting and leaf curling resembling symptoms
of tomato leaf curl disease, as well as reductions in yields, were observed
on tomato plants in the western (Combani and Kahani) and eastern (Dembeni,
Kaoueni, and Tsararano) regions of Mayotte, a French island in the Comoros
Archipelago located in the northern part of the Mozambique Channel. The
whitefly, Bemisia
tabaci, was observed colonizing tomato plants and other vegetable
crops at low levels
there are 7 ToLCNDV isolates that have been reported from India and 2 from
Thailand. Recombination or pseudo-recombination are driving forces in the
evolution of new begomoviruses, especially in tropical regions. Disease
management of ToLCNDV depends in part on preventing movement of Bt-infested
plants (e.g.. tomato transplants) to virus-free areas. Various control
options include removal of infected plants (roguing), removal or burial
of infected crop residues and intercropping in combination with chemical
insecticides and the use of available resistant cultivars. Use of plastic
UV-absorbing screening material to exclude Bt is another method. Genetic
resistance to begomoviruses has been reported in some wild Lycopersicon
species such as L. hirsutum and L. peruvianum, which might
be
transferred to tomato. In Pakistan, resistance to leaf curl virus has
been incorporated into tomato and chili cultivarsref1,
ref2,
ref3,
ref4,
ref5,
ref6
tomato
severe leaf curl virus (ToSLCV) : strains have been reported from Mexico,
Guatemala, Honduras, Nicaragua, and Cuba. Cucumber (Cucumis
sativus) and tomato
(Lycopersicon esculentum) are natural hosts. These strains likely
originated in Central America and the Caribbean region. The genomes of
these viruses are either monopartite or bipartite, the viruses are transmitted
by whiteflies (Bemisia
tabaci), and they infect a range of dicotyledonous plants. Disease
management involves procedures to delay infection, regulated applications
of insecticides, use of biopesticides (parasitoids and predators), and
planting resistant cultivars if they are available.
=> tomato yellow leaf curl (TYLC)ref1,
ref2
is one of the most devastating viral diseases of cultivated tomato in tropical
and subtropical regions. It is spread efficiently by an insect vector (Bemisia
tabaci [Bt]), and the difficulty of its management is compounded
by the existence of distinct biotypes, of which the 'B' and 'Q' biotypes
are of key interest in southern Europe. The disease is difficult to identify
because of great variation in symptom expression. Infected seedling transplants
may serve as the route for long-distance spread of the virus and, when
introduced into areas of high Bt populations, results in extensive and
rapid spread of the virus. High levels of resistance to TYLCV were detected
in 7 of 9 accessions of Lycopersicon
peruvianum and in all 5 accessions of Lycopersicon
chilense tested. In contrast, plants of 7 accessions of Lycoperison
hirsutum and 3 of 4 accessions of Lycopersicon
pimpinellifolium were highly susceptible. Plants of accession CIAS
27 (L. pimpinellifolium) showed moderate resistance to TYLCVref1,
ref2,
ref3,
ref4,
ref5,
ref6,
ref7.
Its introduction into the region is an excellent example of the interaction
between the whitefly vectors (Bemisia
tabaci [Bt] and Bemisia
argentifolii) and tomato that results in rapid spread of a geminivirus.
Bt is an efficient vector of TYLCV; susceptible host plants, such as squash,
can serve as virus reservoirs. TYLCV acquired during a short period of
time by 1-2 day-old Bt adults remain associated with the insect for several
weeks and were detectable for the life of the insect. Although infectivity
decreased with age, Bt was able to infect test plants for > 4 weeks. It
is present in most Mediterranean countries and parts of sub-Saharan Africa,
Middle East, South East Asia, Japan, Australia, Central America, Mexico,
the Caribbean Islands (including Guadeloupe), and locally in the U.S. states
of Florida, Georgia, and Louisiana. Tomato yellow leaf curl disease is
well-established in Reunion Island after 7 years of cropping : Bt predominates
on the island, but some specimens belonged to another biotype (also present
in Madagascar, Mauritius, Seychelles and designated biotype Mascareignes).
Genetic resistance to TYLCV in tomato cultivars appears to controlled by
at least 5 genes, and crossing experiments yielded only tolerant hybrids.
Disease losses can be catastrophic, leading to complete loss. Disease management
includes the use of available resistant cultivars, use of virus-free transplants,
control of the whitefly vector with chemical insecticides, application
of strict phytosanitary measures, avoidance of peak times of vector activity,
changes in cultural practices such as the control of between-season, alternate
hosts, as well as the identification of resistance sources and the production
of transgenic plants containing resistant genes from wild speciesref1,
ref2,
ref3,
ref4,
ref5,
ref6.
tomato yellow leaf curl Morondava virus (TYLCMV) isolates from Madagascar
tomato leaf curl virus (TLCV-Aus) is a begomovirus that has caused
disease in tomato in Australia since 1971 and is described and mapped in
the A2 list of EPPO for TYLCV and similar viruses. TLCV-Aus is known to
be very similar to a strain of TYLCV from Thailand (TYLCV-Thai). It remains
to be seen which of the multiple strains of TYLCV this new Australian isolate
resembles. A summary of the Australia begomoviruses and a set of diseased
tomato photographsref.
Recent outbreaks of begomoviruses causing severe disease in tomato in Indonesia,
Uganda and South Carolina USA
Tomato plants are severely stunted with shoots becoming erect. Leaflets
become reduced in size and pucker. Leaves curl upwards, become distorted,
and have prominent yellow margins. Flowers wither or appear normal, and
the fruits that set either show no symptoms from the viral infection or
they may be small, dry and unsaleable when infections come early in the
season. While it is impractical to completely eradicate a vector-borne
viral disease, a combination of production practices may minimize the impact
of the disease. These include using disease-free transplants, roguing
the infected plants (early in the season), and managing whitefly populations
using various insecticides or reflective mulches. The Ugandan virus is
similar to TYLCV from Dembeni, Mayotte, Comoros Islands but differs from
other African strains. The Indonesian virus is similar to pepper yellow
leaf curl Indonesia virus and an eggplant isolate of TYLCV from Thailand.
The USA - South Carolina virus is similar to TYLCV isolates from Florida,
the Dominican Republic, Cuba, Guadeloupe, and Puerto Rico. The combination
of reports points out the genetic diversity of this virus family. The USA
find in South Carolina seems to be an example of the introduction of a
virus from another state on transplanted seedlings, in this case tomato
and pepperref1,
ref2,
ref3,
ref4
bell
pepper leaf curl virus : begomoviruses are continually evolving in
Asia, especially in India and Pakistan. The combination of high temperatures,
presence of high populations of whiteflies, and suitable natural host plants
apparently results in a mix that is conducive to generating new begomovirus
strains in the region. The begomovirus-beta satellite complexes referred
to above are associated with economically important diseases and have been
isolated from vegetable and fiber crops, ornamental plants, and weeds throughout
Africa and Asia. Their widespread distribution and diversity, coupled to
the global movement of plant material and the dissemination of the whitefly
vector, suggests that these disease complexes pose a serious threat to
tropical and sub-tropical agro-ecosystems worldwide. Collaborative work,
involving research scientists at the Plant Biotechnology Division, National
Institute for Biotechnology and Genetic Engineering (NIBGE), PO Box 577,
Jhang Road, Faisalabad, Pakistan and the Department of Disease and Stress
Biology, John Innes Centre, Colney, Norwich, UK NR4 7UH, contains information
suggesting that these disease complexes are rapidly expanding in geographical
distribution and host range. As an example, cotton leaf curl disease, originally
a major problem in central Pakistan, is now causing extensive damage in
India. In the same region, new diseases are emerging in crops such as tomato,
tobacco, chillies and papaya. The presence of such a diverse population
of begomoviruses in a single region, coupled with the propensity of these
viruses to exchange genetic material by recombination, increases the probability
of new virus diseases emerging in the region. These viruses will likely
cause epidemics in previously unaffected crops, a problem that will be
exacerbated by the selective use of elite cultivars, movement of infected
plant material and widespread
introduction of the whitefly vector (Bemisia tabaci). Continued
growth in international trade and travel could result in these whitefly-transmissible
disease complexes reaching the New World, as was demonstrated when Tomato
yellow leaf curl virus (TYLCV-Is) appeared in the eastern Caribbean in
Cuba, the Dominican Republic, and Jamaica. In the case of the Dominican
Republic, it was believed to have been introduced on infected but asymptomatic
tomato transplants from the eastern Mediterranean region. An isolate of
TYLCV-Is from the Dominican Republic and 98% identical to an isolate from
Israel appeared to have entered the United States in Dade County, Florida,
in late 1996 or early 1997. Subsequently, infected tomato transplants produced
for retail sale at 2 Dade County facilities were rapidly distributed via
retail garden centers throughout the stateref1,
ref2,
ref3
tomato
yellow vein streak virus (ToYVSV) : it is interesting that it took
over 20 years to recognize that ToYVSV and Potato yellow deforming virus
were one and the same virus. In potato, the apical leaves showed yellow
or green mottle which developed into leaf distortion with yellow blotches
(apparently no natural infection have been found on potato). About 20%
of young tomato plants showed virus symptoms. Tomato is an important crop
in the EPPO region, and both indoor and outdoor and the virus vector is
present in many parts of the EPPO region. The disease appears so far, limited
in Brazil but data is lacking about its extent and severity. The original
isolate of PYDV was recorded in the 1980s in southern Brazilref1,
ref2.
About 20% of young tomato plants showed virus symptoms. Tomato is an important
crop in Europe, where production systems are extremely intensive, and yields
can be very high (up to 700 tons/ha). The virus vector [whitefly] (Bemisa
tabaci) is present in the region of the European & Mediterranean
Plant Protection Organization (EPPO). The disease appears, so far, to be
limited in Brazil, but data is lacking about its extent and severity. ToYVSV
infects both tomato and potato crops in Brazil.
Mastrevirus
chickpea chlorotic dwarf virus (CpCDV) is transmitted only by specific
insect vectors (Orosius spp., family Cicadellidae). In addition
to India and Iran, the virus has been reported on chickpea in Egypt and
Iraq. Disease management depends upon an integrated pest management program
(IPM). Management options include use of resistant host plants, biological
control, suitable agronomic practices, and habitat management.
wheat
dwarf virus (WDV) : in Sweden, it is periodically an important pest
on wheat. It is transmitted by the insect Psammotettix alienus,
family Cicadellidae. The genetic diversity among wheat-infecting
isolates of WDV was found to be low throughout Sweden and Europe, while
WDV isolates infecting barley were distinctly different. WDV was also identified
in samples of wild grasses and the insect vector. WDV spreads in Bulgaria,
the former Czechoslovakia, France, Hungary, and the former USSR; found,
but with no evidence of spread, in Swedenref.
Philippines / 1961 / + (devastated many plantations in the
Bicol Region of the Philippines for > 50 years)
Sri Lanka / 1921 / +
Taiwan / 1961 / +
Vietnam / 1969 / +
Africa
Burundi / 1988 / +
Central African Republic / 1996 /
Congo / 1961 / +
Democratic Republic of Congo (formerly Zaire) / 1982 /
Egypt / 1927 / +
Gabon / 1982 / +
Malawi / 1997 / +
Rwanda / 1988 /
It has not appeared in Central or South America or in Western Australia.
BBTV is vectored by the banana aphid (Pentalonia nigronervosa).
Disease management is predicated on integrated pest management (IPM). Strategies
include long-term aphid control (killing of weed hosts for aphid control,
use of predators and parasites, control of aphids on alternate hosts),
frequent scouting for diseased plants, destruction of diseased trees, planting
of virus-free material, and heat treatment of infected tissue cultures
to provide virus-free plantletsref1,
ref2,
ref3,
ref4,
ref5,
ref6,
ref7,
ref8,
ref9.
=> it plays no etiological role in lettuce big-vein disease (BVD)
expression in lettuce (Lactuca sativa)
and does not affect the outcome of MiLV
infection. Both LBVV and MiLV are vectored by the soil-inhabiting fungus
Olpidium
brassicae. LBVV virions are fragile, somewhat rigid rods (320-360
nm long).
unclassified dsRNA viruses
High
Plains virus (HPV) - A newly discovered virus that infects corn and
wheat. It originally was discovered in the High Plains region but since
has been found in Israel, Chile, Florida and many places besides the High
Plains. The fact that HPV has been detected in Australian wheat is not
surprising. It has been recorded in the Americas, and there are unconfirmed
reports of its presence in Russia. HPV can cause severe disease in barley,
maize, oats, rye, and some grasses. Disease management depends upon interrupting
the life cycle of the mite vector (Aceria
tosichella) by plowing down volunteer wheat seedlings at least
2 weeks before seeding the next crop. The mite cannot survive in the absence
of susceptible hosts for more than 24 hours. At present there is no information
on how HPV presence will affect wheat production in Australia. Time will
tell. An intriguing aspect of this report is that HPV appears to share
some properties of a group of filamentous, eryiophyid mite-transmitted
viruses (fig mosaic, thistle mosaic, rose rosette, redbud yellow ringspot,
and wheat spot mosaic, all transmitted by A. tosichella) and possibly
pigeonpea sterility mosaic, transmitted by Aceria
cajani, and known to infect pigeonpea crops in India. There is
little information about the structural properties of HPV and others in
the groupref1,
ref2.
ssRNA negative-strand viruses
Bunyaviridae
Tospovirus : There are at least 15 recognized tospoviruses. The type member,
Tomato
spotted wilt virus (TSWV), has one of the broadest host ranges among
plant viruses. It is well established in many parts of the world and affects
crops such as potato, lettuce, tomato, pepper, groundnut, mungbean, and
tobacco : it constitutes a severe threat to Capsicum cultivation
worldwide. Rough estimates calculate the worldwide loss due to tospoviruses
at USD 1 billion. Lettuce crops in Hawaii have suffered serious damage
due to TSWV for several successive years, forcing growers to switch to
other crops. Annual losses due to peanut bud necrosis virus (PBNV)
in Asia are estimated at more than US$ 89 million. A new approach to disease
management of TSWV is peptide-mediated, broad spectrum plant resistance,
as described by Rudolf, Schreir, and Uhrig at the Max Planck Institute
for Plant Breeding Research, Cologne and Bayer Crop Science in Mohnheim,
Germanyref,
to which the numbered references in this comment refer, and which includes
a comprehensive review). An example is the development of broad spectrum
resistance which is expressed by specific viral proteins. There are unambiguous
examples of protein-mediated virus resistance -- mainly expression of viral
coat proteins (3,4,10) -- but cases of protein-dependent pathogen-derived
resistance due to expression of viral movement proteins or replicases are
also known (9,11,12). In some instances, resistance is based on the expression
of intact, functional proteins; in others the expression of the intact
protein leads only to weak resistance or even to enhanced susceptibility.
In contrast, expression of a dysfunctional protein may lead to strong resistance
(12,13). Presence of the viral gene product in inappropriate amounts, form
or time, is thought to interfere with viral infection. However, in some
cases it is difficult to distinguish between an RNA- and protein-mediated
resistance (8,9). Despite the number of successful examples, the molecular
basis of protein-mediated virus resistance is, in most cases, not understood.
Further research and development are requiredref1,
ref2
=> impatiens necrotic spot in potato is a conundrum, of sorts
because it involves production of potato in an experimental glasshouse
rather than a production field. Under the growing conditions prevailing
in the glasshouse, the virus failed to replicate sufficiently to maintain
the virus in infected potato. The interesting aspect of this disease is
that INSV-infected N. benthiamiana is an effective indicator of
the disease. Disease management would require applications of insecticides
to reduce populations of the insect (Frankliniella
occidentalis). Other thrips have not been identified as vectors,
but that may have changed. The biology of INSV is similar to that of TWSV,
such that the 2 viruses are often recorded togetherref1,
ref2,
ref3,
ref4
iris
yellow spot virus (IYSV) has been reported from over 50 countries worldwide
: in addition to infected onion crops in Washington and Colorado, IYSV
is present in Brazil, Iran, Israel, the Netherlands, and Slovenia. IYSV
has been endemic in south western Idaho and eastern Oregon onion, leek,
and chive seed production fields for over 10 years. IYIS is a major constraint
to onion production in parts of the USA, and new outbreaks continue to
be reported. The economic impact of IYSV varies from low in IYSV-infected
leek in the Netherlands but, in Brazil, IYSV-infected onion crops can range
up to total loss. It has also been detected in onion seed plants from California
and Arizona. The virus is vectored by onion thrips (Thrips
tabaci) but not by western flower thrips (Frankliniella
occidentalis), which are an efficient vector of the virus. Although
there is no cure, diseased plants can still produce reasonable yields through
irrigation and good soil fertility. Not much is known about resistance
to IYSV in onion. Recommended disease management options include removal
of culled onions so as to reduce sources of infection, reduction of plant
stressors so that the crop has sufficient soil and fertility, reduction
of soil compaction and irrigation stresses, and management of thrips populations
by appropriate chemical insecticides. Natural enemies, including predaceous
mites, minute pirate bugs, and lacewings, are often found feeding on thrips.
These beneficial insects are very susceptible to insecticidal sprays, however,
and are thus unlikely to be effective in biological control of insects
in fields treated with insecticidesref1,
ref2,
ref3,
ref4,
ref5,
ref6,
ref7,
ref8.
IYSV attacks a number of vegetable, fruit, and flower crops causing considerable
economic damage. Disease management employs several cultural control options,
including avoiding planting thrips-susceptible crops following small grains,
managing vegetation in fields and field edges, using colored mulches, and
avoiding high nitrogen levels. Some cabbage and onion varieties are somewhat
resistant to thrips attack. Several beneficial insects suppress thrips
levels. Organically-acceptable pesticides are available for thrips controlref.
IYSV is difficult to readily identify. Research results to date have shown:
i) disease incidence varies among varieties; ii) IYSV may be associated
with plant stress (i.e. moisture, temperature extremes, salinity, soil
compaction, pink root, etc. ); iii) in more susceptible varieties, IYSV
incidence is initially higher along field edges and lower in the center
of the field (similar to the pattern of onion thrips). This pattern of
thrips distribution occurs when they immigrate from surrounding vegetation,
but their distribution may become more uniform in the field as the season
progresses. Entomologists at Cornell University are studying the ecology
of onion thrips and their movement patterns within and between fields;
and iv) IYSV incidence decreases as plant population increases, possibly
because onion thrips are challenged to locate a single plant when plant
populations are high. In a IYSV pesticide trial, it was found that Actigard
+ imidacloprid resulted in a 34-38% yield increase of the jumbo class.
A complete integrated approach will be necessary for successful IYSV and
thrips managementref1,
ref2.
IYSV has been reported from North America for several years and recently
in Australia. The virus is mainly transmitted by onion thrips (Thrips
tabaci) and to some extent by the western flower thrips (Frankliniella
occidentalis), which causes considerably more damage to the crop.
Onion seed, bulbs, and roots are not known to carry the virus, but volunteer
onions are often symptomatic in early spring in Colorado. The virus likely
over-winters in perennial and winter annual weeds, over-wintering onion,
and adult thrips. To my knowledge, there is no biological control for IYSV.
Disease management depends upon use of thrips-free transplants, utilization
of crop rotation (at least 3 years between crops), elimination of culls
and weed hosts of the vector, and avoidance of plant stress by providing
appropriate irrigation, and avoidance of soil compaction and saline soils.
There are no completely IYSV-resistant onion cultivars available, but there
are some less resistant ones that can be used. Thrips control may provide
some reduction in Iris yellow spot, but thrips control alone is not sufficient
to economically control the disease. Thrips resistance to commonly applied
insecticides is widespread in Colorado and other onion production regions
of the High Plains in the USAref1,
ref2,
ref3.
It mainly infects onion, garlic, leek, lisianthus and iris (it was 1st
isolated from iris, hence the name Iris yellow spot virus). There is no
evidence of it being seedborne. The industry is concerned about the potential
impact of IYSV in Washington state, particularly because it has been recorded
as present in Colorado, Arizona, Utah and California. IYSV-infected onions
cannot be cured. Infected plants should be removed and destroyed, along
with cull piles and volunteers. Maintaining good cultural management practices
will help to reduce stress on the plants, thus lessening the disease's
effect. Other management practices include maintaining good soil fertility
and adequate irrigation supplemented with good management of thrips and
weeds. Onion thrips are best managed with chemical insecticides. Although
no cultivars are known to be resistant to IYSV, research has shown that
cultivars vary in their susceptibility to both the virus and the thrips
vectorref1,
ref2,
ref3,
ref4,
ref5.
In 2006 it was 1st reported in onions (Allium cepa) in Peru. The
samples tested were collected in 2003 and 2005 near the owns of Superef
and Icaref
in Peru, extending the range of the virus in South America from previous
reports in Brazil (1999) and Chile (2005). The disease distribution map
for other countries, including USA, Spain, and Australiaref.
It causes disease in the crop plants onion and leek and in the ornamental
plant iris (where it was first detected). Affected onion plants show numerous
eyelike spots on the leaves and flower stalks resulting in flower abortionref1,
ref2.
The economic impact of iris yellow spot virus can be severe in Brazil,
where up to 100% loss has been observed in onion fields. Thrips tabaci
can transmit the virus, but Frankliniella schultzei and F. occidentalis
are not thrip vectors. Recent studies showed that onion bulbs and seeds
did not transmit the virus to progeny. Further studies are needed to better
understand the epidemiology of the disease in the field. In order to manage
the disease, infected plants should be removed and destroyed, along with
cull piles and volunteers. Other management practices include maintaining
good soil fertility and adequate irrigation supplemented with good management
of thrips and weeds. Onion thrips are best managed with chemical insecticides.
Although no onion cultivars are known to be resistant to IYSV, research
has shown that cultivars vary in their susceptibility to both the virus
and the thrips vectorref1,
ref2
tomato fruit yellow
ring virus (TFYRV) has an extensive host range (Ghotbi, et al. 2005)
but it is found most often in tomato and in mixed virus infections with
TSWV. It was found infecting tomato in Iran : the virus originated from
the Varamin area where > 30% of the tomato crop was infected with TSWV
tomato
spotted wilt virus (TSWV) is regarded as one of the 10 most economically
destructive plant pathogens. During the past 2 decades, it has spread around
the world by thrips (small insects that feed on plants), causing very high
losses to a variety of vegetable (e.g. tomatillo (Physalis
ixocarpa)), ornamental, and agronomic crops. TSWV is now common
in temperate, subtropical, and tropical regions around the world and is
a major constraint to onion production. 4 thrips species are the major
vectors of TSWV: Frankliniella
occidentalis (western flower thrips); F. schultzei, Frankliniella
fusca (tobacco thrips); and Thrips tabaci (onion thrips).
The western flower thrips (Frankliniella
occidentalis) and the tobacco thrips (Frankliniella
fusca) are major species in Florida. Until recently, growers sprayed
toxic, broad-spectrum insecticides in an attempt to control thrips, but
the chemicals do not prevent virus transmission. The solution is to use
a variety of new, environmentally friendly strategies known as integrated
pest management (IPM). IPM includes new cultural practices (a new plastic
bed cover that reflects UV light and repels thrips : anyway UV-reflective
mulches also repel aphids, drastically reducing both feeding and probing
by them in sweet pepper and baby
marrow (zucchini)), natural insecticides (spinosad is a mixture
of 2 of the most active, naturally occurring metabolites (spinosyns A and
D) produced by the soil-inhabiting actinomycete Saccharopolyspora
spinosa: upon ingestion of the spinosyns, death follows due to
extremely rapid excitation of the insect nervous system), bio-control agents
or natural predators, and a new treatment that boosts the plant's resistance
system against viral and bacterial pathogens (Actigard®).
Resistance to TSWV but not to other tospoviruses, based on a hypersensitive
reaction, has been found only in accessions of Cc 'PI152225' and 'PI159236'.
The resistance, carried by the dominant gene Tsw, is broken at high temperatures
and depends on plant age, with young plants being more susceptible. The
Tsw gene has been introduced into several commercial sweet and hot pepper
cultivars with good agronomic performance. Resistance-breaking strains
of TSWV systemically infecting resistant plants have been found under experimental
conditions and in the fieldref1,
ref2,
ref3,
ref4.
In 2004, leaf samples of a processing tomato variety carrying the Sw5 resistance
gene to Tomato spotted wilt virus (TSWV) were collected from field grown
plants in Mesagne (BR), Apulia (Southern Italy). Leaf extracts were tested
by lateral flow and/or ELISA (Roggero et al. 2002) for TSWV, Impatiens
necrotic spot virus (INSV), Cucumber mosaic virus (CMV), Tobacco mosaic
virus (TMV) and Potato virus Y (PVY). Leaf dips were also observed with
a transmission electron microscope and 2 of these samples were inoculated
mechanically on to a set of test plants. Only TSWV was detected in all
the field samples tested. One of the TSWV field isolates, T992, was investigated
for the ability to overcome the resistance gene Sw5. T992 was mechanically
inoculated onto 20 plants of each F1 hybrid tomato cultivar carrying the
Sw5 gene (Cvs Donald, York, Rovente, Valiente, Hermes, UGX 9233, Diaz,
ISI 19343, Es 5302, Scipio and Herdon); cv Marmande was used as a susceptible
control. Another set ofF1 hybrids was mechanically inoculated with strain
p105; a wild-type strain of TSWV (Roggero et al., 2002). Tomato plantlets
were inoculated at the 4-5 true leaf stage and systemic infection was tested
20 days post-inoculation using ELISA. All hybrids carrying the Sw5 gene
were uninfected systemically by strain p105, with the exception of 4 plants
of F1 UGX 9233. In contrast, T992 systemically infected all F1 hybrids
tested. Marmande was infected systemically by both p105 and T992. These
results showed that strain T992 can overcome Sw5 gene resistance. Portions
of the S and M genome of T992 were cloned and sequenced, and the data deposited
in GenBank (accession numbers AY848922 and AY848921, respectively). Using
a 560-bp fragment corresponding to part of the non-structural protein of
the middle segment (NSm), the closest identity was to the SAN-1 isolate
(AY124966), previously described from Apulia (Finetti-Sialer et al., 2002).
Using a 780 bp N fragment the closest identity was to the LE98-527 strain
from Bulgaria (99.6% identity at the nucleotide level) (Heinze et al.,
2001). T992 was classified as an A-type isolate according to the MaeI restriction
pattern used previously
(Finetti-Sialer et al., 2002). This was the 1st confirmed report of
resistance-breaking (RB) strains of TSWV in tomato in Italy. Previously,
RB strains of TSWV on tomato in Europe were identified only in Spain (Aramburu
& Marti, 2003)ref.
This is the 2nd instance of a resistance-breaking strain of TSWV reported
in Europe in the past 3 years. TSWV resistance-breaking strains have previously
been reported from Italy in Capsicum spp. carrying the Tsw gene
(Roggero et al., 2002) and from Spain in tomato species carrying the Sw5
gene (Aramburu & Marti, 2003). Resistance-breaking strains can spread,
resulting in increased losses in fruit production and quality. Similarly,
in Australia, 3 of 1386 TSWV-infected Capsicum chinense accessions
also expressed systemic symptoms when manually inoculated with specific
TSWV strains. Resistance-breaking strains are a dangerous factor in crop
production systemsref1,
ref2,
ref3.
=> lettuce big-vein disease (BVD) in lettuce
(Lactuca sativa) ? : chlorotic vein banding that become ruffled
and distorted. Symptoms are usually accompanied by reduced plant size and
absence of head formation. Both LBVV and MiLV are vectored by the soil-inhabiting
fungus Olpidium
brassicae. Virions of MiLV are highly kinked filaments, about 3
nm in diameter, that form masses of 2 classes of particles differing in
length that appear to be closed circles, suggestive of tenuiviruses. Disease
management basically requires strict measures to kill the vector in the
plastic growing trays. Other strategies include developing resistant
cultivars using a wild lettuce (Lactuca virosa) in crosses with
cultivated lettuce and a range of biological control agentsref1,
ref2.
ranunculus
white mottle virus (RWMV) is similar to known tenuiviruses such as
citrus psorosis-ringspot virus (CPsV) and tulip
mild mottle mosaic virus (TMMMV), members of the genus Ophiovirus,
family Bunyaviridae. Comparison of the core RNA-dependent RNA-polymerase
(RdRp) motifs of negative-stranded RNA viruses supports grouping CPsV,
RWMV, and MiLV in the Ophiovirus, creating a monophyletic group
separated from all other negative-stranded RNA viruses
=> citrus leprosis (EPPO A1 list) is a devastating viral disease
of citrus. It has persisted in Brazil and Argentina since the early 1930s
and as the previous postings referenced below and the disease distribution
map indicate, it seems to be spreading in South and Central America.
It causes significant mortality of new wood growth, reduction in tree canopy
development, premature leaf and fruit drop, and significant yield reduction.
Citrus leprosis occurred in Florida citrus between the mid-1800s and 1962,
with severe outbreaks between 1907 and 1925. No occurrence of the disease
has been reported over the past 40 years in Florida and recent surveys
in 2001-2002 did not detect the disease. Citrus leprosis differs from many
other plant viruses, which are usually systemic in plant tissues. Sweet
orange varieties are susceptible. Planting resistant citrus cultivars,
pruning to reduce disease inoculum and seasonal acaricide sprays to control
the mite vectors are the only existing means of minimizing the current
impact of this disease. Continued expansion of this viral pathogen
in South and Central America can be seen as a warning that spread could
occur to other citrus-producing areas. Because the disease is strongly
symptomatic on leaves and twigs, this would probably require the introduction
of viruliferous mites, probably on rooted plant materials, into areas that
may already have the mite vector but not the virus. Citrus leprosis is
non-systemic and so far, 3 mite species have been demonstrated to transmit
the disease within and between citrus trees in the orchard, Brevipalpus
phoenicis, B.
californicus, and B.
obovatus (Acari: Tenuipalpidae). In addition to Brazil, the disease
occurs in other South American countries and it was recently identified
in Central America in Panama, Costa Rica and Guatemalaref.
CiLV-infected plants show localized chlorotic lesions with necrotic rings
in leaves, depressed chlorotic or brownish fruits and lesions in the bark
and stems. Fruit drop often occurs and heavy infection can lead to death
of trees. The disease is considered as one of the most important citrus
diseases in Brazil, causing millions of dollar in damage annually to the
citrus industries of Argentina, Brazil, Panama, Paraguay, and Venezuela.
CiLV has been moving northward since 1941 and poses a serious threat to
the billion-dollar U.S. citrus industry. The newly developed PCR procedure
will certainly facilitate rapid detection of CiLV. The major production
cost with citrus in Brazil is miticide applications. Current research in
Venezuela suggests that CiLV may be pass through nurseries, with leaf lesions
developing after the budlings have been planted into the fieldref1,
ref2,
ref3.
Citrus leprosis has cost millions of dollars in damage to crops in South
America, where it is well established. Symptoms include small, chestnut-brown
spots -- commonly referred to as nailhead rust -- that appear on fruit,
leaves, and green twigs of afflicted trees. The resulting loss of tree
canopy growth combined with premature fruit and leaf drop reduce plant
productivity. Sweet orange and some mandarin varieties are most susceptible.
Citrus leprosis virus, which substantially damaged Florida's orange crop
in the early 20th century, is slowly progressing northward from its outbreak
epicenter in South America. The disease's presence in Central America has
raised warning flags among U.S. Department of Agriculture (USDA) scientists
at ARS and at the Animal and Plant Health Inspection Service (APHIS). The
northbound spread of CiLV is considered a serious threat to the citrus
industry of the USA. Brazilian scientists depended upon analyses of symptoms
and transmission electron microscopy (TEM). However, accurate assessment
of symptoms require field experience and can be confused with those caused
by other plant pathogens. A region of the CiLV genome was sequenced and
used to design specific primers that recognize only CiLV. These primers
were used in RT-PCR to test more than 70 citrus plants from different species
and varieties, originating from various geographic locations, and were
shown to recognize only CiLV-infected plants. This is the 1st report on
the development of a molecular-based method for the diagnosis of citrus
leprosis. Disease management depends upon application of miticides and
pruning infected branches from trees. Disease management of citrus leprosis
is by control of the mite vector. Most of the currently available chemicals
used to control mites are effective. Some of the products presently recommended
in Brazil are azocyclotin, cyhexatin, hexythiazox, fenbutatin oxide, propargite
and quinomethionateref1,
ref2,
ref3,
ref4,
ref5,
ref6,
ref7.
=> rhizomania is a disease of beet
(Beta vulgaris subsp. vulgaris). The disease is most
serious on sugar beet, although it is also known to infest fodder beet,
red beet, spinach beet, seakale beet, swiss chard and spinach (Spinacea
oleracea). If left unchecked, there are significant reductions in sugar
beet yields through reductions in root weight and accompanying reduction
in sugar content. 3 different pathotypes (strains) of the virus have been
identified, the 'A', 'B' and 'P' pathotypes. Sugar beet cultivars have
been developed that are both tolerant and show some resistance to infection.
It can greatly reduce sugar yield and tonnage. Further losses to producers
in infested areas can result when movement of agricultural products is
restricted by quarantine laws. The soilborne fungus, Polymyxa
betae (Pb), serves as a vector of BNYVV by carrying the virus to
healthy roots. The association of BNYVV with Pb is an unusual biological
relationship that results in rhizomania development when a susceptible
host is present and conditions are favorable for infection. Sugar beet
serves as a host for both Pb and the virus. Although some weeds, primarily
in the goosefoot family, also serve as hosts, their role in rhizomania
development is not clear. Data from field surveys in Wyoming and Nebraska
showed that Pb is relatively common and, when not carrying BNYVV, usually
causes little damage to the sugar beet. Because BNYVV is spread is favored
by conditions that favor both infection of sugar beet and rhizomania development.
Pb forms 2 types of spores during its life cycle, resting spores and motile
zoospores. Clusters of tiny, thick-walled resting spores, also called cystosori,
enable Pb to survive in soil or in resting spores for 15 years or longer
in the absence of a suitable host. When soil conditions become favorable
for infection, germination of the resting spore is triggered by the presence
of a host-plant root. As resting spores germinate, motile zoospores are
released that actively swim to the root surface where new infections occur.
Once a field becomes Pb-infested, crop rotation will not appreciably reduce
disease risk because of the long-term survival of viruliferous cystosori.
However, some soil fumigants such as those containing 1,3-dichloropropene
may kill enough cystosori to reduce disease development to acceptable levels.
Fumigation treatments are very expensive, and research is being done to
determine their efficacy and conditions under which they should be used.
Expenses associated with fumigant application may be justified, because
significant sugar beet acreage is routinely treated with 1,3-dichloropropene
for nematode control. The use of soil-applied fungicides has not been effective
for rhizomania control in infested fields. Currently available tolerant
or resistant varieties perform satisfactorily in the presence of rhizomania
in some production areas, especially when used in combination with soil
fumigation. However, these varieties must be tested in each production
area to evaluate their performance under local environmental conditions
and production practices. They also must be evaluated for performance after
exposure to local diseases, insects, and weed pests. Research on the development
of resistant varieties is progressing rapidly, with some having dual resistance
to both rhizomania and Beet curly top virus. Management of rhizomania involves
application of phytosanitary measures such as containment of spread in
the affected area, avoiding movement of soil from infested areas,
use of rubber boots or disposable footwear, and cleaning and removal of
adhering soil at the field site. Moreover, soil contractors, machinery,
and highway vehicles should be removed. Removal of soil at the field site
is necessary because resting spores are extremely difficult to kill with
chemical disinfectants, especially when associated with soil. Therefore,
infested soil removed from footwear and equipment is likely to remain infested
and will serve as a potential source of contaminationref1,
ref2,
ref3
Bromoviridae
Cucumovirus
cucumber
mosaic cucumovirus (CMV), the type member of the genus, is worldwide
in its distribution, has the largest host range of any plant virus, infecting
more than 800 species, and is transmitted by > 60 aphid species in a nonpersistent
manner. Virus strains can be subdivided into 2 major subgroups, I and II
(by serological and molecular methods), but all yield essentially the same
subdivisions of isolates. Subgroup I, typified by isolate DTL, occurs predominantly
in the tropics and subtropics, while subgroup II, typified by ToRS, is
prevalent in temperate regions. Both subgroups, however, occur on bananas.
Strains on banana vary from those that are symptomless to those inducing
mild to severe symptoms. The heart-rot strain found in Morocco is particularly
severe. The virus may cause chlorosis, mosaic, and heart rot, and is the
etiological agent of infectious chlorosis disease in banana. In general,
CMV does not have a major impact on banana production, but serious outbreaks
have occurred. Bunch weight reductions of 45-62% have been reported. CMV
has been reported as an emerging threat to the cultivation of banana in
Kerala, India, especially where cucurbitaceous vegetables are cultivated
as intercrops in banana. It is especially important to control CMV where
mass propagation of in vitro banana material is employed, as levels
of CMV in these plantings can be high. While considered worldwide in its
distribution, CMV and CMV strains have been reported for the 1st time on
bananas in a number of developing countries recently, probably due to the
availability of efficient detection and identification methods. Disease
management include planting CMV-free source plants, ensuring plants for
propagation are free of virus, deployment of sensitive diagnostic procedures,
and elimination of weed hosts from plantations and surrounding areas to
control the virus and banana plantations should not be close to crop
hosts of CMV (e.g., cucurbits, tomatoes, and tobacco). Research has been
directed to a program of virus elimination in the Plant Pathology Unit
(FUSAGx, Belgium) in collaboration with the Laboratory of Tropical Crop
Improvement (K.U.Leuven, Belgium). Different in vitro techniques, including
thermotherapy, chemotherapy, electrotherapy or meristem culture, and cryotherapy
were tested for their virus elimination capacityref1,
ref2,
ref3
apple
mosaic virus (ApMV), one of the oldest known and most widespread apple
viruses, is probably distributed worldwide. It used to be rare in European
apple trees but was disseminated by widespread distribution of the 1st
infected Granny Smith clones, where it is latent and produces no symptoms.
It can also cause line pattern symptoms in plum. ApMV is related to Prunus
necrotic ringspot virus. ApMV-infected apple trees develop pale to bright
cream spots on spring leaves as they expand. These spots may become necrotic
after exposure to summer sun and heat. Most commercial cultivars are affected,
but vary in severity of symptoms. Golden Delicious and Jonathan are severely
affected, whereas Winesap and Mclntosh are only mildly affected. Except
in severe cases, a crop can still be produced by infected trees; yield
reductions vary from 0 to 50%. In some cultivars, bud set is severely affected.
ApMV is transmitted by mechanical inoculation and root grafting, possibly
not transmitted by pollen to the pollinated plant. Disease management basically
consists of digging up infected trees and destroying themref1,
ref2,
ref3
Closteroviruses are transmitted by aphids, whiteflies or mealybugs, depending
upon the virus. The outbreak of BnYDV in early 2004 occurred in approximately
20% of all bean-producing glasshouses in 3 Spanish provinces (Almeira,
Granada and Malaga) destined for the fresh market. Yield losses have been
reported from 25-100%, depending on local conditions. Disease management
will depend upon reducing populations of Bt as well has clearing away vegetation
that might support the vectorref
=> leafroll in Vitis
vinifera. It is transmitted by the insect vector mealybug (Planococcus
spp.). GLRaV is probably the most wide-spread virus disease of grapevines
world-wide. There are currently 9 different viruses associated with leafroll,
but GLRaV 1 and 3 are most commonly found. In the U.S. national grapevine
survey
conducted in 1994-1995, GLRaV-1 was present in 1.0% of samples tested,
whereas GLRaV-3 was present in 10.5% of samples tested. Since then Grapevine
leafroll-associated viruses 2, 4 and 5 have been detected in imported grapevines.
Yields of GLRaV-infected vines have reduced yields, and are increasingly
sensitivity to environmental stress. Delayed maturity of grapes may result
in a reduction of 10-70 percent in growth and yield, a 25-50 percent reduction
in sugar content, and poorly coloured fruit. Long distance spread of GLRaV
depends upon movement of infected planting material. Several mealybug and
soft scale insect species have been shown to transmit leafroll-associated
viruses under experimental conditions. Rapid leafroll spread has been reported
in European vineyards having significant insect vector populations. In
California, a very low rate of natural spread within vineyards has been
observed. The common grape mealybug (Pseudococcus maritimus), which
occurs in the Okanagan valley of British Columbia, is a vector of GLRaV-3.
The etiology of GLRaV disease is not well established, but several filamentous
viral particles have been associated with it, including 7 serologically
unrelated closterovirus-like particles referred to as grapevine leafroll
associated viruses 1 to 7 (GLRaV 1 to 7). Grapevine leafroll has also been
associated with grapevine virus A (GVA),
a trichovirus included in the rugose wood complex. 4 mealybug species (Pseudococcus
longispinus,
Planococcus ficus, Planococcus citri, and
Pseudococcus
affinis are known). The only Pseudococcidae reported to transmit GLRaV-3
are Planococcus ficus and Pseudococcus longispinus, but the
scale insect Pulvinaria vitis may also be a vector. Several reports
on field transmission of grapevine leafroll disease have confirmed the
role of mealybugs as vectors of GVA and GLRaV- 3; although, in other studies,
no vectors were identified. Leafroll of grapevines occurs worldwide in
all grape-growing areas. Germany suffered an 80% leafroll infection in
1936. In Nuriootpa, Southern Australia, natural spreading of leafroll symptoms
in Pinot noir clone material was observed. In 1993, 6% of vines displayed
leafroll symptoms, which escalated to 21 and 36% in 1994 and 1995, respectively.
In France some vineyards are reported to be 80% infected with leafroll.
The incidence of leafroll infection over recent years in New Zealand has
increased rapidly. The virus is now causing concern in New Zealand with
possible rapid spread on the North Island. The article chosen from
several in early June 2006 points out that the virus is not new and may
simply be catching the attention of some growers for the 1st time.
Management is by testing of existing groves for the virus, the use of clean
(virus-tested) planting stock when replanting or establishing new vineyards,
and by vector control. Despite the attempt to minimize alarm, it is clear
from the article that the presence and spread of the virus is leading to
systematic and accelerated replanting of some vineyards in New Zealandref1,
ref2,
ref3,
ref4,
ref5
Crinivirus are filamentous viruses containing 2 separate genomic segments
(650-850 and 700-900 nm), both of which are required for infectivity. Tomato
(Lycopersicon esculentum) (field and glasshouse) is the main
host, but other crops such as potato
(Solanum tuberosum) and lettuce
(Lactuca sativa are susceptible. 2 weed species (Jimson weed,
Datura
stramonium and Black nightshade, Solanum nigrum) are also hosts
that may contribute to maintaining these viruses in the wild. Once either
virus is established in an agricultural environment containing susceptible
hosts, it is very difficult to prevent infection. Disease management requires
use of virus-free transplants, avoidance of susceptible hosts (especially
weeds), roguing (physical removal) of infected plants, and control of insect
vectors by insecticides. Criniviruses are an emerging genus worldwide,
containing new species that have evolved over time and are now evident
as causal agents of new plant diseases. Their symptoms are easily mistaken
for those of physiological or nutritional disorders or pesticide phytotoxicity,
thus confounding their identification. Symptoms can vary, depending upon
the host species, to include interveinal leaf yellowing, loss of photosynthetic
capability, leaf brittleness, reduced plant vigor, yield reductions and
early senescence. Criniviruses remain confined to cells associated with
the plant phloem and symptoms are considered to result from plugging of
the phloem with large viral inclusion bodies, thus likely interfering with
normal vascular transport in infected plants. Both TICV and ToCV were first
reported during the 1990s in the United States, and ToCV has been reported
to occur in the Mediterranean countries, Portugal, Spain, and Italy. 4
crinivirus species transmitted by greenhouse white fly (GHWF) have been
identified to date, including Beet pseudo yellows virus (BPYV), Strawberry
pallidosis-associated virus (SPaV), ToCV and TICV. The latter viruses have
exerted significant pressure on vegetable and fruit production in North
America, Europe, and other parts of the world, affecting both greenhouse-grown
crops as well as field crops. 3 viruses, primarily BPYV, SPaV, and TICV,
are transmitted exclusively by GHWF, and are currently responsible for
economic damage to vegetable and fruit production. Although ToCV is transmitted
by the GHWF and impacts tomato production, it is much more efficiently
transmitted by B. tabaci [Bt] biotype B than by GHWF, and its incidence
is associated more closely with the presence of Bt in fields and greenhouses
than with GHWF. These criniviruses have host ranges of varying size, ranging
from quite narrow in the case of SPaV, to extremely broad in the case of
BPYV. Although all GHWF-transmitted criniviruses infect weed species and
wild relatives of cultivated crops, their primary agricultural impact occurs
on 3 major groups of crops. Thus TICV and ToCV exert their main economic
impact on tomato production in both greenhouse and field settings. SPaV
is a problem in strawberry; BPYV, with its extensive host range, infects
numerous cucurbit species, as well as strawberry and blackberry. Disease
management is straightforward; use of virus-free transplants, avoidance
of susceptible hosts, especially weeds, roguing of infected plants, and
control of insects by chemical insecticidesref1,
ref2,
ref3,
ref4.
beet
pseudoyellows virus (BPYV) is transmitted in the semi-persistent manner
by the greenhouse whitefly (Trialeurodes
vaporariorum) and infects melon crops in glasshouses (Cucumis
melo var. reticulatus) and in open fields for the cultivation
of winter melon (Cucumismelo
var. inodorus). The host range of BPYV includes several crop
species such as beet (Beta
vulgaris), lettuce (Lactuca
sativa), endive (Cichorium
endiva), shepherd's purse (Capsella
bursa-pastoris), cucumber (Cucumis
sativus), dandelion (Taraxacum
officinale), and poison hemlock (Conium
maculatum). 1st reported in beet from Salinas, CA, in 1965,
BPYV is spreading in Australia (Tasmania), France, Japan, the Netherlands,
USA (California), and more recently reported from Italy, Crete, and possibly
Spain. BPYV was discovered in 1965 in California and was the 1st crinivirus
reported in the literature. It is transmitted by the greenhouse whitefly
(GHWF) (taxonomically, Trialeurodes vaporariorum [Tv]), which has
since been identified in production greenhouses throughout the world. The
only known vector is the GHWF, which is often a chronic problem. BPYV has
an exceptionally large natural host range among crop and weed species,
infecting plants in at least 12 different taxonomic families, particularly
for BPYV and to a lesser degree, for Tomato
infectious chlorosis virus (TICV) and Tomato
chlorosis virus (ToCV). Typical BPYV symptoms vary among hosts, expressing
severe yellowing, reduced fruit size and possibly early senescence in cucumber
and pumpkin. Greenhouse-grown cucumbers and melons are often infected with
BPYV, which is facilitated by the accumulation of GHWF in closed environments.
Some nurseries employ virus indexing programs and methods for eradicating
viruses through tissue culture techniques. Application of these methods
to GHWF-transmitted criniviruses, coupled with effective vector control,
will reduce spread of these viruses as well as limit damage to susceptible
crops both in greenhouse and field environments. There is little information
on the availability of resistance to GHWF-transmitted criniviruses in any
of the predominantly affected crops. Although a source of BPYV resistance
has been identified in melon, this source has not been advanced into commercial
cultivars. Ongoing research is examining wild tomato germplasm for sources
of resistance to TICV, but no sources of resistance have been identified
to date. Currently, the most effective method for control of criniviruses
is an effective insecticide-based control program. Imidocloprid-based products
are most frequently used for whitefly control, and can be applied as a
foliar spray, a seed treatment or through drip application. While insecticides
effectively reduce whitefly populations, they are inefficient for control
of viruses, since whiteflies can transmit a virus before being killed by
an insecticide. Most GHWF-transmitted criniviruses do not produce symptoms
until 3 to 4 weeks after infection occurs, by which time it may be too
late for implementation of control measuresref1,
ref2,
ref3.
=> tristeza, known as "quick decline" in the USA, is
the most destructive disease of citrus in the western hemisphere and is
worldwide in distribution, causing death and decline of trees on sour orange
rootstocks and a debilitating stem-pitting disease in limes, grapefruit,
and sweet oranges. It affects trees on all rootstocks and reduces yield.
About 25 million trees on sour orange are at risk from CTV decline. Affected
trees may suffer from quick decline, which leads to wilting and death in
a few weeks. Other syndromes are seedling yellows and stem pitting
disease. Only trees on sour orange rootstock are affected by tristeza
decline. CTV causes an incompatibility at the bud union, resulting in girdling
of affected trees. The virus is spread in a persistent manner by Toxoptera
citricida (brown citrus aphid (BrCA)) and Aphis
gossypii (cotton or melon aphid), and Aphis
spiraecola (=citricola, green cotton aphid). Species composition
and seasonal occurrence vary in different countries and regions. T.
citricidus is not found in the Mediterranean area or North America,
while A. spiraecola invaded the Mediterranean region in the 1960s
and has become a serious citrus pest there. T. aurantii is not a
major species, although it is abundant on tea in Japan (Komazaki et al.
1985). The most efficient vector is Toxoptera citricidus. This Old
World species has been in South America for some years and reached Central
America in 1989 and has been spreading through Central America and the
Caribbean since then. Most CTV isolates can be detected by grafting to
plants of Mexican lime (Citrus
aurantifolia), or by ELISA. The monoclonal antibody MCA-13 detects
most CTV strains that affect tops on sour orange rootstocks. Disease management
utilizes certified bud-stock and resistant rootstocks, production of virus-free
trees by shoot-tip grafting or heat treatment, production of trees in areas
known to be free of CTV, inoculation of bud-stock trees with mild CTV strains,
and occasional applications of chemical insecticides to reduce aphid populationsref1,
ref2,
ref3,
ref4,
ref5,
ref6,
ref7,
ref8,
ref9.
Disease management involves removal of declining trees on sour orange and
replacement with trees budded on a tolerant rootstock is recommended when
a tree is no longer economically viable; suppression and eradication of
severe, stem-pitting CTV strains. Other measures include implementation
of mild strain cross-protection; and introduction of virus resistance into
desirable citrus varieties. Immunity to CTV present in Poncirus trifoliata
has been transferred into sweet orange type plants suitable for use as
breeding parents by conventional plant breeding techniques. Symptom
expression in citrus hosts is extremely variable and depends on the environment,
the host and the virus isolate. Mandarins in general are tolerant to CTV
and rarely show any symptoms. Sweet orange, sour orange, rough lemon and
Rangpur lime are normally symptomless but will react to some severe CTV
isolates. Limes, grapefruit, some pummelos,
Citrus
macrophylla, and some citrus hybrids will react to CTV infection.
Symptoms of CTV infection can include total tree collapse, stunting, stem
pitting, leaf cupping, vein clearing, chlorosis and reduced fruit size.
Budwood testing negative for CTV is important in preventing primary infections
of tristeza in CTV-free areas as well as the introduction of new perhaps
more severe isolates in areas where the disease is already present. Detection
and disease eradication or suppression has been effective in areas where
low levels of infection prevail. Where orchards planted with sweet orange
on sour orange rootstocks are declining, they should be replanted using
CTV-tolerant rootstocks such as rough lemon, Rangpur lime, trifoliate orange,
trifoliate orange hybrids of mandarins. Use of mild strain cross-protection
may be a viable option for control.
CTV infects almost all citrus species, hybrids, and relatives. Consequently
there are many strains of the virus that contribute to the diversity of
symptoms associated with CTV infection. Mild CTV strains are basically
asymptomatic in their hosts. Severe CTV strains express a range of symptoms
including one or more of the following: seedling yellows; root stock decline
on sour orange; grapefruit stem-pitting; and sweet orange stem-pitting.
CTV-D strains cause death of the phloem at the bud union, which produces
a girdling effect that can result in overgrowth of the scion at the bud
union, paucity of feeder roots, stunting, leaf yellowing, reduced fruit
size, poor growth, die-back, wilting, and death. Trees affected by decline
on sour orange rootstock may also exhibit pinholing or honeycombing on
the inner face of the bark, or brown discoloration at the bud union. Trees
on sour orange exhibiting decline are routinely removed and replaced. Tolerant
rootstocks include Carrizo citrange, Cleopatra mandarin, and Swingle citrumelo.
Other virulent and damaging CTV strains cause stem-pitting (deep pits in
the wood under depressed areas of bark) in scion cultivars and induce stunting
and reduced production. Twigs on infected trees are brittle and break easily
when intentionally bent or blown off by wind under fruit load. Stem-pitting
may not be apparent until the bark is peeled from twigs. Rope-like external
symptoms can also be caused by stem-pitting strains in grapefruit tree
trunks and/or sweet orange scions. Stem-pitting of scions caused by CTV
results in decline but does not usually cause tree death. The economic
impact of these strains results from reductions in tree size and vigor,
and reduction in fruit set, size, and quality. Stem-pitting is especially
severe in limes and grapefruit, but can affect some sweet oranges. Mandarins
are commonly tolerant, but some hybrids are affected. These CTV strains
commonly occur in Asia, Australia, Southern Africa, Brazil, Columbia, Venezuela,
and other areas. Host resistance is probably the single most attractive
approach to control of virus diseases in long-lived horticultural crops
such as citrus, where short-term measures do not give any benefit. However,
development of new citrus cultivars is difficult because the citrus breeding
cycle is usually 8-10 years. Moreover, most citrus cultivars are highly
heterozygous, and the chances of combining virus resistance with all other
essential horticultural features are low. Genetic engineering offers a
means of incorporating virus resistance into existing desirable cultivars.
Introduction of viral genes into plant genomes to confer resistance is
well established in some systems, e.g. use of CTV coat protein to mediate
cross-protection. Transformation and resistance can be demonstrated in
a relatively short period, but the evaluation of transformed plants for
fruit production is a long-term process. Mild strain cross-protection has
been used successfully in several locations to reduce losses from CTV stem
pitting, but has failed in others. It is difficult to find isolates that
are both mild and protective and then show that these are not harmful to
other cultivars or crops. This has limited the wider application of mild
strain cross-protection. Our inability to predict or control all potential
hazards has also precluded the preventative use of cross-protection. Shoot-tip
grafting, a technique based on the fact that apical meristems contains
little or no virus, has been used successfully to produce virus-free citrus
plants. It is a powerful tool to free existing cultivars of virus
infection. Continued improvement in indexing procedures also makes verification
of virus freedom much easier, and augments other regulatory approaches
to control. Even once a virus is well established, selective certification
or
regulation to curtail movement of the more severe isolates can be an
effective component of management. Suppression of inoculum sources is also
useful in some situationsref1,
ref2,
ref3
cucurbit
yellow stunting disorder virus (CYSDV) is a virus endemic in Portugal
and transmitted by the whitefly Bemisia
tabaci and will spread internally in any area where the virus is
introduced on vegetatively-propagated plants. It is on the EPPO A2 action
list. At present, CYSDV has been detected and causes problems in France,
Spain, Portugal, Morocco, Cyprus, the Arab Emirates and North America.
In Spain, the yellowing symptoms caused by CYSDV are frequently observed
in 100% of the plants when they are found in an affected greenhouse or
screenhouseref1,
ref2
sweet
potato chlorotic stunt virus (SPCSV) is whitefly-transmitted and in
double infections with SPFMV
cause sweet potato virus disease (SPVD), a serious sweet
potato (Ipomoea batatas) disease in Africa. During the past
decade, sweet potato plants showing symptoms similar to SPVD have been
observed in most areas of Spain. SPVD is considered the most damaging virus
disease of sweet potato in Africa and may be the most serious disease in
the crop worldwide. SPCSV has been reported only from Africa (Nigeria,
Uganda, Kenya, Zaire), Asia (Taiwan, China, Indonesia, Philippines), America
(USA, Brazil, Argentina, Peru) and Israel. The fact that both viruses are
present in Spain indicates that SPVD can be expected to spread in the country.
Virus research at the International Potato Center in Peru is focused on
SPVD because of its debilitating effect on resource-poor farms, especially
in sub-Saharan Africa. Unfortunately, SPFMV-resistant cultivars originating
from CIP were found to be susceptible to SPVD. Identification of genes
for resistance to both SPCSV and SPFMV is a high priority. In China, using
healthy planting materials resulted in yields that were 2-3 times greater
than SPVD-infected plants. Similar results were obtained in African trialsref1,
ref2,
ref3
tomato
chlorosis virus (ToCV) is transmitted by several insect vectors, including
the greenhouse whitefly Trialeurodes
vaporariorum, the banded-wing whitefly (Trialeurodes
abutilonea), and by Bemisia
tabaci (biotype A) and Bemisia
argentifolii (biotype B). The virus is a nasty pest, especially
in glasshouse operations. Although it can cause severe crop losses in fresh
market and glasshouse-produced tomatoes, damage is generally minor. It
also infects several other food crops such as lettuce
(Lactuca sativa and potato
(Solanum tuberosum). The fact that ToCV and TICV
induce identical symptoms in tomato requires careful diagnosis to distinguish
between the 2 viruses. Disease management depends upon use of virus-free
transplants, control of susceptible weed species, roguing of infected plants,
and control of insects by chemical insecticidesref1,
ref2.
1st reported during the 1990s in the United States, ToCV has been reported
to occur in the Mediterranean countries, Portugal, Spain, and Italy. Fruit
size and number appear reduced by ToCV infection. Disease management involves
raising and maintaining Bt-free tomato transplants. To prevent entry of
the various vectors into production sites, greenhouses and screenhouses
have to be constantly monitored for the presence of vectors. Use of approved
chemical insecticides can reduce disease incidence. Florida producers can
obtain recommended information from the latest Insect Management Guideref1,
ref2,
ref3,
ref4,
ref5,
ref6,
ref7,
ref8.
bean yellow disorder
virus (BnYDV) was first reported in the autumn of 2003 in French bean
(Phaseolus vulgaris) grown commercially in Spain. Symptoms resembling
nutritional disorders consisted of interveinal mottling and yellowing in
leaves, combined with stiffness or brittleness, were produced on the middle
to lower parts of affected plants. Similar plants infested with whiteflies
(Bemisia
tabaci) were observed in greenhouses. Reproducible symptoms were
observed when the virus was transmitted from bean to bean by Bt (9/10)
but not by mechanical inoculation (0/30)
=> little cherry disease (LChD) occurs in Canada, Germany, Belgium,
UK, the Netherlands and Switzerland, but their relation to the disease
in USA is not known. It has not been reported from Spain, Italy or France,
suggesting a tendency to be confined to northern regions. In USA LChV-1
occurs in both eastern and western cherry-producing areas. Of particular
interest is that ornamental flowering cherries are symptomless carriers
of LChV-1. Symptoms on sensitive cultivars include discolored fruit that
remain small, pointed in shape, and tastelessref1,
ref2.
bean
pod mottle virus (BPMV) causes significant crop losses in soybean.
It is spread primarily by the bean leaf beetle Cerotoma
trifurcata (bean leaf beetle), Colaspis
brunnea (grape colaspis), Diabrotica
balteata, and southern corn root worm (D.
undecimpunctata). BPMV is stable, easily transmitted mechanically
and occurs at relatively high levels in seed coats from seeds of infected
soybean. Yields from infected plants are lowered by 10-40%, grain quality
is reduced both in oil and protein, seed germination is lower and delayed
maturation results in a condition known as 'green stem.' The fact that
BPMV has been reported in Iran is interesting, suggesting that infected
seed may have been used for planting. This report may be the 1st finding
of BPMV outside of North Americaref1,
ref2,
ref3,
ref4.
BPMV was 1st reported in Phaseolus
vulgaris cv. Tendergreen; from Charleston, USA; by Zaumeyer and
Thomas in 1948. It causes significant crop losses in soybean. It is spread
primarily by the bean leaf beetle Cerotoma trifurcata (bean leaf
beetle), Colaspis brunnea (grape colaspis), Diabrotica balteata,
and southern corn root worm (D. undecimpunctata). BPMV is stable,
easily transmitted mechanically and occurs at relatively high levels in
seed coats from seeds of infected soybean. Yields from infected plants
are lowered by 10-40%, grain quality is reduced both in oil and protein,
seed germination is lower, and delayed maturation results in a condition
known
as "green stem." It can also be transmitted by mechanical inoculation,
by grafting, but is not transmitted by seed or by pollen. BPMV spreads
in the North American region. The fact that BPMV has been reported in Iran
is interesting, suggesting that infected seed may have been used for planting.
BPMV undoubtedly entered Iran in virus-infected seed. Growers should consider
a later planting of soybean, especially if BPMV was a yield limiting factor
in 2004. Late planting can result in an increased risk of soybean aphid
activity at a sensitive growth stage. Plant soybean varieties with the
ability to yield in the presence of BPMV. Use good quality seed that is
not mottled, and consider the field history of this problem before making
decisions as to whether to spray for the bean leaf beetle. Sprays must
be carefully timed to be effective. Partial resistance to BPMV exists in
soybean varieties. Partial resistance is expressed as acceptable yield,
low seed mottling and a low incidence of green stem in the presence of
BPMV. Soybean varieties differ in yield and incidence of mottled soybean
seed in the presence of BPMV. Early soybean planting can coincide with
high populations of over-wintered bean leaf beetle adults moving into soybeans
to feed and lay eggs. This timing increases the chance of BPMV transmission
to soybeansref1,
ref2,
ref3,
ref4,
ref5.
radish mosaic virus (RaMV) occurs naturally only in cruciferous
plants (e.g. cauliflower (Brassica oleracea) and turnip (Brassica
rapa)) but can be detected following inoculation in some non-cruciferous
species (necrotic local lesions on Chenopodium amaranticolor, chlorotic
ring spot on Nicotiana tabacum cv. Samsun, and chlorotic local lesions
followed by systemic mosaic on Brassica rapa). It is transmitted
by several beetle species (Phyllotreta, Epitrix hirtipennis,
and Diabrotica undecimpunctata; Coleoptera). It is also transmitted
by mechanical inoculation and by grafting, but, it is not transmitted by
seed. RaMV occurs in Austria, Germany, Hungary, Italy, Iran, Japan, Morocco,
the USA, the former USSR, and the former Yugoslavia. RaMV is common in
turnip crops in Yugoslavia. Disease management is mainly by application
of chemical insecticidesref
=> mild systemic mottling and leaf malformation in Cucumis
quinoa and Nicotiana
tabacum and systemic chlorosis in Cucumis
sativus, andVitis
vinifera. GFLV causes a degenerative disease that is considered
to be the most serious grapevine virus disease. Affected vines are smaller
than healthy vines, and they show progressive decline. Fruit quality is
poor and yield losses range up to 80%. Moreover, the productive life of
vineyards are shortened and winter hardiness is decreased. GVLF is transmitted
by the nematodes Xiphinema index and X. italiae. Natural
hosts are Vitis vinifera, V. rupestris and many other
Vitis
spp. and interspecific hybrids. Symptom expression includes systemic
green or yellow mosaic, ring and line patterns and flecks, leaf and
nodal malformation. GFLV is probably distributed worldwide (in all areas
where Vitis vinifera and American hybrid rootstocks are grown)
=> leaf mottling and flecking, stunting and leaf deformation including
enations. Many infections are latent and plants are symptomless. Symptoms
vary greatly by variety, rootstock and environment conditions. Yield losses
of up to 50% may occur through reduced growth, dieback and severe fruit
drop. Long-distance spread occurs primarily by movement of infected propagative
material. ArMV virus is transmitted by the nematode Xiphinema diversicaudatum,
which is present in permanent pasture and woodland sites in Europe and
parts of the U.S., in scattered locations in Canada, and in Australia.
It also infects many other herbaceous and woody hosts such as raspberry,
strawberry, rhubarb, cherry, peach, and plums.
raspberry
ringspot virus (RpRSV) is transmitted by the nematodes Longidorus
elongatus and L.macrosoma. The virus is transmitted by mechanical
inoculation, by infected seed and by pollen to the seed. RpRSV spreads
in the Eurasian region and the Mediterranean region; Austria, Belgium,
Bulgaria, the former Czechoslovakia, Finland, France, Germany, Greece,
Hungary, Ireland, Luxembourg, the Netherlands, Norway, Poland, Spain, Switzerland,
Turkey, the UK, the USA, the former USSR, the former Yugoslavia. Found,
but with no evidence of spread, in Denmark. Control of this disease includes
pre-plant soil fumigation of vineyard sites to kill the dagger nematode
vector. If diseased vines are present in an established vineyard, all infected
vines will need to be identified and removed. The soil should then be tilled
for one growing season. Fumigate late-summer or autumn soil prior to replanting
with certified virus-tested clean stock. See MSU Extension Bulletin E-806
"Vineyard Preparation for Nematode and Virus Disease Control" and the Michigan
Fruit Management Guide, (Extension Bulletin E-154) for further recommendations
concerning control by soil fumigation
Of the many diseases caused by TRSV, bud blight of soybean is the most
severe and causes the greatest losses. Yields may be reduced by 25 to 100%.
TRSV is the type member of the nepovirus group of plant viruses and is
related to arabis mosaic virus, grapevine fanleaf virus, tomato black ring
virus, and tomato ringspot virus. Several strains of TRSV naturally infect
soybean. TRSV is easily sap-transmissible. Nymphs of Thrips tabaci
transmit it to soybean at a low level of efficiency. The dagger nematode
Xiphinema
americanum also is a vector, but its efficiency in transmitting the
virus to soybean is low. Nematode transmission of TRSV to plant roots may
be of no significance, because the infection generally remains confined
to the roots. Seed transmission is the most important mode of long-range
dissemination and carry-over from season to season. Disease management
involves planting a few soybean cultivars with resistance to a some TRSV
strains. One genotype (PI 407287) of the annual ancestor of soybean (Glycine
soja) is resistant to the virus. Other resistant USDA plant introductions
are 92713 and 154194. Virus-free soybean seeds should be used in
commercial fields, and it may be desirable to avoid fields infested with
dagger nematodes or treat them with an appropriate nematicide, if feasibleref.
=> chlorotic local lesions with systemic top necrosis in Chenopodium
amaranticolor, necrotic local lesions followed by systemic ring
pattern in Nicotiana
tabacum, and chlorotic lesions followed by chlorosis in Cucumis
sativus, andVitis
vinifera. Soil-inhabiting nematodes (Xiphinema
spp.)
acquire the virus during feeding on infected plants and transmit it to
roots of neighboring plants. Long-distance spread is by movement of virus-infected
seed
cherry
virus A (CVA) has been reported in sweet cherry in Germany, Poland,
Canada, and Great Britain. CVA has been detected in leaf and bark material
taken from 15 of 16 sweet cherry trees as well as from apricot and peach.
No data are available on the impact of CVA on fruit yield from sweet cherry
orchards, but it appears to be ubiquitous in the UK. CVA is graft-transmissible,
may also be seed-transmitted, and is widely distributed in sweet cherry
trees in Germany and Canada. CVA may not cause disease in cherry trees,
but it may be a synergist necessary for disease development.
Vector transmission of CPMMV by Bemisia
tabaci appears to be due to virus contamination of the stylet and/or
the foregut following feeding on infected plants. High densities of Bt
would likely increase the rate of transmission. CPMMV is also transmitted
mechanically, and some isolates are transmitted by seed. The virus has
been reported from Asia, Africa, Brazil, and Oceania but is not reported
from EU countries to date. It appears to be unrelated to known members
of the Carlavirus genus. It primarily infects tropical field crops. Its
quarantine pest status in EU countries is very minor, if not doubtfulref.
garlic
common latent virus is of minor significance, but combined with other
viruses can cause severe disease in Europe, South and Central America,
India and China
Foveavirus
cherry
green ring mottle virus (CGRMV) (a.k.a. sour cherry green ring mottle
virus and cherry green ring mottle foveavirus). Usually CGRMV disease remains
latent on sweet cherry and peach, sour cherry and ornamental _Prunus_ species.
It develops leaf yellowing and dark mottles around secondary veins in early
June in the United States. Fruits are often necrotized. On P. serrulata
(Japanese cherry) the disease is very severe with twisting and atrophy
of the youngest leaves. In early summer the bark cracks and the young tips
die. About 5% of cherry and peach cultivars are contaminated with latent
CGRMV. It seems to be evenly distributed in the plant and not epidemic.
Indexing on P. serrulata and recently developed PCR tests are used
for detection of the virus. In Europe, research has established that CGRMV-infected
trees in the Campania region of Italy can also be infected with Apple chlorotic
leaf spot leaf spot virus (ACLSV). At times indicator trees showed irregular
ringspots and a marked clearing of the principal veins. To evaluate the
possible presence of other viral agents, DsRNAs purified from the infected
GF305 indicator trees were used as templates in a polyvalent PCR
detection assay. Besides ACLSV, PCR products corresponding to 2 additional
viral agents could be amplified and sequenced. One of the agents appeared
to be a new Trichovirus, while the other appears to be a Foveavirus closely
related to Cherry green ring mottle virus (CGRMV). A new molecular technique
to detect these 2 cherry flexiviruses in _Prunus_ spp has been developed.
It is sensitive and reliable, and can detect both viruses simultaneously.
The method is more cost-efficient, takes up less space, and is completed
in 2 days instead of 4 monthsref1,
ref2,
ref3,
ref4
Vitivirus are a genus of viruses associated with the rugose wood disease
complex. All are transmitted by mechanical inoculation, those infecting
grapevine with greater difficulty. Transmission is by grafting, and dispersal
through propagating material is common with grapevine-infecting species.
Detection technologies include grafting to indicator hosts, serology (primarily
ELISA) and PCR. Disease management depends upon use of certified healthy
stock or known to be virus-free. Trees should not be planted in soils where
viruses have been found previously. Trees exhibiting suspicious symptoms
should be removedref1,
ref2,
ref3,
ref4,
ref5.
grapevine
virus A (GVA) is associated with Kober Stem Grooving and affected vines
may show swelling at the graft union and fail to thrive. Ungrafted vines
may be infected, but usually do not show symptoms. GVA has also been associated
with
grapevine leafroll-associated
virus
grapevine
virus B (GVB) is transmitted in a semi-persistent manner by different
species of pseudococcid mealybugs in the genera Pseudococcus and
Planococcus.
GVB is widely distributed. Vitviruses are presently linked with rugose
wood disorders, and some progress has been made in the understanding of
their basic genome structure. Full-length infectious molecular clones of
GVA and GVB from Italy have been used to inoculate grapevines in an attempt
to provide essential pathology
=> corky bark in grapevine. The disease affects only grafted
vines. The severity of corky bark is more pronounced in vines infected
with other rugose wood complex viruses. Corky bark causes an incompatibility
to develop at the graft union. Leaf symptoms resemble those of Leafroll
but are more severe. Leaves on cultivars such as "Pinot Noir" may develop
a yellow chlorosis before they turn red. The wood at the base of canes
may swell slightly, causing the bark to split. Depending on the cultivar,
various wood groovings also may occur.
Neither GVC nor GVD have been proven to cause disease in grapevine,
but their structure and genetic profiles have shown that they belong to
the Vitivirus genus.
soybean
dwarf virus (SbDV) causes widespread economic losses on soybean (Glycine
max (L.) Merr.) in Japan, and has been reported on soybean in Virginia,
in various legumes in the southeastern United States, and in peas in California.
SbDV is transmitted by an aphid (Acyrthosiphon (Aulacorthum)
solani
(some isolates also by Acyrthosiphon pisum) in a persistent
manner. Both
aphid species are present throughout the USA and also worldwide. Common
names of Acyrthosiphon (Aulacorthum) solani are
pea aphid and green pea
louse. For Aulacorthum solani, the common name is the foxglove
aphid. SbDV has been reported from Australia, Japan, New Zealand, and the
USA (California). The 1st natural appearance of SbDV was in Blacksburg,
Virginia in 1999. SbDV is serologically related to beet western yellows,
barley yellow dwarf (strains RPV and MAV), bean leaf roll, potato leaf
roll, and tobacco necrotic dwarf viruses. A 50% incidence of field infection
may result in as much as 40% reduction in crop yield. Subterranean clover
red leaf virus is so closely related that it is often
considered to be the same species. Regarding the reproductive (R) stages
of soybean, there are 6 stages: R1, beginning bloom; R2, full bloom; R3,
beginning pod; R4, full pod; R5, beginning seed; and R6, full seedref.
Polerovirus
cucurbit
aphid-borne yellows virus (CABYV) has isometric particles of 25 nm
in diameter. The genome of CABYV consists of a single molecule of positive
sense ssRNA. CABYV was widely distributed with high frequency (nearly 50%
of samples tested) in these 4 cucurbit species in the major growing areas
of Iran. This conclusion is based on an extensive survey by ELISA
throughout Iran conducted during 2001 to 2004. CABYV was first reported
in France in 1992 (Lecoq et al. 1992). So far, it has been recorded in
other European countries (including Greece, Spain and Cyprus) and African
countries (including Tunisia, Morocco, Sudan, and Zambia) and in the USA
(California). Typical symptoms of CABYV on cucurbits include yellowing
and thickening of old leaves. The major veins of these leaves remain green.
These symptoms can be masked by mixed infection with other cucurbit viruses,
and this was noted in the current study. Yield reduction in infected cucumber
crops can reach about 50%. Major vegetable species susceptible to CABYV
include watermelon, muskmelon, cucumber, zucchini squash and lettuce (Lactuca
sativa). CABYV can be transmitted persistently by the aphid Aphis
gossypii with great efficiency and also by the aphid Myzus
persicae. CABYV is not transmitted mechanically. The source of
the virus is unknown, possibly wild cucurbits. Resistant curcubit cultivars
are not available, but sources of resistance to CABYV have been identified
in melon accessionsref1,
ref2,
ref3,
ref4,
ref5.
So far, it has been recorded in a few African countries that include Morocco,
Sudan, and Zambia (Lecoq, personal communication). Typical symptoms of
CABYV on cucurbits include yellowing and thickening of old leaves. Yield
reduction in infected cucumber crops can reach about 50% (Lecoq et al.
1992). It has a narrow host range. Major vegetable species susceptible
to CABYV include watermelon (Citrullus
lanatus), muskmelon (Cucumis melo), cucumber (C. sativus),
zucchini
squash (Cucurbita pepo), and lettuce
(Lactuca sativa). CABYV is not transmitted mechanically. According
to Abou-Jawdah and colleagues at American University, Beirut and INRA,
France, viral diseases are the major cause of economic losses in commercial
cucurbit production in Lebanon. A survey revealed that Zucchini
yellow mosaic potyvirus (ZYMV) and CABYV are the most common viruses
of field-grown cucurbits in Lebanon. Other viruses involved were watermelon
mosaic virus (WMV), papaya
ringspot virus-watermelon strain (PRSV-W) and cucumber
mosaic cucumovirus (CMV). Inoculation of squash with a mild strain
of ZYMV (strain WK) gave significant protection against severe virus symptoms
and resulted in significant yield increase as compared to the control,
as did silver plastic mulch. The best protection and highest total yield
were obtained with floating row covers (flexible nets or other types of
screens). Integration of cross-protection with silver mulch or floating
row covers improved the protection obtained with either approach. Cross-protection
is still a useful disease management option for reducing yield loss and
maintaining reasonable quality of product. Resistant curcubit cultivars
are not available, but sources of resistance to CABYV have been identified
in melon accessionsref1,
ref2,
ref3.
Resistance towards CABYV in Sudanese melons was only detected in the wild
agrestis melons. Among different melon genetic resources collected from
different parts of the world and evaluated for resistance against CABYV,
the Sudanese Humaid accession T-EK 92-2 was found segregating for resistance
(Dogimont et al. 1996). Further, the wild melon (Humaid) line HSD 2445-005
was found to be homogenously resistant, while the Humaid accession HSD
2441 was also found segregating for CABYV resistance. Yield reduction in
infected cucumber crops can reach 50%. According to Abou-Jawdah and colleagues
at American University, Beirut and INRA, France, viral diseases are the
major cause of economic losses in commercial cucurbit production in Lebanon.
pepino
mosaic virus (PepMV) was originally described from pepino (Solanum
muricatum) in Peru (found in 2 tomato
(Lycopersicon esculentum) crops in 1974 and then no longer observed)
it was identified in 1999 as the causal agent of a severe tomato disease
in commercial greenhouses in the Netherlands and has been reported as a
serious problem in greenhouse tomatoes throughout Europe (Bulgaria, Hungary,
Germany, UK, Belgium, France, and Spain), Canada, and the USA . The prevailing
assumption is that PepMV was brought to Europe from South America by unknown
means. In most of these countries it is under control or has been eradicated.
Unfortunately, pepino mosaic is present in outdoor tomato production areas
in Spain, where it causes serious crop loss in localized areas. Results
of studies (symptoms on plant indicator hosts and % homology in a 547-bp
PCR fragment derived from the RNA-dependent RNA polymerase gene) all of
15 PepMV isolates from countries within Europe and elsewhere are considered
members of the same strain, designated as the tomato strain of PepMV. Moreover,
the high similarity between the various isolates suggests that the outbreaks
in Europe likely originated from a common locus. Pepino mosaic is difficult
to manage as it is a very contagious disease that spreads easily by use
of contaminated tools, shoes, clothing, hands, and plant-to-plant contact.
Moreover, movement of workers can spread the virus by brushing against
infected plants. While a high density of bumblebees has been associated
with PepMV spread in a crop, the risk of spreading the virus via hand pollination
may be greater. PepMV can be transmitted by grafting or pinching suckers
from mother plants. Virus can be spread over long distances by transportation
of infected tomato fruits or contaminated seeds. Very strict phytosanitary
procedures (use of virus-free seed and transplants, sterilization of equipment
and facilities, and disinfection of circulated irrigation water) are required
to maintain healthy plants, especially in glasshouse operations. Also infects
tomato seeds, vegetables in Chile, Sweden, UK, Netherlands, France, and
Spain (detected in a shipment of tomato seeds originating from China).
PepMV is extremely contagious, and infectious virus is present on seed
surfaces, in seed pulp, and in wash water from infected seeds. Transmission
through seed is considered unlikely. As a precaution, tomato seed in commercial
production is treated with acid under controlled conditions to eradicate
any virions on the seed surface. According to the International Seed Health
Initiative for Vegetable Crop's Manual of Seed Health Testing Methods Detection,
testing for PepMV on seeds is a 2-stage process: an ELISA, and, a bioassay,
in that order. During drying, storage, and, with disinfection treatments,
the majority of seed-borne PepMV virions degrade and lose infectivity.
Both infectious and non-infectious virus particles are detected in ELISA.
Hence, a negative (but not a positive) ELISA result is conclusive on the
seed health status of the seed lot. In the bioassay, only infectious PepMV
is detected. Hence, both a negative and a positive bioassay result are
conclusive on the seed health status of the lotref1,
ref2,
ref3,
ref4.
PepMV has been detected for the 1st time in Ecuador in wild populations
of Lycopersicon pimpinellifolium along the Pacific coast of the
South American continent in 2005. Potexviruses are extremely infectious
but they are not known to be naturally spread by vectors. PepMV is easily
spread via contact with infected plants. PepMV has been detected in the
potato cultivar 'Yungay' growing in the Andes in Peru. Moreover, 14% of
tested accessions in the potato germplasm at the International Potato Center
in Peru are infected with PepMV. More research is required to determine
the risks of PepMV infection in potato. Spread from tomato to potato may
be possible under field conditions in southern Europe. PepMV induced serious
losses in tomato fruit quality in trials at Efford in the UK in 2003. In
the 'worst case' scenario, these losses could be in the order of GBP 37.5
million [USD 64.4 million] in the GBP 79 million [USD 135 million] UK industry,
assuming that the disease becomes endemic in all tomato fruit production
areas. In practice, losses may not be as great. Because the UK industry
is based almost exclusively on production of high-quality fruit, with virtually
no tomato processing industry, any losses of quality would be significant.
Any drop in quality could be catastrophic for producers. Contrary to experimental
results in the UK, numerous field and several experimental observations
in the Netherlands and a few other EU countries indicate that PepMV has
only a very minor or a non-significant economic impact on tomato production
on average. More damage might be expected if PepMV-affected plants are
also attacked by Verticillium sp. The economic impact due to PepMV
is also influenced by the marketing system in a country. In the UK, only
Class 1 fruit is profitable. This is not the case in several other EU Member
States where, as a consequence, the grower can still profitably sell fruit
of less than top quality.
barley
mild mosaic virus (BaMMV) are transmitted by the soil-inhabiting and
spore-forming bacillus Polymyxa
graminis. Both viruses occur on barley in Europe and Asia and are
economically important, soilborne pathogens of winter barley. Until recently,
laboratory diagnosis of these pathogens has relied upon ELISA using polyclonal
antiserum. Because of inherent virus particle instability, combined with
the inability to sap-transmit BaYMV, high quality antiserum has been difficult
to obtain and ELISA is often unsatisfactory. As an alternative approach,
2 TaqMan assays (1 BaYMV-specific and the other BaMMV-specific) have been
developed. These assays have been validated for 3 seasons, by testing samples
in parallel with ELISA. TaqMan assays are a more reliable detection method
than ELISA, especially with late-season and mixed infection samples. Both
fungi acquire the viruses following encystment on host roots, which then
germinate to form a pre-penetration swelling termed an adhesorium. The
protoplast is "injected" into the plant host cell by a bullet-like mechanism,
causing infection in the root. The protoplast then grows into a multinucleate
plasmodium which eventually converts into a sporangium to release further
zoospores. As an alternative, the multinucleate plasmodium can convert
into numerous thick-walled resting spores which are released when the host
cells decay and can survive as an inoculum pool for many years in soilref1,
ref2,
ref3,
ref4,
ref5,
ref6
Ipomovirus
beet
virus Q : Polymyxa betae (Pb) is thoroughly established in Iranian
soils. During a survey on soilborne viruses in sugarbeet, 2 viruses with
rod-shaped particles were isolated, in addition to beet necrotic yellow
vein furovirus (BNYVV). The Ahlum isolate proved to be serologically closely
related to beet soilborne virus (BSBV), which was 1st described in England
and has since been found in all sugarbeet growing areas worldwide. Recent
data revealed that the 2nd serotype (Wierthe) should be considered a distinct
virus species named Beet virus Q (BVQ). These 2 pomoviruses are also transmitted
by Pb. Although their contribution to rhizomania remains a matter of debate,
it is not uncommon to find them associated with rhizomania-infested fields.
Moreover, occurrence of 3 different viruses, transmitted by a similar vector,
within a single sugar beet raises questions regarding the epidemiology
of rhizomania syndrome. Virus particle of the Genus Pomovirus are morphologically
similar to other rod-shaped viruses, i.e. in the genera Furovirus, Pecluvirus,
Hordeivirus, Tobravirus, Tobamovirus and Benyvirus. The derived amino acid
sequences for the putative RNA 1-encoded proteins also suggest relatively
close relationships to the genera Furovirus, Pecluvirus, Hordeivirus and
somewhat more distant ones to the genus Tobamovirus. Affinities not only
to genera Pecluvirus, Hordeivirus and Benyvirus, but also to genera Potexvirus
and Carlavirus, are suggested by the derived amino acid sequences of their
triple gene block-encoded proteins. The folding properties of the 5-UTRs
of their genomic RNAs suggest affinities to the genus Tymovirus, those
of the 3'-UTRs to genera Tymovirus, Tobamovirus and Hordeivirus. BVQ was
isolated together with BNYVV from a sugarbeet tap root obtained from a
rhizomania field near Braunschweig, Germany. Like BNYVV, it causes local
lesions on C. quinoa, but those of BVQ appear about 5 days earlier
after mechanical inoculation. They both have a more irregular shape with
a tendency to spread along the veins. Systemic infections of C. quinoa
were not observed. BVQ and BNYVV were separated from originally mixed infections
by single lesion transfers. BVQ could not be transmitted to Nicotiana
benthamiana or Nicotiana clevelandii, nor could it be re-transmitted
by mechanical means to sugarbeet leaves or roots. It is possible that this
isolate can be transmitted only by a soilborne vector, or it may have lost
its infectivity for beets after several years of cultivation on C. quinoa.
BVQ proved to be extremely difficult to purify; nevertheless, an antiserum
was obtained with a partially purified virus preparation which, despite
some additional reactivity with constituents of healthy C. quinoa,
could be used in immunocapture RT-PCR, immunosorbent electron microscopy
(IEM) and the immunoelectron microscopical decoration test. BVQ has been
repeatedly observed by IEM repeatedly during the past decade in sugarbeet
samples from various areas in Germany and abroad, indicating that it is
widely spread. The most frequently detected virus was BSBV, followed by
BVQ and then BNYVV. In no case was BVQ found alone. BVQ has been found
in Bulgaria, Belgium, France, Germany, Hungary, Italy, and the Netherlands,
but not from Turkey. From an epidemiological point of view, although the
role of BNYVV in rhizomania syndrome is well established, there is controversy
regarding the role of Pb in seedling growth and in severe stunting of sugar
beet, and still others reject the notion that Pb has any effect on sugar
beet growth. The controversy is emphasized by the study of 2 other viruses,
which were possibly undetected in the Pb used in previous studies. Our
study confirms the ubiquitous presence of BSBV in sugar beet fields. It
was present in > 80% of the analyzed samples, with a frequency much higher
than that observed for BNYVV. The limited number of samples tested does
not preclude further detection possibilities on different sugar beet cultivars
or on different species. In all cases, BNYVV occurred with BSBV and often
with BVQ as well. It would be very interesting to check a possible interaction
of pomoviruses with BNYVVref1,
ref2,
ref3
cassava
brown streak virus (CBSV) : 1st reported in cassava
(Manihot esculenta), by Storey from East Africa in 1936. A devastating
virus that causes cassava brown streak disease (CBSD), it is gaining
in severity, threatening food and livelihood securities for millions of
farmers and cassava consumers in Sub-Saharan Africa. CBSD is considered
the most important disease of cassava disease in coastal lowlands of Eastern
and Southern Africa, and, is also found along the shores of Lake Malawi
in Malawi and Tanzaniaref1,
ref2,
ref3.
In Tanzania, the rate of infection of CBSD ranges up from 2 - 83%, depending
on cultivar and location. The peak period of disease spread occurs in cassava
planted in April and May, and this correlates very well with peak populations
of whiteflies (primarily Bemisia
tabaci), confirming that it is indeed the vector. A recently developed
RT-PCR assay can detect CBSV in symptomless germplasm and planting material
with good success. Research efforts are being directed to increase the
availability and utilization of improved cassava varieties, and to strengthen
the national germplasm generation and deployment capacities in Kenya, Tanzania,
and Mozambique. Interspecific crosses between domesticated cassava and
the wild Manihot melanobasis at the Amani research station in Tanzania
have resulted in good levels of resistance to CBSV. Local tolerant cultivars
in southern Tanzania and Mozambique are also of use in disease managementref1,
ref2,
ref3.
bean
common mosaic virus (BCMV) infects Phaseolus
vulgaris crops in many regions of the world. It is transmitted
in a non-persistent manner by aphids and is also readily seed-transmitted.
The disease it causes decreases crop production. In Australia, BCMV has
been reported in New South Wales, Queensland, Tasmania and Victoria, based
on serology and amino acid composition. BCMV almost certainly entered Western
Australia via infected seed. Its seedborne nature guarantees its spread,
and infected seedlings are sources of virus inoculum. Many BCMV strains
have been distinguished (Drijfhout et al., 1978). Those once grouped as
serotype A are now considered isolates of a separate potyvirus species
-- Bean
common necrosis virus -- and several viruses, once considered to be
distinct, have now been shown to be strains of this virus (McKern et al.,
1992). The latter include: azuki bean mosaic virus, blackeye cowpea mosaic
virus, cowpea (aphid-borne) mosaic virus, cowpea (blackeye) mosaic virus,
cowpea vein-banding mosaic virus, peanut blotch virus, peanut stripe virus
and some isolates from soybean. Genetic studies using F2 populations of
P.
vulgaris from crosses between differential cultivars of P. vulgaris
and novel isolates of BCMV and Bean common mosaic necrosis virus (BCMNV)
from Africa have revealed that there are previously undescribed resistance
genes in P. vulgaris. These genes are currently under investigation
using other novel isolates of BCMV and BCMNV. The primary aim of research
on the molecular genetics of legume viruses is for the genetic improvement
of Phaseolus vulgaris in Africa for resistance to viruses. Disease
management is basically planting of virus-free seedref1,
ref2,
ref3
=> cassava brown streak disease (CBSD) in cassava
(Manihot esculenta) no insect vector has been identified. As
is the case with cassava mosaic disease, the CBSD virus may be transmitted
by whiteflies -- a group at the University of Bristol (U.K.) has
reported transmission of the virus by whiteflies. CBSD infection causes
a dry necrotic rot in the storage roots, decimating yields, often leading
to complete spoilage or significant reductions in quality. Disease management
involves planting of stem cuttings from healthy plants without leaf chlorosis,
shoot tip die-back, cankers, fungus patches, or streaks on the stems. The
International Institute of Tropical Agriculture (IITA) has begun a major,
proactive emergency program to combat the disease and stabilize production
of this important food crop. Locally grown cassava cultivars with apparent
resistance -- or tolerance -- to CBSD have been identified in Tanzania
and Mozambique and are being evaluated. These less susceptible cultivars
have been made available to selected farmers in villages in Tanzania, and
in Mozambique for evaluation by National Agricultural Research Services
and the International Institute for Tropical Agriculture (IITA) programmes
to screen a wide range of cassava material for resistance to CBSDref1,
ref2,
ref3,
ref4,
ref5,
ref6.
chilli
veinal mottle virus (ChiVMV) : a aphid-transmitted potyvirus reported
in chili pepper (Capsicum chinense)ref
in Hainan Provinceref,
China from samples collected in 2003 and 2004ref.
ChiVMV is one of the most predominant viruses of peppers in Asia. Surveys
in 16 Asian countries have shown that 30% of pepper crops are affected
by this disease. Flower drop is normally severe following infection with
this virus and therefore crop loss can be heavy. Growing transplants in
insect-proof facilities, avoiding weeds and other solanaceous crops (e.g.
tomato), planting early to avoid aphid flights, and using mineral oil sprays
are methods used in attempts to manage the disease. Capsicum chinense,
the crop plant infected, remains the least understood of the domesticated
pepper taxa with respect to center of origin and its probable progenitor.
Fruit shape can vary from long and slender to short and obtuse. Fruit can
be extremely pungent and aromatic, with persistent pungency when eaten.
The best-known cultivars are the very hot Habanero peppers, such as Scotch
Bonnetref1,
ref2,
ref3,
ref4,
ref5
leek
yellow stripe virus causes severe disease in autumn and winter leek
crops in western Europe and is probably present in leek production areas
worldwide.
onion
yellow dwarf virus (OYDV) is transmitted by Myzus persicae and
other aphid species, or mechanically to onions and other crops such as
garlic, leek and some narcissus species. It is not spread by seed, but
infected bulbs (transplants and volunteers) always produce diseased plants
and serve as a source of contamination for following seasons, especially
when aphid populations are high. Disease management relies on use of disease-free
transplants and crop rotation out of onion production for at least 3 years.
Other disease management recommendations include isolation from other susceptible
crops or volunteer self-sown onions. Insecticides may suppress vector populations
but generally are not necessary or effectiveref
papaya
ringspot virus (PRSV) cucurbit isolate (W) and papaya isolate (P) infects
only hosts in the Cucurbitaceae (e.g. watermelon
(Citrullus lanatus) and bottlegourd (Lagenaria
siceraria)). PRSV-W is transmitted by aphids in a non-persistent
manner, following acquisition of virus particles from a host reservoir,
and are capable of transmitting it for 10-15 minutes in most cases. PRSV-W
has been reported from Hawaii, Taiwan, Brazil, Thailand, the Caribbean
islands and the Philippines. It is the major limiting factor in production
of the crop. Disease management includes (1) the application of quarantine
measures (prevention of the introduction of infected plants into a clean
area; (2) preventing movement of papaya plants from areas known to be infected
with the virus; (3) roguing of infected plants; and (4) use of tolerant
and resistant cultivars which do not produce severe symptomsref1,
ref2,
ref3,
ref4
Pennisetum
mosaic virus (PenMV) isolated from a perennial grass (Pennisetum
centrasiaticum) : maize from only 1 region (Shanxi Province in northern
China) has been found to be infected and the symptoms it caused, especially
on sorghum, were significantly milder when compared to those of SCMV. Because
it is a potyvirus, PenMV can be expected to spread via several aphid species,
and seed transmission should be examined in maize and perhaps other species
such as Panicum, Eleusine, and Setaria. Sequence comparisons
and phylogenetic analysis showed 3 distinct groups of Chinese SCMV sequences
(sugarcane isolates from Zhejiang province, a maize isolate from Guangdong
and maize isolates from other provinces). It will be interesting to know
more about the genomic relationships between PenMV and other maize-infecting
potyviruses such as Maize dwarf mosaic, Johnsongrass mosaic, Sugarcane
mosaic, and Sorghum mosaic.
plum
pox virus (PPV) infects apricot, plum and peach trees. Plum pox
is the most devastating viral disease worldwide of stone fruit including
peaches, apricots, plums, nectarines, almonds, and sweet and tart cherriesref1,
ref2.
The disease significantly limits stone fruit production in areas where
it is established. > 100 million stone fruit trees in Europe are infected.
The virus can infect many wild species. It is transmitted by aphids and
therefore extremely difficult to control. The Slavic name for plum pox,
Sharka,
is the most commonly used name for the disease around the world. PPV has
been known in Europe since the beginning of the 20th century. First described
on plums in Bulgaria in 1915, plum pox has spread to a large part of Europe,
the Mediterranean, the Middle East (Egypt and Syria), India, and Chile.
Since 1950, spread became more rapid, and in 1999 it reached Canada and
the USA. An estimated 100 million trees are infected in Europe. Symptoms
depend on the cultivar, the age of the plant and the nutrient status. On
leaves, light green discolorations and yellow or light green rings may
appear. Fruits develop pigmented rings or line patterns and are often deformed.
For plums, premature fruit fall is abundant. Trees can remain without symptoms
for up to 3 years after infection. At least 4 major strains of the virus
are known, named PPV-D, PPV-M, PPV-C and PPV-EA, differing in symptom severity
and patterns of spread. All strains are considered to be worldwide quarantine
organisms, and fast eradication of infected trees is the most important
instrument to manage the disease. In this report, PPV-D is the strain detected
from samples collected from a single grove in November 2004 in Argentina.
PPV was found in 1992 in neighboring Chile but is now eradicatedref.
In the fall of 1999, plum pox was detected for the 1st time in North America
in a Pennsylvania orchard, and has subsequently spread to several provinces
in Canada (Ontario in June 2000). 4 PPV groups have been described to date:
PPV-D in apricot trees from southeastern France, PPV-M in peach trees from
Greece, PPV-EA in apricot trees from El Amar, Egypt, and PPV-C in sour
cherry trees from Moldova. PPV-M isolates are more aggressive in peach,
are aphid-vectored more efficiently, and spread more rapidly in an orchard.
PPV-M has been reported to be seed-transmitted, while other PPV strains
are known not to be transmitted through seeds. Both PPV strains M
and D infest peach, plum, and apricot. The strain present in Pennsylvania
has been determined to be PPV-D. PPV-C infects sweet and tart cherry naturally
and has infected other Prunus hosts experimentally. To date,
no other PPV strains have been reported to infect cherry naturally.
Scientists use several techniques to distinguish PPV strains, monitoring
the behavior of host trees, ELISA and molecular tests such as PCR, and
sequencing of PCR products or cutting PCR products with enzymes at locations
in the DNA sequence that are unique to each strain. Control and prevention
measures for PPV include field surveys, use of certified nursery materials,
use of resistant plants (when available), aphid control, and elimination
of infected trees in nurseries and orchards. Sources of resistance exist
in Prunus but are not abundant. A team of scientists from
the USA and France has genetically engineered a PPV-resistant plum (otherwise
known as C5), and the resistance can be transferred through hybridization
to other plum trees. This provides a unique source of germplasm for future
breeding programs worldwide. There has been no similar success in attempts
to genetically modify other Prunus species. The disease is very
difficult to manage. Management strategies include prevention of spread
to virus-free areas, eradication of infected trees, decreasing spread by
aphids, and breeding for virus resistance. There is no cure or treatment
for the disease once a tree becomes infected; infected trees must be destroyed.
Several aphid species can transmit plum pox within an orchard and over
short distances (about 1000 feet [300 m]) to trees in nearby orchards.
Long-distance spread usually occurs as a result of the movement of infected
nursery stock or propagative materials. Strain typing of detected isolates
was especially important, because an unusual and potential new strain of
PPV was detected recently in plum that originated from Eastern Europe.
It is interesting that, in spite of identification as D strain based on
RFLP analyses, the Kazakhstan plum and apricot isolates displayed atypical
electrophoretic mobility of the CP subunits, migrating similar to that
of the M isolate. The DAG motif was detected in both the plum and apricot
isolates of PPV from Kazakhstan, indicating that they have the potential
for aphid transmission. The 6-nt (2 amino acid residues) deletion observed
in the plum isolate of PPV described in this study is the 1st deletion
of this nature observed among isolates of PPV, but its biological significance
is not known at present. The plum and apricot isolates appear to be closely
related, sharing a number of nucleotides that appear to be unique to the
Kazakhstan isolates. Based on these results, it is possible that the plum
isolate was derived from the apricot isolate, because the latter appears
to be more typical in terms of the number of nucleotides in the CP coding
region of the genomeref1,
ref2,
ref3,
ref4,
ref5,
ref6,
ref7
soybean
mosaic virus (SMV) : resistance-breaking strains of SMV is a blow to
plant breeders and pathologists. SMV is one of the most widespread viruses
in soybean, and new resistance-breaking strains continue to emerge. An
example is the cultivar Hutcheson, developed in Virginia, that is resistant
to the common strains of SMV, but new resistance-breaking (RB) isolates
of SMV have emerged in natural infections to break the resistance of Hutcheson
containing the Rsv1 allele. Resistance to SMV is controlled by single dominant
genes at 3 distinct loci, Rsv1, Rsv3, and Rsv4. The Rsv3 gene induces extreme
resistance, hypersensitive response, or restriction to virus replication
and movement, which are strain-specific. The Rsv4 gene functions in a non-strain
specific and non-necrotic manner, restricting both cell-to-cell and long-distance
movement of SMV. The Rsv1, Rsv3, and Rsv4 resistance genes exhibit a continuum
of SMV-soybean interactions that include complete susceptibility, local
and systemic necrosis, restriction of virus movement (both cell-to-cell
and long distance), reduction in virus accumulation, and extreme resistance
with no detectable virus. Cultivars containing 2 genes for resistance (Rsv1
and Rsv3 or Rsv1 and Rsv4) were resistant to multiple strains of SMV tested
and show great potential for gene pyramiding efforts to ensure a wider
and more durable resistance to SMV in soybeansref1,
ref2.
sugarcane
mosaic virus (SCMV), the prevalent potyvirus infecting maize across
China : mosaic followed by reddening and necrosis of the lamina
zucchini
yellow mosaic virus (ZYMV) (originally named muskmelon yellow stunt
virus), first observed in 1981 in France and Italy, has since been
reported from most southern and southwestern states in the US as well as
and has been found in at least 22 countries on 5 continents, especially
in Mediterranean countries, Central Europe and USA : France, the USA, Lebanon,
Japan, Taiwan, Jordan, Singapore, Greece, Nepal and likely in other counties.
It is one of the major members in the Potyvirus genus infecting cucurbits.
It induces extreme symptoms on all melon types, including severe yellow
mosaic on leaves, which is usually associated with distortion, deformation
and fruit blistering. Plants are often stunted and fruit set is poor. The
first few leaves affected on rockmelons may progress from chlorosis to
full necrosis. A number of ZYMV variants have been described, some
strains of which may induce lethal wilting, others can cause cracks on
fruits or mosaic and hardening of the fruit flesh. The virus has characteristics
very similar to watermelon mosaic virus
(WMV)-1 and Watermelon virus 2 (nonpersistent aphid transmission, etc.),
and like WMV-2, its host range is not limited to cucurbits. Currently,
none of the genetic factors that confer resistance to WMV-1 or WMV-2 are
able to control ZYMV, but other resistance sources have been identifiedref1,
ref2,
ref3.
It affects crops in. Cucurbita
pepo (pumpkin), Cucumis
melo (melon) and watermelon
(Citrullus lanatus) are the predominant susceptible hosts. ZYMV
is often associated with papaya
ringspot virus (PRSV) or with watermelon
mosaic virus (WMV) in tropical countries. The virus is transmitted
by several aphids including (Aphis
citricola, Aphis
gossypii, and Myzus
persicae). Evidence of seed transmission is equivocal. Symptoms
include mosaic, yellowing, shoestringing, stunting, and fruit and seed
deformations. Typical of aphid-transmitted viruses, it is extremely difficult
to control with insecticides, reflective mulches, or mineral oils. Disease
management involves use of resistant cultivars and control of infected
weeds from which aphids can acquire the virus. Application of chemical
insecticides is usually not economical. Disease management utilizes reflective
mulches, judicious application of insecticides, and resistant cultivars.
Some wild cucurbits are sources of ZYMV resistance genes, which may have
application for developing resistant cultivarsref1,
ref2,
ref3.
Resistance is present in some lines of Cucumis sativus from China
and in an accession of C. melo from India. Unfortunately, this resistance
is strain-specific and thus not effective against a 2nd pathotype. Resistance
is available in a wild squash (Cucurbita ecuadorensis) and in a
C.
moschata line from Nigeria. All tested commercial cultivars of
Citrullus
lanatus (watermelon) are susceptible, but resistance is available in
some accessions of C. colocynthis from Nigeria. A very high level
of resistance was found in some races of C. lanatus from Zimbabwe,
but it confers resistance to the Florida strain only. In recent years,
new squash lines possessing the coat protein gene of this virus have been
developed and proved to be resistant under field conditions. The ZYMV coat
protein gene has also been incorporated into melon and cucumberref.
wheat
streak mosaic virus (WSMV) infects wheat, barley,
maize,
oats
and rye and some pasture and weed grasses.
WSMV causes severe disease in some winter wheat crops in the Great Plains
of North America, with average losses of 3%. There is one report from South
America. It occurs throughout the Mediterranean Basin at low incidence
and is reported from Eastern Europe and Australia. The virus is transmitted
by the eriophyid mite Aceria
tosichellaref.
Characteristic WSMV particles (700 x 15 nm) were observed in electron micrographs
from infected wheat and confirmed by serological tests. Damage to wheat
crops can range from complete crop failure to severe reduction in yield.
The outbreak in Argentina was observed in cvs. ACA 223, Baguette and Buck
Guapo in wheat fields in Cordoba province. WSMV has been reported from
Canada, China, Czech Republic, Hungary, Iran, Jordan, Mexico, Poland, Rumania,
Russia, Turkey, Ukraine, USA, the former Yugoslavia and Syria. In South
America the first report occurred in 2004 in Argentina. In North America,
conditions favoring spread of the disease are the presence of a source
of infection coupled with early planting of winter wheat. Severe losses
can occur in early planted fields of winter wheat and spring wheat. A.
tosichella needs living plants to survive year-round. Nymphal mites
can acquire the virus after feeding for 15 minutes or more on infected
plants, and they remain viruliferous for several days in the absence of
infected plants. High sequence identity of US and Turkish WSMV genotypes
suggests that humans assisted the movement of WSMV across the Atlantic.
Immigrants from the Crimea initiated the hard red winter culture in South
Dakota, Nebraska, and Kansas in the 1880s, and germplasm exchange was frequent
between the Great Plains of North America and the Black Sea. WSMV is reportedly
seedborne at low rates (0.1-0.2%) in maize and wheat, and both the virus
and its vector could have been transported across the Atlantic in grain
shipments. Disease management depends upon eliminating or destroying volunteer
wheat and susceptible weeds before the new crop is sownref1,
ref2,
ref3,
ref4,
ref5,
ref6
unclassified Potyviridae
cucumber
vein yellowing virus (CVYV)ref1,
ref2,
first reported from Israel in 1960, has subsequently spread within the
EPPO region (Israel, Jordan, Portugal, Spain, Turkey) and Sudan. The disease
affects cucumber, pumpkin, squash, and watermelon
(Citrullus lanatus). CVYV wreaks havoc on cucurbit hosts in
the eastern Mediterranean region, causing considerable crop loss. Information
on disease management is meager. Attempts to reduce losses center on use
of virus-free seedlings, provision of screens in glasshouse production
systems to prevent viruliferous whiteflies (Bemisia
tabaci) from feeding on plants, use of chemical insecticides, implementing
a period of at least a month between seeding new crops, and biological
control using predacious insects (Encarsia
formosa), a parasitic wasp, and the beetle Delphasutus pusillus.
The fact that cucumber vein yellowing disease is present across the southern
flank of Europe is of concern to plant pathologists and entomologists.
CVYV is well established in Israel, Jordan, Turkey, Spain and Portugal.
Symptoms in both cucumber and melon have been described as vein yellowing,
vein clearing and stunting, with a corresponding yield reduction. Sudden
death, an uncommon outcome for plant virus disease, was observed on melon
in Spain. Avoiding infected propagation plants, management of whiteflies
and weed reservoirs are the main ways to manage disease problems. Attempts
to select or engineer useful tolerant or resistant varieties are being
maderef1,
ref2,
ref3
Sequivirus
Dandelion yellow mosaic virus (DaYMV) was isolated from dandelion
and lettuce in Europe. Lettuce mottle virus (LeMoV), a putative sequivirus,
is often found in mixed infections with Lettuce mosaic virus (LMV) in Brazil.
DaYMV, LeMoV and LMV cause similar mosaics in field-grown lettuce. Differences
in biology and sequence suggest that DaYMV and LeMoV are distinct species.
Plants of lettuce (Lactuca sativa) cv 'Veronica' showing mottle
symptoms were submitted to biological, serological and physicochemical
tests as well as electron microscopy to determine a possible association
of a virus matching the expressed symptomatology. Mechanical inoculation
of sap extracts resulted in local lesions on Chenopodium quinoa and
isometric virus particles were observed. The host range was restricted
to a few species of Asteraceae, Chenopodiaceae and Solanaceae, and most
commercial lettuce cultivars developed mottle symptoms when mechanically
inoculated with the virus. Helichrysum bracteatum (strawflower),
a spontaneous Asteraceae, was found to be a potential differential host
since it is susceptible to the virus and not to Lettuce mosaic virus (genus
Potyvirus). A serological relationship with Dandelion yellow mosaic virus
was demonstrated by plate-trapped antigen-enzyme linked immunosorbent assays
(PTA-ELISA). The fact that LeMoV has spread to the western side of the
Cordillera de Los Andes is of significance to growers in that region, as
is the finding that this is the 1st report of a sequivirus infecting field
lettuce in Chileref.
Sobemovirus
rice
yellow mottle virus (RYMV) causes symptoms of the disease yellow
mottle in the crop plant rice, Oryza sativa. Symptoms include
stunting, reduced tillering, mottling and yellowish streaking of the leaves,
delayed flowering or incomplete emergence of the panicles and, in extreme
cases, death of plants. The disease is a major constraint to rice production
in Africa. RYMV was 1st reported in Kenya in 1966 and later found in most
countries in Africa where rice is grown. RYMV is transmitted mechanically
and by chrysomelid beetles but not by seed (a property of some Sobemoviruses).
Chaetocnema
pulla Chapuis is thought to be an important vector of the disease in
Tanzania. Much of the spread may not be due to transmission by beetles
but rather by mechanical inoculation. Very few rice varieties are resistant
to RYMV. The highest level of resistance was provided by a cultivar of
Oryza
sativa indica, "Gigante," and a few cultivars of Oryza glaberrima
series Tog. These varieties showed a natural high resistance characterized
by a low virus titre and the absence of symptoms. In this 1st report of
RYMV in Uganda, 4 samples were collected from symptomatic plants growing
in a subsistence rice field north east of Lake Victoria, close to the Nile
River, in 2000. The samples contained RYMV serotype 4, a serotype found
in eastern Africa (Madagascar, Kenya, and Tanzania). It differs from (88%
identity) the basal strains from eastern Tanzania. Rice is a relatively
new crop in Uganda. It was introduced on a large scale in the 1960s and
is now widely grown in many parts of the country, especially in the eastern
and northern regions. To meet the increasing demand for rice, Uganda imports
about USD 100 million worth of rice every year. The presence of RYMV will
not be good news for those making efforts to increase rice production in
Uganda, including expansions into the upland areasref1,
ref2,
ref3,
ref4,
ref5,
ref6,
ref7,
ref8,
ref9
Southern
bean mosaic virus (SBMV), 1st reported in common bean in samples from
USA (Louisiana and California) in 1943, also infects Vigna unguiculata,
[Vu] V. mungo and Glycine max,
causing mosaic and/or mottle, and stunting (especially in Vu). It is transmitted
in a semi-persistent manner by bean leaf beetles (Ceratoma trifurcata
and Epilachna varieties), mechanical inoculation, grafting, by seed
(3-44%) and by pollen. SBMV has been reported from Africa (Morocco) and
from regions in the Americas (North, South and Central), and France. SBMV
is transmitted to bean seedlings if germinating seeds are in contact with
infective extracts or are planted in soil near roots of infected plants.
Disease management essentially involves use of virus-free seedref.
SBMV was 1st reported in Phaseolus
vulgaris from samples collected in Louisiana and California, USA
by Zaumeyer and Harter in 1943. There are several strains (cowpea strain
(strain C), Ghana strain (strain G), severe bean mosaic strain or Mexican
strain (strain M) and the type strain (strain B). Symptoms persist in P.
vulgaris,
Vigna unguiculata, V. mungo and Glycine
max. Symptoms include mosaic and/or mottle, and stunting (especially
in Vigna unguiculata). SBMV is transmitted by beetles (Ceratoma
trifurcata and Epilachna variestis). It can also be transmitted
by mechanical inoculation, by grafting, seed (3-7% in V. unguiculata
cv. Early Wilt Resistant Ramshorn), by pollen to the seed and transmitted
by pollen to the pollinated plant. It has been reported from the African
region, the North American region, the South and Central American region
and France. SBMV probably entered Iran via infected seed. The strategy
for disease management involves managing the bean leaf beetle. Resistance
to SBMV is not yet available
tomato
mosaic virus (ToMV), usually expresses characteristic mosaic symptoms,
leading to considerable plant damage and yield losses. 3 resistance genes,
Tm-1, Tm-2 and Tm-2(2) have been identified in crosses between wild and
cultivated tomato species in efforts to prevent systemic infection and
losses in fruit yield and quality caused by Tobacco mosaic virus (TMV)
and ToMV. The Tm-2(2) resistance gene is used in most commercial tomato
cultivars for protection against infection with tobacco
mosaic virus (TMV) and its close relative tomato mosaic virus (ToMV).
Observations suggest that the resistance conferred by the Tm-2(2) gene
against ToMV depends on specific recognition events in this host-pathogen
interaction rather than interfering with fundamental functions of the 30-kDa
MPref1,
ref2,
ref3.
Tobacco mosaic and odontoglossum ringspot viruses are closely related,
and cucumber green mottle mosaic and sunn-hemp mosaic tobamoviruses are
distantly related. Disease management involves application of phytosanitary
measures, especially avoiding contact between infected and virus-free plants.
Production benches and equipment used in glasshouse production systems
must be sterilizedref1,
ref2,
ref3
Tombusviridae
Aureusvirus
Pothos
latent virus (PoLV). The scientific name for pothos is Epipremnum
aureum; its common name is devil's ivy
=> black scorch in sugarbeet
(Beta vulgaris). BBSV was first reported in the late 1980s in
China. The virus is responsible for serious damage to the sugar beet crop
in the Xinjiang, Ningxia, Inner Mongolia, Gansu, and Heilongjiang provinces
of China. BBSV infects sugar beet plants systemically through the roots
after transmission with Olpidium brassicae zoospores and causes
black scorch symptoms on the leaves. Sugar beets are grown as a commercial
source of sucrose (sugar). BBSV can result in significant loss of
root yield and sugar recovery. BBSV has been reported in China and in 2006
in the USA and possibly elsewhere. It remains to be seen if this becomes
a major disease problem. The USDA is seeking the development of a
suitable test for BBSVref,
which is an indication that there are concernsref
unclassified Tombusviridae
cucumber
leaf spot virus (CLSV), previously classified as definitive species
in the genus Carmovirus. Aureusviruses are soil-borne viruses readily transmitted
by sap inoculation to a moderate range of hosts. Natural transmission of
CLSV is by the chytrid fungus Olpidium
bornovanus [Ob], (previously O. radicale), whereas PoLV
infects the host without the apparent intervention of a vector. A bulk
culture of Olpidium radicale (now classified as Ob) from melon roots
collected at Montfavet, France did not transmit CLSV or the cucumber fruit
streak strain of CLSV (CLSV-FS). CLSV is sap-transmitted, and is seed-borne
(c.1%) and soil-borne. Found naturally only in cucumber. Reported from
Germany, Greece, Great Britain and Jordan (Weber et al., 1982, 1986; Gallitelli
et al., 1983) and Spain. CLSV is most likely related to Melon necrotic
spot carmovirus (MNSV), red clover necrotic mosaic dianthovirus (RSNMV)
and cucumber necrosis tombusvirus (CNV). CLSV is an Aureusvirus in the
family Tombusviridae and is most closely related to Pothos latent
virusref1,
ref2,
ref3,
ref4,
ref5,
ref6
=> banana streak disease was first described in Morocco and
the causal virus, Banana streak badnavirus, was described in 1986. BSV
has subsequently been recorded in Africa, Europe (Canary Islands and Madeira),
Asia, North America (Florida), Central and South America, and the Pacific
Islands. Infection of Musa
by BSV limits development of new Musa hybrids in breeding programs
worldwide. BSV has been transmitted experimentally by mealybugs (Planococcus
citri and Saccharicoccus
sacchari) [Ss] both of which colonize banana. Results of surveys
in Uganda show that Dysmicoccus brevipes
[Db] and Ss were the most prevalent mealybugs, and the incidence of
banana streak was correlated with the presence of Db. Disease managementis
complicated because infected plants may be symptomless; but use of PCR
and ISEM has facilitated rapid detection of BSV. 400 million people in
developing countries depend on bananas and plantains as a staple food.
Plant breeders need access to as much diversity as possible in order to
develop higher-yielding varieties with resistance to pests and diseases.
For bananas, the world's biggest collection is maintained in trust for
humanity at the Katholieke Universiteit in Leuven, Belgium.KUL sends plants
to researchers worldwide through IPGRI's International Network for the
Improvement of Banana and Plantain (INIBAP). International guidelines,
however, allow only movement of disease-free plants, but a substantial
part of the collection has been blocked because it is infected with BSV.
Researchers from KUL and the Gembloux Faculty of Agriculture have already
developed several techniques for eliminating viruses from sterile cultures
in the banana collection. These techniques are effective against other
diseases, but BSV remained a problem. Knowing that BSV is quite closely
related to HBV, and uses some of the same chemical processes, the
banana scientists got together with the Rega Institute for Medical Research
at KUL. This institute was responsible for developing adefovir and tenofovir,
antiviral compounds tested and approved for the treatment of hepatatis
B and AIDS. The researchers grew infected banana cells in the presence
of small doses of the drugs for 6 months. Testing of whole plantlets produced
from those cells demonstrated that up to 90% of the plantlets showed no
sign of BSV.
Caulimovirus
cauliflower
mosaic virus (CaMV) is found worldwide, especially in temperate areas
of the USA and Europe. Its natural host range is limited to the Cruciferae
(cabbage, cauliflower, Brussels sprouts, and others). The main sources
of CaMV are infected brassica crops or cruciferous weeds on which any of
several aphid species have overwintered. It is often found as a mixed infection
with turnip mosaic virus (TuMV),
resulting in more severe synergistic symptoms than when either virus is
present alone. Disease management requires adequate weed control and sanitation,
especially the rapid plowdown of previous crops. Transplant beds should
be isolated from commercial crop fields and overwintering cruciferous weed
hosts. Symptoms of CaMV are often confused with those of TuMV. Resistance
to CaMV is found in most cabbage cultivarsref1,
ref2,
ref3,
ref4.
=> sterility mosaic disease (SMD) is the most damaging disease
of pigeonpea endemic in the Indian subcontinent. It causes yield losses
exceeding USD 300 million per annum in India and Nepal alone. SMD-affected
plants show severe stunting and mosaic symptoms on leaves, with complete
or partial cessation of flowering. The SMD causal agent is spread by the
arthropod mite vector Aceria
cajani. Cultivating SMD-resistant genotypes is the most viable
way to manage this serious disease of pigeonpea. Pigeonpea (Cajanus
cajan), is a grain legume that is a very important subsistence
crop in marginal farming systems adopted by millions of smallholder farmers
in the Indian subcontinent. It is grown for its seed for human consumption
and for income generation by trading surpluses in local and commercial
markets, but is widely used for diverse purposes, including as animal fodder
and for soil conservation. It is grown on about 5.25 million ha, yielding
3 million tonnes, and contributes to about 5% of total world production
of pulses. About 90% of global pigeonpea is grown in India and Nepal, and
the remainder is cultivated in Africa, the Caribbean and Southeast Asia.
There are no reports of SMD from Africa or the Americas. Infection by SMD
in plants < 45 days old results in 95-100% loss, while older plants
suffer losses of 26-97%. SMD is the most significant disease of pigeonpea
in India, causing losses over of USD 280 million in 1993. A previously
undescribed virus, Pigeonpea sterility mosaic (PPSMV), shows properties
similar to viruses in the genus Tenuivirus. However, all tenuiviruses are
phloem-limited, are transmitted by Delphacid planthoppers and only
infect species in the Poaceae, thus ruling out PPSMV as a tenuivirus.
Ultrastructural studies of PPSMV-infected pigeonpea showed 100-150 nm quasi-spherical-membrane-bound
bodies (MBBs) and fibrous inclusions (FIs). The filamentous VLPs of PPSMV
resemble the nucleoprotein particles of Tomato spotted wilt virus (TSWV),
and PPSV VLPs are slightly larger than those of TSWV. PPSMV shows no serological
relationship to Maize stripe virus tenuivirus or Peanut bud necrosis tospovirus.
PPSMV and High plains virus share some common properties: transmission
by the eriophyid mite A. cajani, 4-7 similar-sized MBBs and similar
morphology. Similar MBBs have been detected in plants infected with fig
mosaic, wheat spot mosaic, thistle mosaic and rose rosette, suggesting
that these viruses may constitute a new virus genus. Disease management
of SMD will depend upon identification of broad-based resistant genotypes.
These are relatively rare in the pigeonpea gene pool, but a related wild
species,
Cajanus
scarabaeoides (a.k.a. C. indicus) has high levels of resistance
to several pigeonpea biotic constraints. SMD thrives readily in crops under
irrigation or near irrigated fields, and such crops are at risk of early
infectionref
unclassified :
mature vine decline and fruit rind necrosis in cucurbits in Florida
(the second largest producer of watermelon
(Citrullus lanatus) in the United States)ref1,
ref2
eggplant mottled dwarf virus
=> a virus that is widespread in the Middle East has now been detected
in tomato and potato in Slovenia. It has previously been reported in Bulgaria
and Italy in pepper and cucumber and is known to infect tobacco and cucumber
in Greece and eggplant in Turkey. EMDV was first reported in eggplant
(Solanum melongena) in southern Italy in 1969. In addition to
cucumber and pepper, the natural host range of the virus includes black
nightshade (Solanum nigrum), and S. sodomaeum that, in Morocco,
may be a perennial source of infection. The virus is transmitted by contact
inoculation and grafting but not by seed. It spreads in Algeria, Italy,
Morocco, Tunisia, Turkey, and the Canary Islands. The vector of ECMV
is unknown, but because percentage of infection is generally low, a polyphagous
insect with low vector specificity may be involved in transmission. Transmission
was achieved by the agallian leafhopper (Agallia vorobjevi) in a
study in Iranref1,
ref2,
ref3.
=> bacterial canker in Lycopersicon
esculentum and pepper affects field and greenhouse production systems,
often inducing severe, in some cases total, crop loss, in Thailand, France,
Turkey. The primary source of the pathogen is contaminated seeds
and transplants. The pathogen can survive in non-decomposed tomato
crop residues and on seed for up to 5 years. Infested seed is the principal
means of long-distance spread. Solanaceous weeds can be alternate hosts
of the pathogen. Strategies for avoiding the disease include pre-season
sanitation of all equipment, pipes, containers etc., use of certified seed
and transplants, use of available tolerant cultivars, use of seed that
has been treated to inactivate the pathogen, rogue out volunteer plants
and solanaceous weeds near production glasshouses, and crop rotation in
tomato fields (3 years of planting non-host crops). If disease occurs in
glasshouses, eradicate entire production. If disease is present in fields,
use appropriate bactericides, plow down the crop and incorporate into soil
for active decomposition. Some degree of control can be obtained by applying
chemical and antibiotic treatments, but they should be used sparingly so
as to prevent development of resistant strains of the pathogen. According
to the manufacturer, Virkon S (source : Antec International) is effective
in disinfecting tomato seeds from canker infection without any adverse
effects on seed germination or seedling stand.
=> bacterial ring rot (BRR) : Cms occurs throughout Europe,
after being identified in recent years in France, the Netherlands, Slovakia
and Denmark. 3 outbreaks have occurred in the UK since November 2003. Defra
officials consider it one of the most serious diseases of potatoref1,
ref2,
ref3.
Cms is spread by infected tubers, and a major concern for plant pathologists
in Wales and other parts of the UK is the possibility that seed potato
stocks could be infected. Sanitation is the key to disease management.
Only classified seed should be used for planting; all machinery, equipment,
vehicles, containers such as potato sacks, storage facilities such as bins,
and any other possible source of the pathogen must be identified and rigorously
cleaned and thoroughly disinfected. Finally, if possible, dispose of all
potato waste at an approved tip (dump) or by incineration. The disease
is especially damaging to seed producers since disease-free seed is the
foundation of any seed potato production program. Disease management depends
upon zero tolerance of the pathogen and application of very strict phytosanitary
measures to maintain freedom from contamination. Quaternary ammonia, bleach,
chlorine dioxide, iodine, and phenol groups are useful disinfectants. Cms
can remain latent in tubers, so adequate laboratory testing of seed lots
is required. Damage is caused by destruction of vascular tissues and subsequent
wilting and dying of plants and secondary rotting of tubers. Crop losses
have been mainly reported from North America (up to 50%) and from Russia
(15-30% of plants infected, up to 47% crop loss). Where ring rot occurs
in the EPPO region, the disease appears more sporadically and at low levels
of infection. The low disease occurrence in this area is due to the fact
that cutting of potato seed, and use of pricker-type planters, is uncommon
in Europe. When tubers are cut, however, higher levels may also occur (up
to 30% crop loss in France). Economic losses are due to wilt and tuber
rotting in the field and in storage. Indirectly, expenses related to the
disinfection of sacks, machinery, stores etc., prohibition of potato cultivation,
and restriction, or prohibition, of export trade may increase economic
lossref1,ref2,
ref3,
ref4.
According to Antec International, a balanced, stabilised blend of peroxygen
compounds, surfactant, organic acids, and an inorganic buffer system [Virkon-S
(source : Antec International)] is recommended as a means of controlling
Cms. Sanitation, cleanliness, and disinfection are the keys to eradication
of bacterial ring rot. If either pathogen is confirmed on a commercial
farm, a thorough clean-up of storage and equipment must be carried out
to reduce the chance of any bacteria remaining and causing contamination
of incoming certified seed lots destined for the following year's potato
crop. Access to seed storages and equipment by commercial growers and their
trucks should be limited and controlled. Equipment should not be shared
between commercial and seed farms, and all trucks from commercial potato
farms should be cleaned and disinfected before they enter seed storages
or seed handling areas
Curtobacterium
Curtobacterium flaccumfaciens
Curtobacterium
flaccumfaciens pv. flaccumfaciens [Cff] causes bacterial
tan spot in bean (Phaseolus vulgaris) and soybean (Glycine max).
It is internally seedborne in legumes. Pathogenesis is facilitated by higher
temperatures (25-30°C). Disease incidence can be reduced by planting
pathogen-free seed or by using seed of less susceptible cultivars. Cff
grows throughout the water-conducting tissues of the plant and impedes
water movement, resulting in a wilt. Symptom development is favored by
temperatures > 32°C. Infection is often caused by the planting of infected
seed, but Cff may also survive in infested crop debris. Cff bacteria
are more confined to internal infection of plant vascular tissue, and apparently
are not spread as readily by rain or movement of machinery among wet plants
as compared to the halo blight pathogen (Pseudomonas syringae pv.
phaseolica)
or the common bacterial blight pathogen (Xanthomonas campestris
pv.
phaseoli). Infection through natural openings on the plant are
rare, but hailstorms and wounding favor infection. Cff is disseminated
among fields by irrigation water and movement of infested crop debris or
contaminated seed. Disease management strategies include planting high-quality
certified seed free from the bacterial wilt pathogen. There are varietal
differences in their susceptibility to bacterial wilt, and resistant or
tolerant varieties should be planted if available. A 2-year crop
rotation to non-hosts such as small grains is recommended. Avoid reuse
of irrigation water if possible and practice strict sanitation of crop
debris and volunteer beans to reduce pathogen survival between bean crops.
Antibiotic seed treatment can reduce surface contamination of seed, but
chemical controls are most effective when integrated with sound cultural
practicesref1,
ref2,
ref3,
ref4,
ref5
=> ratoon stunting disease (RSD), a difficult pathogen to detect,
and tissue blot immunoassay are required. RSDis considered by many to be
the most important disease affecting sugarcane production worldwide. It
can cause a 5-15% loss in crop yield without the grower even knowing his
fields have been infected. The disease is caused by a bacterium. RSD has
no easily recognized external symptoms, only stunting of growth, which
may not always be apparent in the field. Although RSD has been reported
in Jamaica since 1961, presence of the pathogen had never been confirmed
in symptomatic tissues before 2005ref1,
ref2.
Bacillus / Clostridium group (low G+C Gram-positive Bacteria)
Bacilli (facultative anaerobes or strictly aerobes spore-forming Bacteria)
=> melting decay in grapes. Initial symptoms are usually observed
after 2 weeks of cold storage (-0.5 to 0°C and 90-95% relative humidity).
The fact that the incidence in cold storage has increased dramatically
from the 1990s to 2003, suggests that perhaps a new strain of Bs has evolved
under those conditions. There is a report in 1992 of Bs being associated
with soybean seed, but that requires confirmation. Infection of grapes
by the 2 yeast species is of interest and may be related to environmental
conditions in the field as well as in cold storage. Bs is widely used as
a fungicide on flowers and vegetables, including crop plants.
Firmicutes
Mollicutes
Acholeplasmatales
Acholeplasmataceae
Candidatus Phytoplasma (plant yellows agents) : phytoplasma-induced diseases
are being recognized as significant pathogens of food crops. Phytoplasmas
are a group of prokaryotic, microscopic plant pathogens that cause over
700 diseases of food, fiber and ornamental plants. They are found mainly
in the phloem sieve tubes of their plant hosts and in certain sucking insects,
which can act as vectors. They can also be spread by grafting, by parasitic
plants or by seed transmission. Detection of phytoplasmas is by grafting
to susceptible host plants, microscopy, serology (ELISA), nucleic acid
hybridization or DNA amplification using the polymerase chain reaction
(PCR). Symptoms displayed by plants infected with phytoplasmas include
foliage yellowing, petal greening, shoot proliferation, stunting, little
leaf formation, necrosis and a decline of vigor leading to deathref1,
ref2,
ref3
16SrI (aster yellows (AY) group) aster yellows group (16SrI) phytoplasmas
are associated worldwide with > 100 diseases, several of which are quarantine-regulated
and economically important. Scientists from the Molecular Plant Pathology
Laboratory at Beltsville, MD, USA found that combined use of 16S rRNA and
ribosomal protein gene sequences enabled differentiation of 18 distinct
subgroups in the AY group. A new species, 'Candidatus Phytoplasma asteri',
was proposed to represent the AY phytoplasma group. This accomplishment
will aid plant quarantine agencies in implementing new regulations to prevent
these pathogens from being introduced into new regions. Ing-Ming Lee, a
USDA scientist specializing in mycoplasmas, and his colleagues constructed
the first comprehensive phytoplasma classification system in 1993, based
on RFLP analysis of 16S rDNA. Further work led to an expanded system by
2000 that included 15 major phytoplasma groups and over 40 subgroups, providing
the most comprehensive phytoplasma classification system available. In
northern Tunisia, grapevines
(Vitis vinifera) were found exhibiting symptoms of grapevine
yellows that included plant weakness, incomplete lignification, flexible
shoots and drooping. Affected leaves were thicker than normal, brittle,
rolled downward and showed veinal yellowing and necrosis. In addition,
grape bunches became dry and shrivelled before fruit could fully develop
and ripenref
a new phytoplasma causes hoja de perejil (parsley leaf disease)
of tomato (Lycopersicon
esculentum) cv 'Rio Grande' and Calotropis
little leaf (Morrenia variegata (Mv)) in the Bolivian provinces
of Santa Cruz and Sucre. An infection rate of 60% suggests that the disease
may be widespread in some areas, but there are no data on crop loss in
tomato. Obviously the phytoplasma is well-established in Mv in affected
areas of Bolivia and constitutes a source of inoculum.
=> peach yellow leafroll (PYLR) was 1st described in 1948, occurring
primarily in Butte, Placer, Sutter, Yuba and San Juaquin and Stanislaus
counties of Bolivia. It caused moderate losses in the 1950s and 1960s,
killing approximately 4800 trees, but the incidence of PYLR increased dramatically
in the late 1970s when a major epidemic killed over 35 000 trees in 1979.
The incidence of PYLR has declined but continues to be a chronic problem
in the northern California counties of Yuba, Sutter, El Dorado and Placer
=> coconut lethal yellowing (LY) disease : symptoms include
premature nutfall, necrosis of immature inflorescences, progressive frond
yellowing, and eventual palm death. It spreads rapidly, destroying coconut
and other palms. Millions of coconut
palms (Cocos nucifera, Atlantic tall ecotype) have been killed
in the Caribbean region over the past 40 years. LY disease has swept through
the coconut-growing regions of Jamaica, Cuba, the Cayman Islands, and Florida
and is presently destroying palms in the Yucatan Peninsula, Honduras, Guatemala
(however, the syndrome differed from that reported for LY, as inflorescence
necrosis was evident after, rather than before, frond yellowing), as well
as mainland Belize. Similar diseases have been identified in Africa (Kenya,
Mozambique, Tanzania, Nigeria, Ghana, and Cameroon). If unchecked, LY disease
may spread to South America. Millions of coconut palms on the Caribbean
and Atlantic coasts are endangered, because the common cultivar is highly
susceptible to the phytoplasma. LY, described by some as the "dengue of
palm trees," is spread by the planthopper Myndus crudus, but other
planthopper species are being assessed for their role as vectors. Infected
palms die within 6-9 months after symptoms are 1st expressed. The vascular
systems of infected palms are plugged with the phytoplasma thus stressing
the palms and accelerating the onset of death. Research scientists at Ft.
Lauderdale, FL, and Meridia, in Yucatan, have identified other phytoplasma
strains associated with coconut palm that express leaf-yellowing syndromes
in southern Mexico that are distinct from LY phytoplasmas. There is no
effective cure for LY-infected palms. Previously ravaged areas have been
replanted with resistant cultivars and hybrids such as 'Maypan'. There
is some work being done on genetic modification of palms, but transformation
of palms with genes of interest including LY resistance, and other traits,
is still in the offingref1,
ref2,
ref3
=> grapevine yellows (GY) FD and boid noir phytoplasma (BN) are common in European vineyards,
FD being more important. The principal host of FD is grape
(Vitis vinifera). Of considerable significance is that Convovulus
arvensis (field bindweed) and Solanum nigrum (black nightshade)
are common in German vineyards, thus providing an inoculum source. The
principal vector for the FD phytoplasma is Scaphoideus titanus (vine
leafhopper), but the vector for BN is Hyalesthes obsoletus, also
known as the vector for potato stolbur. Local spread of FD is about 5-10
km per year, while that of BN is much slower. Uncontrolled spread of FD
is usually catastrophic, particularly in the cultivars Chardonnay and Pinot
Blanc. BN spreads much more slowly, and its economic impact is much less.
Management of the disease is based on use of suitable planting material
and control of vectors by chemical insecticidesref1,
ref2
16SrVI (Clover proliferation group) Subgroup A (16SrVI-A)
=> dry bean phyllody (DBPh) disease in dry bean
(Phaseolus vulgaris L.) cultivars of Andean origin grown in
Mattawa and Paterson, WA. Symptoms of DBPh became apparent during mid-to-late
pod development and were characterized by leafy petals (phyllody)
and aborted seed pods resembling thin, twisted, and corrugated leaf-like
structures. Deformed sterile pods that were small, sickle-shaped, upright,
and leathery were also observed. The infected plants generally exhibited
chlorosis, stunting, or bud proliferation from leaf axils. Phyllody describes
a retrograde metamorphosis of the floral organs to the condition of leaves.
Because floral tissues in phytoplasma-infected plants revert to vegetative
tissues, no seeds are produced, and crop losses due to phyllody can be
very high. Phyllody-affected crop plants can be cured of phytoplasmas by
heat treatment or by subjecting cuttings to tissue culture. The beet leafhopper,
Circulifer
tenellus (Ct), is the only known vector of Vinca
virescence phytoplasma / beet leafhopper-transmitted virescence agent (BLTVA),
although not much is known about other vectors. Phytoplasmas infect and
multiply in their leafhopper vectors. The BLTVA is vectored in the same
manner as other phytoplasmas are by other leafhoppers. Ct acquires
BLTVA only by feeding on infected plants. Prophylactic use of insecticides
is the only known means to prevent transmission of BLTVA. The Washington
vegetable seed industry has been plagued with BLTVA for years, and even
the prophylactic use of insecticides has not always successfully managed
it. Some vegetable seed crops are no longer grown in the Columbia basin
due to inadequate control of BLTVA.
=> potato purple top (PPT) / aster yellows / haywire / purple dwarf
and Purple-top wilt : upright terminal shoots, upward leaf rolling,
chlorosis, red or purplish discoloration of new leaves, proliferation of
axillary shoots with basal swelling, and the formation of aerial tubers.
It has been a factor in disease losses for many years in Washington state
but is seldom a major factor affecting potato crops in the Columbia Basin.
However, PPT is endemic in potato crops in Mexico, where it ranks 2nd to
late
blight caused by Phytophthora infestans.
=> potato hair sprouts (PHS) is found in Mexico. PHS has the
greater impact, since infected, but symptomless, tubers generally fail
to sprout or may sprout poorly. Moreover, PHS-infected stems are weakened
because they are deficient in chlorophyll (etiolated). Moreover, psyllid
nymphs inject a toxin into potato tissue, causing PPT-like symptoms, which
confounds diagnosis. Disease management basically depends upon planting
certified seed in areas free of phytoplasmas or, in the case of areas infested
with infected weeds and leafhoppers, use of insecticides to reduce vector
numbers. Development of resistance to phytoplasmas may offer a measure
of controlref1,
ref2,
ref3.
=> apple proliferation (AP) is one of the most important phytoplasma
diseases of apple (Malus)
in Germany and France, affecting almost all cultivars, reducing size (by
about 50%), weight (by 63-74%) and quality of fruit, as well as reducing
tree vigour and increasing susceptibility to powdery mildew (Podosphaera
leucotricha). It is transmitted by grafting and is disseminated in
budwood (both scion and rootstock). The plant louse Psyllid Cacopsylla
melanoneura (Homoptera: Psyllidae) has been implicated as a vector,
and the overwintered adults are probably important in the spread of AP
in apple orchardsref1,
ref2.
In Europe apple proliferation phytoplasma is an EPPO A2 quarantine organism
and is known in Austria, Bulgaria, Czech Republic, France, Germany, Greece,
Hungary, Italy, Moldova, Poland, Romania, Slovakia, Slovenia, Spain, Switzerland,
UK (eradicated), Ukraine, Yugoslavia. Further spread or propagation of
the disease in infected budwood or plant material could lead to considerable
yield losses throughout the European and Mediterranean apple cultivation
areas. It has not been detected in the USAref1,
ref2,
ref3,
ref4,
ref5,
ref6
Candidatus
Phytoplasma pyri / pear decline (PD) phytoplasma : is vectored by the
pear psylla (Cacopsylla
pyricola). Expression of the disease depends on rootstock susceptibility,
tree vigor, and psylla numbers. Poor shoot and spur growth, shoot dieback,
upper rolling of leaves, reduced leaf and fruit size, and premature leaf
drop characterize pear decline. Sudden tree collapse can result from tissue
damage at the graft union on highly susceptible rootstocks such as Pyrus
serotina or Pyrus
ussuriensis, but slow decline of trees is more common. Management
of the disease is based on use of tolerant pear root stocks and Pyrus
betulaefolia. Pyrus betulaefolia is a rootstock that is
tolerant of infection by pear decline (PD). Consequently it is used in
orchards as the rootstock underlying the tree. In addition to P. betulaefolia
seedling Bartlett and Winter Nelis are also used as rootstocks. Apparently
there is no known biological control for pear decline phytoplasma. The
phytoplasma apparently does not multiply in pear trees as well as it does
in pear psylla. Control of pear psylla usually results in disease remission
even when rootstocks are highly susceptible. Poor shoot and spur growth,
shoot dieback, upper rolling of leaves, reduced leaf and fruit size, and
premature leaf drop characterize PD. Trees on tolerant rootstocks may show
mild to moderate symptoms that occasionally become severe if very high
psylla populations occur in conjunction with other tree stresses. Commercial
pear rootstocks, with the exception of Pyrus calleryana, are available
which are essentially tolerant to PD and produce excellent crops in spite
of recurring pear psylla populations and exposure to PD. To keep PD in
remission on susceptible rootstocks, control pear psylla and maintain trees
in good vigor, and reduce stress caused by inadequate irrigation, nutrient
deficiency, weed competition, lack of pruning, and pest damage. There is
no known biological control of the PD phytoplasma. Indirectly, biological
control of pear psylla can reduce disease expression. Based on dissimilarities
of restriction sites detected by rDNA RFLPs, 9 primary 16S rDNA groups
(termed 16Sr groups) and 14 subgroups were recognized in a classification
scheme proposed by Lee, Hammond, Davis, and Gundersen. At least 14 primary
16Sr groups consisting of 16SrI, aster yellows; 16SrII, peanut witches'-broom;
16SrIII, X-disease; 16SrIV, coconut lethal yellows; 16SrV, elm yellows;
16SrVI, clover proliferation; 16SrVII, ash yellows; 16SrVIII, loofah witches'-broom;
16SrIX, pigeonpea witches'-broom; 16SrX, apple proliferation; 16SrXI, rice
yellow dwarf; 16SrXII, stolbur; 16SrXIII, Mexican periwinkle virescence;
16SrIV, Bermuda grass white leaf, and at least 32 strain subgroups have
been recognized. 45 subgroups were identified when ribosomal protein gene
RFLP data were also considered in the analysesref1,
ref2,
ref3
=> potato stolbur (PS ; a.k.a. tomato stolbur) disease
incidence in potato (Solanum tuberosum)
can be high, leading to significant crop loss, but the disease tends not
to persist in stocks. PS is one of a group of phytoplasmas causing yellows-type
diseases in Europe within the broad concept of European aster yellows.
Parastolbur
and metastolbur are strains of stolbur; northern stolbur
is probably caused by potato witches' broom phytoplasma, pseudoclassic
stolbur is poorly defined, and pseudostolbur is a physiological
disorder. A little leaf disease of tomatoes, Capsicum, and eggplants
in southeastern France has been attributed to a phytoplasma distinct from
stolbur. PS infects 45 species in the Solanaceae; principal hosts
are potato (Solanum tuberosum),
tomato,
peppers
and eggplant. Of concern to
plant pathologists are infected plants species in the Asteraceae,
Convolvulus
arevensis and Fabaceae (Trifolium spp.) that are sources
of inoculum. PS occurs in 15 countries of the EPPO region, Asia (8 countries)
and the EU. The most important vector in eastern Europe is Hyalesthes
obsoletus, but there are several others that are of concern. Local
spread in a field appears to originate from infected weed species rather
than from crops. PS can be detected using specific stains in infected tissues,
by indirect immunofluorescence, and by a tissue blot techniqueref1,
ref2
Candidatus Phytoplasma asteris
apple
sessile leaf phytoplasma (AsPL). Considering the fact that apple is
a very popular fruit cultivated in many countries worldwide, the most significant
aspect of this report is that ApSL may become a threat to apple production
in states of the European Union. ApSL obviously occurs in Lithuania, and
I would suspect that it occurs in other areas in Europe, but there are
no other reports of its occurrence to my knowledge. Phytoplasmas are transmitted
by leafhoppers, planthoppers and psyllids. Development of PCR for detection
of ApSL is a major step forward in detecting the phytoplasma in the food
crops featured in this piece and will certainly facilitate its detection
in budwood and propagation nurseriesref1,
ref2
=> aster yellows (AY) is the most widespread plant disease among
those known to be caused by phytoplasmas. AY phytoplasmas are associated
with diseases in more than 100 plant species worldwide, predominantly in
herbaceous dicotyledonous plants. In North America, AY diseases are attributed
primarily to phytoplasma strains belonging to subgroups 16SrI-A (termed
Eastern AY phytoplasma) and 16SrI-B (termed California AY or Western AY
phytoplasma) in the AY group (16SrI). Both 16SrI-A and 16SrI-B phytoplasmas
are transmitted by a variety of polyphagous leafhopper species and have
a wide range of plant hosts. On the basis of RFLP patterns of the 16S rDNA,
the OatP phytoplasma was classified as a member of group 16SrI (group I,
aster yellows phytoplasma group). The RFLP patterns of the 16S rDNA were
indistinguishable from those of 16S rDNA from tomato big bud (BB) phytoplasma
and other phytoplasmas classified in group I, subgroup A (subgroup I-A,
tomato big bud phytoplasma subgroup). Disease management depends upon the
crop involved. Monitoring of leafhoppers and early detection of AY yellows
symptoms are important for those crops in which hand-removal of diseased
plants is feasible. For field crops, there are very few management options
available. Crop rotation will not reduce aster yellows, because it is not
a soil-borne disease, and most crops are susceptible to the phytoplasma.
There are no fungicides available to control aster yellows. I rather doubt
that there are varieties that possess resistance to the AY phytoplasmaref1,
ref2.
tomato
big bud phytoplasma (a.k.a. tomato big bud mycoplasma-like organism),
reported mainly from regions outside the EPPO region, causes a disease
similar to potato stolbur and some taxonomists regard them as synonymous.
a new phytoplasma related to potato stolbur phytoplasma was detected in
potato (Solanum tuberosum) using PCR samples collected in Texas
and Nebraska in 2005. The report is noteworthy because the pathogen causes
discoloration of potato tubers that may result in rejection of a shipment
for the chipping industry. The main vectors are insects of the leafhopper
family (Macrosteles sp., Hyalestes sp.). The disease is found
in Central and in southern Europe, as well as the Middle East, the USA,
Australia, and Asia. Stolbur is classified as a quarantine parasite in
the European Union. Destruction of alternative hosts and the use of certified
seed pieces are the main tools to manage these kinds of diseasesref1,
ref2,
ref3
=> corn stunt disease (CSD) : beyond stunting of plants, it
causes production of multiple ears that fail to fill. In the fall, leaves
in the upper portion of infected plants take on a reddish color. It is
of significant economic importance in a number of Latin American countries.
It occurs from the southern U.S. states to Brazil and Peru. Sk and the
maize
bushy stunt phytoplasma (MBSP) together with maize
rayado fino virus constitute the CSD complex. Using a PCR assay
for Sk, the pathogen was found in El Salvador, Guatemala and Panama. Significant
yield reductions can follow from dual infections of Sk and MBSP. Disease
management depends heavily on cultural practices (disking fields containing
volunteer corn, herbicide applications to eradicate alfalfa). In California,
all current commercial cultivars of field and sweet corn are susceptible.
Generally, insecticides are ineffective in controlling the corn leafhopper
(Dalbulus
maidis), which is common throughout the southeastern and southwestern
U.S. : brownish or tan in color and less than one-eighth of an inch long,
it is the only vector of corn stunt disease in California.
Proteobacteria
Alphaproteobacteria
Rhizobiales
Rhizobiaceae
Candidatus Liberibacter is a fastidious prokaryote that remains
refractory to culture on artificial media
Candidatus
Liberibacter africanus (South African form/strain, which induces
severe disease symptoms on citrus between 22-24°C), vectored mainly
by Trioza
erytreae
Candidatus
Liberibacter asiaticus (heat-tolerable Asian form, which induces
symptoms in warm climates (27-32°C)), vectored mainly by Diaphorina
citri (Dc). Dc has been recorded in South, Central, and North America
(Florida and Texas), West Timor, in several districts of Timor-Leste and
in the north of the Indonesian province of Papua (formerly Irian Jaya)
on the island of New Guinea. HLB was recently found at Sorong and Jayapura
in northern Papua.
=> citrus huanglongbing (HLB) / citrus greening disease. The HLB
agent is spread by propagation, and, by 2 citrus psyllids which can vector
either pathogen. Most citrus cultivars, except pumello, are susceptible
to the Asian form. There is no cure for the disease at present. Trees gradually
decline in vigor and yield, and eventually die. The best control for HLB
is exclusion. In areas where HLB has been established, management to reduce
losses include propagation of HLB-free trees for planting, reduction of
the psyllids populations by removing species which continually flush, application
of insecticides when threshold population levels are attained, and by pruning
symptomatic sectors from the trees. Use of parasites to control psyllid
populations has been successful in Reunion and some other areas. Before
the development of shoot tip-grafting methods to eliminate graft-transmissible
pathogens, budwood was therapeutically treated at an elevated temperature,
up to 60 deg C, for a few minutes before propagating. > 20 plant diseases
are associated with, or known to be caused by, these bacteria-like organisms,
which range in size from 0.25 to 0.5 by 0.8 to 4.0 mm.
HLB has been reported in India, Asia (Papua New Guinea, East Timor, but
not Australia), Southeast Asia (including Indonesia and The Philippines),
the Arabian Peninsula, in South Africa, in south Miami-Dade County (Florida,
USA) and in in Sao Paulo's orchards, Brazil (the state produces about 90%
of Brazil's frozen concentrated orange juice (FCOJ) exports, and, around
half of the world FCOJ market). A similar disease (cucurbit yellow vine
disease) has been reported to infect cantaloupe, pumpkin, squash and
watermelon in the USA (Oklahoma, Texas, Tennessee, Massachusetts). HLB
is the major constraint to citrus production, affecting 29 countries in
Asia and Africa. Infected citrus trees in Brazil have been by officials
to be infected with the most dangerous strain of HLB (Candidatus Liberibacter
asiaticus). Its arrival in Brazil signals probable spread to citrus
groves in Brazil and possibly to other citrus-growing areas in South America,
thus possibly exposing citrus groves in Central and North America to infection.
The HLB bacterium infects nearly all citrus species, cultivars, and hybrids
and some citrus relatives. Prevention of spread is the best control for
HLB. HLB symptoms are similar to other decline diseases such as citrus
blight and citrus tristeza and develop slowly, and infected trees may not
be recognized as those of a new disease. In areas where HLB has been established,
management to reduce losses include propagation of HLB-free trees for planting,
reduction of psyllid populations by removing species which continually
flush, application of insecticides when threshold population levels are
attained, and by pruning symptomatic sectors from infected trees. Disease
management includes heat treatment to eradicate the pathogen in budwood.
The most effective method of preventing the disease is to control the insect
vectors. Agricultural practices, including the careful selection of vector-free
production areas, good crop husbandry, and careful selection of trees,
are key to successful management. The HLB bacterium can cause catastrophic
losses of an important crop. Infection rates of up to 95% have been seen
in Thailand, and crop losses of 100% have been reported in some areas of
South Africa, resulting in destruction of entire crops. It invades conducting
tissues, causing a decline of citrus trees and rendering them unproductive.
Affected trees citrus trees may live for 5-8 years and never produce usable
fruit. HLB probably originated in China. Once a tree has been infected,
it cannot be 'cured' of HLB. Where the disease exists, management strategies
rely on preventing its spread into uninfected areas. A variety of measures
are employed, including regulation of the movement of propagating material,
destruction of infected trees, and control of insect vectorsref1,
ref2,
ref3,
ref4,
ref5,ref6,
ref7,
ref8,
ref9,
ref10,
ref11,
ref12,
ref13,
ref14,
ref15,
ref16,
ref17,
ref18.
The Asiatic or oriental citrus psyllid, Diaphorina citri [Dc], is
widely distributed in southern Asia where it has been a major pest of citrus
in several countries, particularly India, where there has been a serious
decline of citrus in recent years. Dc had not been recorded to occur in
North America or Hawaii but was reported in Brazil, by Costa Lima (1942;
Rio de Janeiro) and Catling (1970). However, in June 1998, Dc was detected
in Florida, distributed along Highway 1 on the east coast of Florida, from
Broward to St. Lucie counties, but was apparently limited to dooryard host
plantings at the time of its discovery. By September 2000, Dc had spread
to 31 counties in Florida (Halbert 2001). Dc and one of its parasites are
also present in the Rio Grande Valley of Texas. Both species appear to
have been accidentally introduced in the spring of 2001 on potted Murraya
originating in Florida. The fastidious bacterial pathogen Serratia marcescens
[Sm], which causes HLB, exists in sieve tubes. Electron microscopy, using
serial sections and a 3-dimensional configuration confirms the presence
of mature forms of the pathogen, generally rigid rods with dimensions ranging
from 0.25 to 0.5 by 0.8 to 4.0 mm. The cells
are pleomorphic, and produce flexible elongated rods which grow into new
organisms. Multiplication is generally accomplished by budding, less frequently
by binary fission or beading. Since 1988, cucurbit crops, particularly
watermelon, cantaloupe, and squash grown in Oklahoma and Texas have experienced
devastating losses from cucurbit yellow vine disease (CYVD), caused by
Sm. Squash bug [Anasa tristis] is a putative vector of the pathogen.
In 2000-01, overwintering populations of the squash bug collected from
DeLeon, TX were tested for their ability to harbor and transmit Sm. Individual
squash bugs (n = 76) were caged for a 7-day period on a series of at least
4 squash seedlings. 3 studies were conducted, one with insects collected
in November placed on 1st leaf-stage seedlings and the 2nd and 3rd with
insects from an April 2001 collection placed on 3-5 leaf-stage squash.
Controls consisted of squash seedlings caged without insects. Squash bug
transmission rates of the pathogen in Studies I-III were, respectively
20, 9.1, and 3.6%. Overall, 10.5% of the squash bugs harbored and successfully
transmitted the bacterium to squash seedlings. All control plants were
negative for CYVD symptoms or presence of Sm. Female squash bugs killed
a significantly greater proportion of young 1st leaf-stage seedlings than
males. Feeding on 3-5 leaf stage squash resulted in no plant mortality
regardless of squash bug gender. This study demonstrated that the squash
bug harbors Sm in its overwintering state. The squash bug/Sm overwintering
relationship greatly elevates the pest status of squash bug and places
more importance on development of integrated strategies for reducing potential
overwintering and emergent squash bug populations. Dc is often referred
to as "citrus psylla", but this is the same common name often applied to
Trioza
erytreae, the psyllid pest of citrus in Africa. To avoid confusion,
T.
erytreae should be referred to as the African citrus psyllid or the
2-spotted citrus psyllid (the latter name in reference to a pair of spots
on the base of the abdomen in late stage nymphs). These 2 psyllids are
the only known vectors of the etiologic agent of citrus greening disease
and are the only economic species on citrus in the world. 3 other species
of Diaphorina have been reported on citrus (2 in Swaziland, one
in India), but these are non-vector species of relatively little importance.
Dc ranges primarily in tropical and subtropical Asia and has been reported
from the following geographical areas: China, India, Myanmar, Taiwan, Philippine
Islands, Malaysia, Indonesia, Sri Lanka, Pakistan, Thailand, Nepal, Cecum,
Hong Kong, Ryukyu Islands, Afghanistan, Saudi Arabia, Reunion, Mauritius,
and Brazil. The discovery of Dc in Saudi Arabia (Wooler et al., 1974) is
the 1st record from the Near East. T. erytreae also occurs in Saudi
Arabia, preferring the eastern and highland areas where the extremes of
climate are present, whereas Dc is widespread in the western, more equitable
coastal areasref1,
ref2,
ref3,
ref4,
ref5,
ref6,
ref7,
ref8,
ref9
Epidemiology : Rs is thought to have originated
in the temperate highland regions of Peru but has subsequently spread to
Europe, Asia, South and Central America, and Australia, as 25-30°C
is the optimum temperature for the strains. In February 2003, Rs race 3,
biovar 2, not known to occur in the USA, was detected and confirmed in
geraniums imported from Kenya and eradicated. Subsequently it occurred
again in late December 2003 in geranium imported from Guatemala. Some control
actions have already taken place, and importations into the United States
have ceased. Most races of the bacterium, and their associated diseases,
appear to be limited to tropical, sub-tropical and warm temperate climates,
and thus pose no long-term threat to agriculture in cool temperate climates.
However, Rs race 3, biovar 2A, which has a very wide host range, is now
considered to be a quarantine pest in the more temperate regions of Europe,
Canada, and the United States, primarily on potato and tomato as well as
on some weed species which would serve as inoculum sources. Bacterial wilt
of potato has been estimated to affect about 3.75 million acres in around
80 countries, with global damage estimates currently exceeding $950 million
per annum. Consequently, race 3 (biovar 2A) is listed as a quarantine pest
in Canada, Europe and the USA. Of major significance is that race 3 infects
also geranium (Pelargonium spp.), and infected plants have entered
the flower trade. Disease management requires regular disinfection of all
hand implements, use of disinfectant foot baths at entry points to each
production glasshouse, washing of hands, wear newly laundered clothing
daily, destroy weeds that are potential hosts of Rs in and around glasshouses,
and use effective disinfectants such as quaternary ammonia, peroxygen compounds
and bleachref1,
ref2,
ref3,
ref4,
ref5.
=> wilt disease in several important agricultural crops such
as potato (potato brown rot
(PBR)), tomato, pepper,
and eggplant.
Rs can survive for several years in the soil and also remain alive
on host plants belonging to the Nightshade family (tomato, nightshade,
capsicum, aubergine, tobacco, etc.) as well as other plants. It is spread
by irrigation water or by infected seed potatoes. There are 3 races of
Rs on the basis of pathogenicity. Within the species 38 RFLP groups have
been distinguished, and they form 2 genetically
distinct major divisions with origins in Australasia and the Americas.
The host range, which includes over 200 plant species, is one of the widest
of all the phytopathogenic bacteria. Species infected by Rs include the
Solanaceae,
but > 50 other plant families also contain susceptible species. Worldwide,
the most important are: tomatoes, Musa spp., tobacco, and potatoes.
Many weeds are also hosts of the pathogen and therefore increase the potential
of Rs to build up inoculum. Different pathogenic races within the species
may show very limited host ranges.
race 1 affects tobacco, tomatoes, potatoes, aubergines, diploid bananas,
and many other (Solanaceous) crops and weeds, and has a high growth temperature
optimum (35-37°C)
race 2 affects triploid bananas and Heliconia spp., and has a high
temperature optimum (35-37°C)
race 3 biovar 2 has a lower temperature optimum (27°C) and affects
mainly potatoes and tomatoes.
A considerable number of additional symptomless weed hosts have been reported,
which may enable race 3 biovar 2 to survive in latent form, or in their
rhizosphere. Several weed species commonly inhabit edges of waterways,
thus providing an inoculum source. There are also reports of natural occurrence
of race 3 biovar 2 in Pelargonium hortorum. Within the EPPO-region,
race 3 biovar 2 (equivalent to biovar 2), is present and has potential
for spread. Rs is a contentious topic in agricultural trade negotiations
in the EU and is subject to strict quarantine and eradication regulations
in the USA. No economically feasible controls exist. Avoid planting on
land with a previous history of BW. Instead, grasses, legumes, and cucurbits
should be planted to reduce inoculum of Rsref1,
ref2,
ref3.
Transmission : through soil, contaminated
irrigation water, equipment, or personnel. Rs does not readily spread from
plant to plant via splashing water, casual contact, or aerially.
Signs : in geranium are wilting of leaves
and/or abnormal yellowing of lower leaves
Moko disease of banana
is caused by Rs, race 2 (biovar 1). The disease occurs in Trinidad, Amazonian
Brazil, Peru, Guatemala, southern Mexico, Grenada, Philippines, and Central
and South America. Moko disease is considered a greater threat to both
commercial and subsistence farmers than Fusarium spp. and Sigatoka
leaf spot of bananas. > 85 000 farmers grow bananas on about 10 000 hectares
of land in several parishes. The industry earned > USD 27 million in 2003
and is a constant cash flow for thousands in barely marginal existence.
Rs also infects tomato, taro, and coconut. Unfortunately there is no known
resistance to Rs. The pathogen is spread rapidly by insects contaminated
with bacteria following foraging on infected floral tissues. Disease management
is difficult and expensive, and can only be effectively implemented on
large commercial plantations due to cost. Recommendations to restrict the
spread of the disease include weekly inspection of crops for symptoms and
strict implementation of standard phytosanitary measures. Replanting of
any field with banana, plantain or other host crops should be prohibited
for > 1 year after infected plants have been killed. Movement of vehicles
from an infected farm to other banana or plantain fields should be prohibitedref
Prevention : spread can be controlled in greenhouses
by application of sound sanitation practices. Key management strategies
include use of strict phytosanitary regimens to eliminate the pathogen
and the use of certified disease-free seed. According to Antec International,
a balanced, stabilised blend of peroxygen compounds, surfactant, organic
acids, and an inorganic buffer system [Virkon-S (source : Antec International)]
is recommended as a means of controlling Rs. A continuing problem in some
circumstances is infection of solanaceous plants near potato washing and
waste operations. Runoff of contaminated water leads to infection of reservoir
hosts such as Solanum dulcamara (climbing nightshade) along waterways,
thus perpetuating these 2 pathogens.
=> a quarantine pest for Israel, has been found infecting watermelon
(Citrullus lanatus) and melon (Cucumis melo) at a limited
number of production sites. Bacterial fruit blotch has great potential
to cause significant economic losses to cucurbit production and has been
responsible for up to 90% losses of marketable yield in some watermelon
fields. Although all cucurbits are susceptible, bacterial fruit blotch
is only a problem on watermelon. The fruit symptoms (irregularly shaped
water-soaked lesions with cracks) that are most obvious and distinctive.
Fruit blotch can be introduced in infected seeds as part of the international
seed trade. PCR-based detection methods in seed are being developed.
Use of clean seed and disease-free transplants is necessary in order to
manage the disease. Because the pathogen is seedborne, and a significant
portion of commercial watermelon fields are planted with seedlings raised
in greenhouses or other transplant production facilities, recognition of
symptoms on seedlings is important. Control in the field involves rotation
out of cucurbits and control of volunteer watermelon plants. Sprinkler
irrigation can lead to spread through the fieldref1,
ref2,
ref3,
ref4.
=> fire blight in apple and pear. Management of Ea is a major
problem for tree fruit growers and an irritating nuisance for growers of
ornamental fruit trees. Removal and burning of all blighted tree limbs
and cankers is essential. There is no effective chemical control of the
disease, but elemental sulphur or copper may be of some use. Streptomycin
has been used for controlling Ea on apple and pear trees. Prevention strategies
include removal of suckers and water sprouts, avoidance of excessive water
or high-nitrogen fertilizers, and clean cultivation below trees. Resistant
cultivars, if available, should be plantedref1,
ref2.
Erwinia
persicina [Ep] (previously known as Erwinia persicinusref)
was first described in 1990 after being isolated from a variety of fruits
and vegetables, including bananas, cucumbers, and tomatoes. In 1994, Ep
was shown to be the causative agent of necrosis of bean pods and was also
reported to be the 1st human isolate of Ep. The strain was isolated from
the urine of an 88 year old woman who presented with a urinary tract infection.
By the hydroxyapatite method, DNA from this strain was shown to be 94.5%
related at 60°C and 86% related at 75°C to the type strain of Ep.
The biochemical profile of Ep is most similar to those of 2 plant pathogens,
Erwinia
rhapontici and Pantoea agglomerans, and species of
Enterobacter.
It is negative in tests for lysine, arginine, ornithine, dulcitol, and
urea and is motile and positive in tests for D-sorbitol
and sucrose. It is susceptible to the expanded-spectrum cephalosporins,
aminoglycosides, and fluoroquinolones, but it is resistant to ampicillin,
ticarcillin, and cefazolin. There have been several other bacterial plant
pathogens reported to be involved in human infectionsref1,
ref2,
ref3
=> infection of pulse crop seeds such as lentil and chickpea
is reported to cause reduced germination and stunting of seedlings. Concern
has been expressed by plant pathologists regarding spread of Er to pulse
crops in western Canada. Plants are most susceptible to Er infection at
the young pod stage. Er overwintered well in experiments conducted in western
Canada. Viable Er cells were found in 47% of seeds and in 59% of stems
left on the soil surface during the winter of 2000-2001, and survival percentage
increased markedly in seed buried at a depth of 6 cm. The fungus is an
opportunistic pathogen, reported also on bread wheat, durum wheat, and
onion. Use of disease-free seed is the best method of disease management
=> Stewart's wilt (a.k.a. bacterial leaf blight of maize) is transmitted
primarily by corn flea beetles (Chaetocnema
pulicaria) and by seed. Disease management includes using resistant
cultivars and insecticides to reduce flea beetle populations
Pectobacterium
brittle leaf is a new lethal disease of date palm (Phoenix
dactylifera). The fact that no pathogen has been identified is
not too surprising, given that other priorities may be more urgent. Efforts
will have to be directed at finding the causal agent(s). Reference to a
low molecular weight dsRNA in affected date palm is of interest but there
are dsRNAs in apparently healthy crops (for example, black-seeded common
bean) which seem to have no apparent relation to disease expression. Presumably
Fusarium
oxysporum f. sp. albedinis, the causal agent of Bayoud disease,
Fusarium
proliferatum and Erwinia
chrysanthemi have been considered as possible pathogens. The date
palm is often the only available staple food for the inhabitants of desert
and arid lands, and thus it is vital to millions throughout North Africa
and the Middle East. According to FAO, there are 90 million date palms
in the world, each of which can grow for more than 100 years. 64 million
of these trees are grown in Arab countries, which produce 2 million tons
of dates between them each year. Trees start producing after 4-5 years
and reach full production after 10-12 years. Major Arabian date palm producers
include the Maghreb countries (Morocco, Algeria and Tunisia), Egypt, Libya
and Saudi Arabia.
=> bacterial stem rot. Ecc is ubiquitous, causing disease in
glasshouse crops and appears to be present at low frequency in various
regions of Italy. 2 greenhouse pepper
(Capsicum annuum L.) isolates of Ecc characterized in this report
were pathogenic in tomato, thus possibly putting that crop at risk. Diagnosis
of the disease requires careful analysis, because the tomato pith pathogen,Pseudomonas
corrugata can be confused with Ecc. Ecc survives readily in field
residues. Disease management depends upon use of hypochlorite-treatment
of seeds, avoidance of wounding, and early detection of the pathogen. Should
an outbreak occur in glasshouse production units, all plants should be
destroyed, and the crop should be treated with fixed copper sprays. At
the close of production, all plant residues should be removed and subjected
to solarization for at least 45 days during summer.
Pseudomonas
fluorescens : strains of Pf suppress plant diseases by protecting
seeds and roots from fungal infection This occurs as a result of the production
of several secondary metabolites including antibiotics, siderophores and
hydrogen cyanide. Competitive exclusion of pathogens as the result of rapid
colonization of the rhizosphere by Pf may also be an important factor in
disease controlref1,
ref2,
ref3,
ref4.
Pseudomonas fluorescens (Pf-5) naturally safeguards roots and seeds from
infection by harmful microbes that cause plant diseases : the genome of
this microbe is composed of 7.1 million base pairsref
Pseudomonas
viridiflava [Pv] causes bacterial leaf blight of melon,
tomato
and eggplant and other food
crops. It is rarely found in the region of Asturias in northern Spain
and has been traditionally considered an epiphyte or opportunistic pathogen.
Pseudomonas
strains with an atypical LOPAT profile (where LOPAT is a series of determinative
tests: L, levan production; O, oxidase production; P, pectinolitic activity;
A, arginine dihydrolase production; and T, tobacco hypersensibility) have
been differentiated. Since 1999, a new Pseudomonas type with
an atypical LOPAT profile (convex colonies with uncharacteristic yellowish
mucoid material in hypersucrose medium [L test]; O negative; P variable;
A negative; and T positive) was frequently isolated from and associated
with disease in plants in common bean (Phaseolus vulgaris). It has
also appeared in material from other plants with disease symptoms, including
kiwifruits (from spring of 2000) and lettuce (from 2001). A novel family
of peptide antimycotics, termed ecomycins, is described from Pv. Ecomycins
B and C have molecular masses of 1153 and 1181, and they contain equimolar
amounts of hydroxyaspartic acid, homoserine, threonine, serine, alanine,
glycine and an unknown amino acid. Fatty acids were detectable after hydrolysis,
methylation and gas chromatography and mass spectroscopy. The ecomycins
have significant bioactivities against a wide range of human and plant
pathogenic fungi, including Cryptococcus neoformans and
Candida
albicans. Pv also produces what appears to be syringotoxin, an antifungal
lipopeptide previously described from
Pseudomonas syringaeref1,
ref2,
ref3,
ref4,
ref5.
=> tomato pith necrosis, is one of the most destructive diseases
of tomato in Europe. Symptoms are yellowing and wilting of lower leaves
which progressed upwards, brown areas on stems and yellow-brown discoloration
of the pith
Pseudomonas syringae pv. syringae (Pss) is a pathogen on
mango and causes citrus blast disease on trees of orange (Citrus cinensis
cv. Washington) and mandarin (Citrus reticulata cv. Marisol). Pss
is an epiphytic bacterium and usually causes damage following an injury,
such as wind damage, frost, hail, etc. Frost causes the removal of the
epidermis thus allowing the bacterium to invade floral tissues. Low temperature
and wet conditions favor disease development. Boron deficient trees are
more susceptible to disease. Disease management involves protection from
frost, removal of contaminated shoots, and use of copper sprays (Bordeaux
mixture) at bud-swelling stage. In years of heavy rainfall, a 2nd application
of Bordeaux mixture may be necessary. The 2nd link shows good pictures
of diseased tissues on pear; I could not find good photographs for citrus,
but the photographs of pear are useful and should give you a good idea
of disease symptomsref1,
ref2,
ref3.
=> bacterial speck disease in tomato.
Small (1 to 2 mm), water-soaked, dark brown-to-black spots similar to those
observed in the greenhouses of commercial seedling companies and commercial
greenhouses that produce tomato develop on the young expanding leaves of
inoculated plants within 7 to 10 days. There are 2 possible routes for
infection. The 1st is that tomato seed contaminated with Pst was used to
establish seedling transplants. The 2nd is that the seedling production
facilities were contaminated by the Pst. In either case, the bacterium
can be efficiently spread. Disease management includes use of seed produced
on disease-free plants, disease-free transplants, crop rotation with non-solanaceous
crops for at least 2-3 years between tomato crops, and resistant cultivars.
Proper sanitation such as disinfecting interior glasshouse surfaces is
strongly recommended before seeding or transplantingref.
PCR methods were developed in USA for the detection, differentiation
and quantification of Xf strains. 5 PCR systems were developed based on
the currently available genomic sequences of 4 strains: Pierce's disease
of grapevine, almond leaf scorch, oleander leaf scorch and citrus variegated
chlorosis. These PCR systems were able to differentiate each strain specifically
in suspensions containing a mixture of strains (whole bacteria or DNA)
and in DNA extractions from field-collected samples. Brazil currently produces
> 1/3rd of the world's oranges. Citrus production in several states in
Brazil is threatened by Citrus variegated chlorosis (CVC), a bacterial
disease that affects primarily sweet orange (Citrus sinensis) cultivars.
A xylem-limited gram-negative bacterium, Xf is the confirmed pathogen of
CVC. CVC symptoms include foliar necrotic spots, leaf scorch, tree-stunting,
and reduction of fruit size and yield. Xf is spread from plant to plant
by grafting with infected bud material and by sharpshooter leafhoppers
(Hemiptera: Cicadellidae). Xf causes citrus variegated chlorosis disease
in Brazil and Pierce's disease of grapevines in the USA. Both of these
diseases cause significant production problems in their respective industries.
The recent establishment of the glassy-winged sharpshooter in California
has radically increased the threat posed by Pierce's disease to California
viticulture. Control of CVC by pruning of symptomatic branches is effective
under certain circumstancesref1,
ref2,
ref3.
Xanthomonas
campestris
pv. armoraciae [Xpa] is present in the USA, Ukraine, Australia,
Japan, Brazil, China, Turkey, and India and causes cabbage leaf spot.
The disease is favored by cool temperatures in fall and winter, although
it infects susceptible hosts over a wide temperature range. Infected plant
debris is a source of inoculum and Xpa is known to be soil- and seed-borne.
Disease management involves use of bacteria-free seed, planting in well-drained
soils, and rotation of non-cruciferous crops on a 3-year cycle. Apparently
there are no tolerant or resistant cultivars.
Australia : 4 outbreaks in 2004, 1993, 1991, and 1924ref1,
ref2,
ref3.
Because symptoms are generally similar, separation of these types from
each other is based on host range, cultural and physiological characteristics,
bacteriophage sensitivity, serology, plasmid fingerprints, DNA-DNA homology,
and, by various RFLP and PCR analyses. The latter DNA-based assays demonstrate
that these strain types are genetically, as well as pathologically, unique.
The decision to destroy non-commercial citrus trees is a major departure
and it will profoundly affect residential homeowners. There is no option
but to destroy citrus trees in private backyards in order to reduce or
eliminate CC. The outbreak began almost 12 months ago; the cost so far
to growers is about $100 million; and the cost to government is another
$13 millionref
USA : Xac continues to spread in southern Florida. Eradication of infected
citrus trees is the primary means of disease management. Local spread of
Xac is primarily by wind-driven rain, overhead irrigation and contaminated
equipment and long-distant movement is by infected plant material. Much
success was achieved by implementing a policy of destroying infected trees
and pruning all green wood on trees within 50 feet of the infected trees,
but in the latest eradication program with citrus leafminer involvement,
the general policy of removing infected trees plus exposed trees within
a 1900 ft radius is now in place. This epidemic of citrus canker (1995
- present) has impacted many areas of Florida including 15 counties. Citrus
canker has erupted again in Martin County. The disease was reported on
7 Dec 2004 in 1 tree in a grove near the Indian River/St. Lucie county
line. On 25 Jan 2005 a routine Sentinel Tree Survey conducted by USDA found
3 suspected citrus trees on 2 adjacent properties in Sebastian. Officials
of the State Citrus Canker Eradication Program immediately launched a comprehensive
survey of these areas to identify the extent of the infection and to prevent
further spread. Commercial control actions (quarantine removal) were implemented
to remove 16 878 trees including 226 trees confirmed to be infected by
the citrus canker bacterium. In Florida, the predicted negative economic
impact of allowing citrus canker (CC) to become endemic clearly favors
eradication. The Florida approach to CC eradication has evolved over time.
In the first program from 1915 to 1933, infected trees were usually doused
with an incendiary fuel and burned in place. In later programs, infected
trees have been burned in place or removed mechanically. The necessity
of removing exposed -- in addition to obviously infected -- trees was recognized
in the 1986 program, and a guideline calling for removal of all citrus
within 125 ft of infected citrus was adopted based on studies of inoculum
dispersal in Argentina. In the latest eradication program with citrus leafminer
involvement), even the 125-ft radius was deemed inadequate for eradication
in most situations. The "1900-foot rule" was established in January 2000
and put in practice in March 2000, requiring the removal and destruction
of diseased citrus trees and of all citrus trees within a 1900-ft radius
of a diseased tree). The 1900-ft rule presently serves as the operational
basis of the CC eradication program. Each circle of 1900 ft radius represents
0.41 square miles (1.06 square km). The implementation of the 1900-ft rule
results in removal of the majority of dooryard citrus within infected areas.
Through risk assessment, exposure zones are determined commensurate with
the amount of disease, age of infection, inoculum dispersal opportunities,
environment, susceptibility of hosts, physical access to potential hosts
for regular inspection, plus other factors. In these exposure zones, all
citrus is removed. Guidelines call for quarantine areas to extend one to
2 miles in all directions from infected citrus. No citrus material is allowed
to move into or out of the quarantine zone unless risk-assessed. Survey
and inspection crews should practice rigorous sanitation of hands, shoes,
clothing, or any equipment that comes in contact with citrus before moving
from property to property. Quaternary ammonium disinfectants are available
for use on both inanimate surfaces and for application to bare skin and
clothing. In areas of the world where CC is endemic, disease management
involves use of resistant varieties, windbreaks to hinder inoculum dispersal
and timely applications of copper-containing bactericides. Selective pruning
of infected tissues is also utilized in citrus growing areas where labor-intensive
practices prevail. CC has been present in Florida for over 100 years :
CC may be spreading throughout the state because humans are the main mode
of its spread. Other modes of spread include overhead irrigation, flooding,
insects, and birds. Long-distance spread of CC has to be managed by preventing
the transportation of infected plant material and by using decontamination
procedures. There is no cure for CC. In areas of the world where CC is
endemic, disease management involves use of resistant varieties, windbreaks
to hinder inoculum dispersal, and the timely application of copper-containing
bactericides. These strategies are costly and not completely reliable.
Currently, the only management option for CC in Florida is to eradicate
the disease. CC has caused exceptionally high crop losses in the Florida
citrus industry. The hurricane seasons in 2004 and 2005 have taken a heavy
toll on growers. Eradication is the only option for managing the disease
for citrus growers. John-Thor Dahlburg, a Los Angeles Times staff writer,
likened 2004's hurricanes to dropping a bacteriological bomb on Florida's
already sorely challenged citrus industry, widely dispersing a virulently
contagious germ that causes CC. Florida officials say the possibility that
hurricanes could further scatter the bacteria has created the most serious
threat in decades to the state's signature crops. State agriculture officials
say they have no yardstick to determine when -- and if -- they should abandon
the attempt to wipe out citrus canker despite spending 10 years and about
$650 million in what has, so far, been a losing battle. Florida has not
decided the conditions under which it would drop its controversial eradication
policy in favor of other approaches. The ultimate cost of the eradication
program could top $1 billionref1,ref2,
ref3,
ref4,
ref5,
ref6,
ref7,
ref8,
ref9,
ref10,
ref11
=> citrus canker (CC)ref
is one of the most destructive bacterial diseases affecting citrus fruits
in Florida and other citrus-producing areas of the world. CC affects all
types of citrus, including oranges, sour oranges, grapefruit, tangerines,
lemons (Citrus
limon) and limes. Infected citrus trees undergo progressive decline
in health and fruit production and, ultimately, cease to produce fruit.
Transmission : spread locally primarily
by wind-driven rain, overhead irrigation, and contaminated equipment. Long
distance spread is by movement of infected planting material. Citrus leaf
miner (Phyllocnistis
citrella) may help spread Xac because of leaf damage due to mining
activityref1,
ref2,
ref3,
ref4,
ref5.
strain "A" affects members of the plant family Rutaceae,
including most citrus species and hybrids, especially, grapefruit, lime,
sweet lime, and trifoliate orange. All known U.S. infestations have been
associated with the "A"
strain "B" infects lemons in Argentina, Uruguay, and Paraguay
strain "C" (more cosmopolitan) infects a wider range (Mexican or
key lime, sour orange, Rangpur lime, sweet lime, citron, and occasionally,
sweet orange, and mandarin orange) and infects only Mexican lime in Brazil
strain
Disease management relies on the use of more
resistant types of citrus, such as Valencia oranges and mandarins, use
of cultural practices that reduce disease severity (allowing vegetation
to reduce wind-blown sand, planting of windbreaks, and, avoidance of working
in infected areas when trees are wet from dew or rain, because bacteria
ooze from lesions onto moist surfaces). Frequent applications of copper-containing
bactericide sprays have been shown to be somewhat effective in suppression
of the disease but are not cost effective. There is no known chemical compound
that will destroy the bacteria within the plant tissue. In order to eradicate
the disease, infected and exposed trees must be cut down and disposed of.
Xanthomonas
axonopodis pv. phaseoli [Xap] : comparative tests (1995-1998)
have evaluated several semi-selective media for use in the detection in
bean
seed. 2 media XCP1 and MT have been chosen for their ease of use and selectivity
for Xap. Both media rely on the ability of Xap to hydrolyze starch. The
fact that a PCR-based system for detection of Cff was recently developed
in Italy suggests that development of a similar system for Xap might be
worth investigating
Xanthomonas
axonopodis pv. vesicatoria [Xav] has been in Turkey for
some time. Long-distance spread of the pathogen in the country is likely,
mainly by movement of infected or infested tomato seed. The fact that Xav
has infected tomato may be the consequence of environmental conditions.
Xav is comprised of strains (races) that infect only sweet pepper
or tomato (Lycopersicon
esculentum), or both crops
=> banana bacterial wilt (BBW), 1st reported in Ethiopia, caused
only minor damage, because banana
production was practiced on a small-scale basis. It is also known to cause
wilt of ensete, a variety of banana found in Ethiopia. Its spread to Ugandaref
and other areas of eastern Africa is a direct threat to banana, which is
a staple food crop, and over 90% of production is from smallholders for
home consumption or local trade. BBW erupted in Bulyanti village, Kyabaala
parish, in Mukono district in September 2001 and has spread to 21 of the
56 districts by August 2004 and 33 in August 2005. In the 1970s, Uganda
produced between 15 to 20 tonnes of bananas per acre but yields are currently
about 6 tonnes per acre. High-density production of banana in Uganda is
intensive and thus disease spread is rapid and difficult to control. The
mode of transmission suggests that Xcm may spread by aerosol or by insects.
Although the only eradicative procedure is burning of affected plants,
disease management in the long term must depend upon selection or development
of resistant cultivars. It would be interesting to know whether there are
differences in the genotypes of Xcm collected from different areas in Africaref1,
ref2,
ref3,
ref4.
. Major banana-producing countries such as Uganda, with 10 million tons
annually, Rwanda, with 1.5 million and the Democratic Republic of the Congo
(DRC), with 1 million, are experiencing sharp losses due to attacks by
Xcm. At Goma, in the DRC's eastern province of Nord-Kivu, the price of
wine bananas and cooking bananas has doubled, resulting from losses of
60%. Production in Kichanga and Rutshuru has fallen by around 60%, and
they have been forced to turn to producers in the area of Bweremana, 50
km from Goma. Even with that, they are not managing to satisfy the increasingly
important Rwandan and Ugandan demands. According to initial estimates,
only 8 of 2500 hectares of the region's plantations already infected have
had their plants uprooted. It is difficult to eradicate BBW once it has
become established in smallholder production systems, and outbreaks must
be managed effectively and quickly to prevent the spread of the disease.
Disease management strategies used include disposal and destruction of
infected plants, disinfection of tools in managing the plantation, avoidance
of planting materials from infected fields, removal of male buds (to reduce
insect transmission of the disease), keeping browsing animals out of infected
fields, replacing bananas with another crop for at least 2 years, and use
of quarantine measures to prevent introduction of BBW into new areas. Strict
discipline by farmers to avoid transmission on contaminated tools and crop
residues can help halt the advance of BBW. Infected trees have to be burned.
For him and his neighbors, it is a matter of preventing the disease spreading
from plant-to-plant. Farmers are not always prepared to make such a sacrifice.
Reluctance to uproot their banana plants makes the battle against this
scourge difficult. There are no known resistant cultivars. Strict application
of phytosanitary practices are requiredref1,
ref2,
ref3,
ref4,
ref5,
ref6,
ref7,
ref8,
ref9,
ref10
=> bacterial leaf blight [BLB] of rice.
They have reduced Asia's annual rice production by as much as 60%. In Japan,
about 300 000 to 400 000 hectares of rice were affected by BLB in recent
years. 20-50% yield losses have been reported in severely infected fields.
In Indonesia, losses were higher than those reported in Japan and in India,
millions of hectares were severely infected, causing yield losses = 6-60%.
Removal of weed hosts, rice straws, ratoons (sprouts from the root or crown),
and volunteer seedlings is important to reduce infection. Maintaining shallow
water in nursery beds, providing good drainage during severe flooding,
and plowing under rice stubble and straw following harvest are also useful
management strategies. Proper application of fertilizer, especially nitrogen,
and proper plant spacing are recommended for management of BLB. Planting
resistant varieties is the most common and effective approach to management
by farmers in Asia. When different strains of bacteria are present, it
is recommended to grow resistant varieties possessing field resistance
genes. Let the paddy go to fallow and allow it to dry thoroughly. Seed
treatment with bleaching powder (100 mg/ml)
and zinc sulfate (2%) reduce bacterial blight. Control of the disease with
copper compounds, antibiotics, and other chemicals has not proven highly
effective.
=> clubroot (CR) remains one of the important diseases affecting
members of the mustard family (Cruciferae). It is a soilborne disease
of field crops such as canola, mustard, cabbage, broccoli, cauliflower,
radish, and turnip. Clubroot is not a new disease and is common in British
Columbia and eastern Canada. Given the previous reports of clubroot in
home and market gardens, it is possible that vegetable gardens may be acting
as initial foci of infection, particularly if growers are unknowingly importing
contaminated transplantsref1,
ref2,
ref3.
CR is a soil-borne disease that affects crucifer crops, including cabbage,
broccoli, cauliflower, canola and mustard. The disease is found in many
parts of the world. In Canada, it has been a problem for commercial vegetable
producers in British Columbia, Quebec and Ontario. According to Kent MacDonald,
P.Ag., CCA, crop specialist with Agriculture Alberta, there were no reported
disease problems with canola during 2004. In 2005, however, there were
reports of CR in several new fields in the Edmonton area. CR is especially
problematic because the fungus persists in soil for many years, and there
are no crop protection products currently registered for its use in Canada.
Plasmodiophora
brassicae Woronin causes CR. It infects the roots and causes formation
of irregular club-like galls. These galls restrict the flow of water and
nutrients to leaves, stems and pods. Plant symptoms include wilting, stunted
growth, yellowing, premature ripening and shriveled seed. Plants infected
early in the growing season may resemble those suffering from heat or drought
stress. Crops that have finished flowering may express symptoms resembling
sclerotinia stem rot or possibly fusarium wilt. In most cases, CR can be
diagnosed by a close examination of the root system. Based on using CLIMEX,
a computer software program designed to predict potential distribution
and relative abundance of species (insect, disease, etc), the Edmonton
region was likely regarded as one of the few areas of western Canada where
CR would induce significant economic crop loss. Other Alberta areas with
similar climatic conditions still have the potential for CR development
and need to be aware of the potential significance of the disease. Although
CR problems are not widespread, the economic impact of the disease can
be significant for individual producers. MacDonald says that canola yield
losses from research data indicate that CR infestations are approaching
100 per cent, leading to yield losses of 50%. The percentage of yield loss
from CR is generally half of the percentage of infected plants. There is
no real cure for CR. The best management strategy is prevention, and that
includes: long rotations (4 years) between canola crops as the single most
important preventative strategy. Fields that have CR problems have a history
of short (often 1-in-2 years) canola rotations. Lengthening the canola
rotation may reduce profitability in the short term, but the long-term
gains will be substantial if the longer rotation prevents CR. Field equipment
requires application of phytosanitary measures such as cleaning soil from
equipment, including tires; and avoiding hay and straw purchases from regions
known to be infested or suspected to be infested with CR because straw
and hay could be carrying soil and the CR pathogen. Once land is infected
with CR, management strategies are more difficult and/or expensive. Canola
should not be seeded on infected land for 5-7 years. The CR pathogen can
survive in soil for up to 17 years, so a 5-7 year break from canola may
not eliminate the problem. The extended rotation away from canola must
also include diligent control of species susceptible to CR. Volunteer canola,
weeds in the mustard family, dock, hoary cress, orchardgrass, red clover,
red-top, and perennial ryegrass will minimize soil erosion with zero or
minimal tillage. Since CR is a soil-borne disease, the fungus will move
with wind or water-eroded soil. There is evidence that liming
soils to pH 7 or higher will reduce the viability and longevity of
spores in the soil. CR is a very difficult disease to manage, and heavily
infested areas may have to be abandoned for crucifer production. Some control
may be achieved with the following measures: use a good crop rotation program,
growing crucifers on the same soil no more than every 3rd or 4th year,
is essential to retard development of a large population of spores on land
not already heavily infested; liming (calcite) soil to pH 7.2 or above
may be helpful but avoid raising the soil pH too high so as to interfere
with growth of succeeding crops other than crucifers; planting with pathogen-free
plants in pathogen-free seedbeds and uninfected plants is essential to
prevent introduction of the disease; application of a fungicide in transplant
water or rototilled in a band prior to planting may help to reduce disease
development; clean and disinfect all machinery before moving it from infested
to non-infested land and use resistant cultivars if available, although
plant resistance has not been very useful in CR control because of rapid
development of new races of the fungusref1,
ref2,
ref3,
ref4,
ref5
Macrophomina
phaseolina (Mp) is a highly variable fungus, with isolates differing
in microsclerotial size and the ability to produce pycnidia. The pathogen
infects and causes diseases of canola,
corn/maize,
soybeans,
and sunflower. It
is a weak pathogen killing plants that are stressed, especially by high
temperatures. It is an important pathogen in southern USA, Mexico, and
Africa. Sclerotia survive in soil, thus providing inoculum for future infections
of the crop. Crop rotation, use of early maturing varieties to avoid late
season heat/drought stress, and water management are methods used to manage
the diseaseref1,
ref2
The fungus associated with mango scab in Queensland has been compared
with the type collection of Sphaceloma mangiferae, and found to
be conspecific with that taxon. Morphological characteristics indicate
that it is placed incorrectly in Sphaceloma, and the new combination
Denticularia
mangiferae is proposed. Pathogenicity to mango leaves has been demonstrated
with a culture isolated from mango in Queensland, and with inoculum taken
directly from sporulating leaf lesions. Elsinoe mangiferae has also
been reported to cause a similar disease in Australia in January 1997 as
a result of intense investigation into severe scarring and distortion of
mangoes in the Darwin rural area of the Northern Territory. Both pathogens
can cause severe infections, resulting in development of scar tissue and
fruit drop. Mango scab is usually not important in commercial groves, because
fungicides containing copper also control scab. Infection in nurseries
can be prevented by frequent sprays of neutral copper on young leavesref1,
ref2,
ref3
=> grape
anthracnose. The fungus overwinters in infected plant material. In
the spring when the temperature is > 2.2°C, spores are spread by wind
and splashing rain and can infect all aboveground parts of the plant. However,
warmer conditions (up to 32.2°C) promote more severe infections. The
primary winter survival mode for the fungus is in mummified berries and
in other infected plant material. Management of grape anthracnose disease
consists of the following procedures: 1) pruning and destroying diseased
plant material while they are dormant to reduce the potential for disease
in the following year; 2) removing wild grapes in the vicinity because
they can harbor pathogens; 3) avoiding planting anthracnose-susceptible
grape cultivars; 4) and promoting drying of the canopy by pruning, training,
row orientation, and proper spacing. Grapes in New Zealand are treated
with regular dormant and regular fungicide sprays during the seasonref1,
ref2,
ref3,
ref4
Leptosphaeria
maculans (a.k.a. blackleg of rapeseed fungus) (anamorph = Phoma
lingam) causes the most important disease of canola
(Brassica napus) worldwide, especially prevalent in Australia,
Canada, France, Germany, and the United Kingdom). Isolates can be categorized
into 4 pathogenicity groups (PGs) on the basis of the interaction phenotypes
(IP) on the differential canola cvs. Westar, Glacier, and Quinta by using
a standard screening protocol in the greenhouse. Isolates in PG1 are weakly
virulent as they generally cause superficial lesions on the leaves. However,
isolates in PG2, PG3, and PG4 are highly virulent because they can produce
stem canker at the base of the canola plant, causing significant yield
loss.
=> black leg / Phoma stem canker. Disease management includes
cultural control, fungicides, and genetic resistance. Weeds and volunteer
canola must be controlled. Pathogen-free seed should be used. Lm survives
on stubble, so fields affected by the pathogen should undergo crop rotation
for at least 3 to 4 years, and new plantings should be at least 500 metres
from such fields. Seed treatment with fungicides (benzimidazole, dicarboximide,
and morpholine) results in almost complete elimination of seed transmission
of the pathogen. Resistant cultivars are the most important and sustainable
means of blackleg control, but the choice of cultivars depends upon availability
and the strain of Lm in the production area. Blackleg in western Canada
will continue to change, and new strains will continue to appear in canola
fields. Farmers will have to be prepared to adapt to new varieties and
means of identifying new strains of the pathogen. The industry's action
plan for coping with new disease strains includes ongoing evaluation of
varietal resistance over time, developing a system to identify new strains,
and developing polygenic resistance to the blackleg pathogen. New strains
(PG3 and PGT) were identified in 2003. Most current commercial varieties
appear to have resistance to the new PG strains, but pathologists agreed
they can't yet advise growers which ones may be resistant. Disease management
depends upon planting canola no more than once in 3 years and choosing
varieties rated as resistant or moderately resistant to blacklegref1,
ref2.
Most isolates of L. maculans in western Canada belong to PG2, but
PG3 and PG4 isolates were recently found in Manitoba. PG3 isolates are
aggressive to Q2 and Defender, and additional susceptible cultivars will
undoubtedly be identified in future. This does not mean that all varieties
will be attacked by PG3, because genes conferring resistance to PG3 have
been probably incorporated into many current canola varieties. Varieties
originating from areas where PG3 is endemic have long been used to breed
Canadian canola, so resistance genes have almost certainly been introduced.
PG3 distribution in western Canada is currently unknown, but the strain
may already be present in Canadian blackleg nurseries, so many varieties
may have already been "pre-screened" for resistance. The appearance of
PG4 may be evidence of pathogen population changes occurring under high-selection-pressure
exerted by resistance genes in commercial cultivars, or through importation
of PG4 isolates with canola seed. Australian plant breeders identified
a new source of blackleg resistance Brassica
sylvestris [Bs], a wild relative of canola. The
resistance was successfully incorporated into canola, resulting in
an almost immune response to blackleg. After further breeding, Pacific
Seeds released varieties for the Australian market in 2000, and their adoption
by growers has led to substantially reduced yield losses associated with
blackleg. However, in early 2003, Pacific Seeds issued a press release
stating that blackleg stem cankers had been observed on these varieties
which had previously been immune to blackleg. In addition to the 2 sites
identified by Pacific Seeds (Port Lincoln, SA and Cudal, NSW), Agriculture
WA also reported the breakdown of Bs resistance at Mt. Barker in Western
Australia. During
2003, the strain of blackleg able to attack the Bs resistance spread
across Eyre Peninsula, causing an estimated cost of 20 million dollars
to local farmers. At some locations, varieties based on this type of resistance
are now very susceptible to blackleg and may experience almost complete
yield loss. Blackleg strains able to attack plants containing the Bs resistance
appear to be unable to infect varieties containing polygenic resistance.
This development is of considerable concern to farmers and pathologists
to the say the
leastref1,
ref2.
Canola is the major oilseed crop grown in the Prairie Provinces in Canada
and its coverage area is expanding. It is also an economically important
and serious disease of canola (Brassica napus) in Australia, France,
Germany, USA and the United Kingdom. It is the most serious disease of
anola/rapeseed in the prairies, and may cause major crop losses in some
years. The infections of blackleg may occur on cotyledons, leaves, stems
and pods. Stem canker is the most serious symptom, as it can girdle the
stem, causing plant lodging leading to yield loss. 3 disease prevention
methods -- crop rotation, genetic resistance and seed treatment with fungicide
have proven to be effective. In Manitoba, L. maculans population
consists mainly of PG2 (virulent on cv. Westar; avirulent on cvs. Glacier
and Quinta) and a few PG1 isolates (avirulent on all 3 differential hosts).
PG3 isolates (virulent on cv. Westar and Glacier; avirulent on Quinta)
are found in Europe, Australia, USA and eastern Canada. The existence of
PG3 in western Canada had not been established until its isolation in 2002)ref1,
ref2.
Phaeosphaeriaceae
Phaeosphaeria
Phaeosphaeria
nodorum (a.k.a. Septoria nodorum) : an investigation spanning
some 160 years of data has shown how air pollution is linked to plant diseases.
The study reveals that industrial emissions directly affect which microbes
attack wheat. Each year, US wheat farmers lose some US$250 million as a
result of damage caused by the fungus
Mycosphaerella
graminicola. And European farmers spend about US$400 million annually
on fungicides to control the spread of this pathogen and
Phaeosphaeria
nodorum, which similarly hits crop yield. Over the course of the past
century, European farmers have seen P. nodorum become more prevalent,
and the once dominant M. graminicola fall into the background. The
prevalence of P. nodorum DNA in an archive of British wheat samples
that was started in the autumn of 1843 doesn't correlate with rising temperatures
due to global warming, but rather with changes in air pollution,
specifically with levels of sulphur dioxide, an air pollutant spewed out
by industrial installations such as coal-fired power stations. In 1844,
for example, sulphur dioxide emissions in Britain were about 1 million
tonnes a year, and M. graminicola was 3 times as common as P.
nodorum. But as this figure climbed to 6 million tonnes in 1970, the
M.
graminicola virtually disappeared, and P. nodorum exploded to
100 times its 1844 amount. With reduced coal burning over the past 2 decades
(and a subsequent drop in sulphur dioxide emissions), the ratio of these
wheat pathogens in Europe has returned to more or less the same as it was
in pre-industrial times. How exactly might pollution exert this influence
on plant disease? The fungi may react differently to increases in rain
acidity caused by sulphur dioxide, particularly when it comes to forming
reproductive spores. But he adds that the mechanism is likely to be very
intricate, involving ozone as well as sulphur dioxide.
Alternaria
alternata (Aa) is the most frequently reported Alternaria
species causing plant disease. It is primarily a weak pathogen, attacking
already stressed plants, but may also be pathogenic on healthy plants.
It is interesting to note that all of the previous posts related to Aa
concern citrus. Wounding is required, especially during harvest, leading
to post-harvest and storage infections of tubers and fruits, or by insects
and nematodes. Insects facilitate infection and act to stress the entire
host-plant system, thereby reducing overall plant resistance. Furthermore,
insects may act as vectors by dispersing inoculum throughout the crop.
Infection pathways include nutrient, water, or microclimate-originated
stresses. Recommendations for disease management include a 3-year crop
rotation for tomato or potato, planting of crops that are not hosts of
Aa, removal and burning of infected debris and eradication of weed hosts
to further reduce inoculum. Combining resistant cultivars and other control
measures greatly decreases disease progressref1,
ref2.
In India, the present approach has been to find bio-pesticides that are
free of hazardous residues and environmental pollution. In the light of
increasing awareness about adverse effects of pesticide residues in food
on human health, which is often reflected in adoption of more and more
stringent regulations by many countries, a well equipped pesticide residue
laboratory was establish at Tocklai which will direct research towards
integrated approach to pest and disease management through uses of, biocides,
parasites, predators, cultural methods and safer chemicals. For biological
control of pests, survey for natural enemy complex of pests is in progress.
Experiments on mass breeding of promising species of parasitoids and predators
of the major tea pests are also in progress under controlled laboratory
conditions. Fungal pathogens such as Trichoderma spp. are being
effectively used for the control of Poria hypobrunnea, which causes
stem canker in North-East India. Application of bioformulations of T.
harzianum
and Gliocladium virens to the soil and for wound dressing at
the time of pruning suppresses the development of canker. The bacterium
Bacillus
subtilis is effective in the control of black rot disease caused by
Corticium
invisum and C. theae. Blister blight disease caused by
Exobasidium
vexans is an important leaf disease leading to heavy crop loss in South
India and Darjeeling. Manipulation of the micro climate by shade regulation
contributes greatly reduces disease incidence. However, it will be necessary
to spray copper oxychloride to control this disease under the agroclimatic
conditions of South India. In the new planting areas, it is necessary to
avoid the planting of cultivars which are highly prone to the incidence
of major pests and diseaseref1,
ref2,
ref3
Alternaria brown spot (ABS) of tangerine hybrids is known to occur
in South Africa, Turkey, Israel, Spain, and Colombia as well as Florida
and possibly in other citrus-growing regions. The disease first appeared
in Florida citrus groves about 30 years ago and has become a serious problem
on some varieties in recent years. It was first reported in Australia in
1962, but it is not known when the fungus arrived in Florida. It is assumed
that the conditions in Iranian citrus groves are similar to those in Florida.
Fungicides are the primary means of controlling ABS. However, there are
many management practices which are helpful in reducing disease severity.
New groves should be established with disease-free nursery stock. If Alternaria
is present from the outset, it increases to high populations during the
period of vegetative growth on young trees and is difficult to control
on fruit. For new groves, it is best to locate susceptible varieties in
high areas where air drainage and ventilation are good and leaves can dry
more rapidly. Less vigorous rootstocks such as Cleopatra mandarin should
be selected rather than vigorous ones like Carrizo citrange. Groves of
Minneola tangelos in low, wet areas have conditions so favorable for
disease that ABS may be virtually uncontrollable. Trees of susceptible
varieties should be spaced more widely than oranges to promote rapid
drying of the canopy. In existing plantings, it is important not to promote
excessive vegetative growth. Overwatering and excessive nitrogen fertilization
should be avoided. Light hedging should be done frequently rather than
hedging severely but less often. For products registered for control of
Alternaria
brown spot, see the Florida Citrus Pest Management Guide. The number of
fungicide applications needed for control varies greatly with the susceptibility
of the variety and the severity of the infestation. In the worst cases,
the 1st spray should be applied when the new shoots are about 4-6 inches
long to prevent buildup of Alternaria on the spring flush. The 2nd
application should be made at petal fall. Thereafter, applications may
need to be made as often as every 10 days to achieve good control on fruit
and foliage. When frequent applications of copper fungicides are being
used, rates can be reduced to as little as one pound of metallic copper
per acre. During dry periods which often occur in April and early May,
pray intervals can be increased. Likewise, less susceptible varieties or
less severely affected groves do not need such intense spray programs.
Groves of susceptible varieties should be monitored frequently to determine
the disease status. Spraying can be discontinued in late June, since fruit
usually become resistant to Alternaria in July as fruit growth slows. It
is probably not economical to try to control the disease on late summer
flushes of growthref1,
ref2,
ref3,
ref4
=> gray leaf spot / black spot is present in all canola and
rapeseed production areas. The disease overwinters on plant debris and
seed. All above-ground plant parts are susceptible to infection from the
spores produced on plant debris or infected seed. Polish-type canola cultivars
are more susceptible than Argentine-type cultivars. Argentine varieties
have a higher yield potential and are also taller and have a higher oil
content than Polish varieties. Argentine varieties require about 95 days
to reach maturity, while Polish varieties need approximately 80 days to
reach maturity. Disease management depends upon planting certified, disease-free
seed, a rotation of 1-4 years, and control of weedy mustards and volunteer
self-sown canola. It is most likely that the introduction of grey leaf
spot was the result of planting infested seed. Fungicides containing iprodione
and azoxystrobin are registered for control of gray leaf spot on canola,
but I do not know if they are recommended for use in Argentina. Using fungicide-treated
seed may help to increase stand establishment when infected seed is plantedref1,
ref2.
Alternaria
mali (Am) is a common saprophyte (an organism capable of growth
and survival without the aid of another living organism) which can become
somewhat infectious to apple fruit that has been predisposed to infection
because of injury to the host. Common injuries that can lead to Am rot
include mechanical or chemical injury, sunscald, or chilling. Infection
can occur before or after harvest, although it is more commonly a post-harvest
problem. Am leaf spot is aggravated by European red mites. Disease management
consists of mite control, application of fungicides, and adequate tree
spacing and other cultural practices that enhance drying conditions. The
disease is managed by avoiding injury during harvest and packing. Additionally,
post-harvest fruit dips in chlorine solutions can help to prevent post-harvest
disease problems. Controlled cold storage is another good practice that
will reduce disease problemsref1,
ref2,
ref3
=> Alternaria leaf blight (ALB) of wheat
(Triticum aestivum) is generally regarded as a weak, minor pathogen
that mainly affects old local cultivars, particularly of durum wheat. The
disease is common in the eastern and central areas of the Asian Subcontinent.
ALB can be very severe if environmental conditions are favorable for disease
development; major losses can result when susceptible cultivars are grownref
Bipolaris incurvata (syn. Helminthosporium incurvatum or
Drechslera
incurvata causes coconut leaf blight (CLB). It is a minor pathogen
of coconut (Cocos nucifera)
but it can be severe in nurseries. There are no alternate hosts of CLB.
CLB is present in Australasia, Central and South America, Pacific and Seychelles.
It is an invasive pathogen and is listed as a new emerging and re-emerging
plant disease in the United States. Researchers realized that NaCl applications
could help restore infertile soils in the Philippines back to productive
plantings. In the mid-1970's, researchers found applications of NaCl would
suppress leaf spot disease caused by CLB on coconut seedlings and that
this treatment worked as well as fungicides. The relative cost of NaCl
versus chemical fungicides resulted in significant savings to farmers.
Because of lethal yellowing disease, growers are advised to plant resistant
Malayan strains, often called dwarf or pygmy coconuts, and labelled yellow,
golden, red, and green, according to the color of their fruits, such as
'Golden Malayan Dwarf'. The Malayan palms are very similar to the Jamaican
Tall except for having straight trunks. The red strain is the most rugged
of the 3 but has the least attractive foliage. The variety `Maypan', a
hybrid of Malayan x Panama Tall, has the most robust and rapid growth yet
retains its resistance to lethal yellowing disease. All Coconut Palms are
highly salt-tolerant and make nice street trees if planted when they are
tall enough. Be aware that falling fruit can damage vehicles or hit pedestrians
and the flower stalks (in spring) or developing fruit (summer) may need
to be removed. Lethal yellowing disease, virus diseases, and fungi all
affect coconut palms. Ganoderma butt rot can infect the lower trunk
and roots, and can kill the palm. Avoid injury to the palm in this area.
There is no control for butt rot, only preventionref1,
ref2,
ref3,
ref4
Bipolaris
sacchari (Bs) (Sivanesan, 1987) causes eye spot disease
in sugarcane, and wheat
stem-base disease
Bipolaris
sorokiniana (teleomorph Cochliobolus sativus) is the causal
agent of common root rot, leaf spot disease, seedling
blight, head blight, and black point of wheat and barley.
That fungus is one of the most serious foliar disease constraints for both
crops in warmer growing areas and causes significant yield losses. High
temperature and high relative humidity favour the outbreak of the disease,
in particular in South Asia's intensive irrigated wheat-rice production
systems. In general, disease management would involve use of approved seed
treatment, plowing down of crop residues, and several years of rotation
to non-cereal crops.
.. are important foliar pathogens of barley. Estimated losses worldwide
are up to 20%. Isolates derived from single conidia were evaluated for
their virulence phenotypes on 25 differential barley genotypes. In general,
the Ptft isolates exhibited a broader spectrum and a higher level of virulence
on the host differentials than the Ptfm isolates. 8 barley genotypes were
resistant to all 19 pathotypes identified and should be useful in breeding
barley for resistance to both forms of P. teres. Genetic variation
was also examined by restriction fragment length polymorphism (RFLP) analysis.
A 0.46-kb DNA fragment (ND218) generated by PCR from genomic DNA of a California
isolate of Ptft was used as a probe. Every P. teres isolate tested
with ND218 exhibited a unique RFLP pattern. Cluster analysis, based on
both the virulence phenotypes and RFLP patterns, indicates that P. teres
possesses a high degree of diversity at the species and subspecies levels.
The high degree of polymorphism revealed by ND218 will make this probe
a useful tool for the DNA fingerprinting of P. teres isolates. Sequence
analysis of the 18s rDNA revealed 100% homology between the 2 forms. This
intron distinguishes P. teres from the barley leaf spot pathogen
Cochliobolus
sativus, the symptoms of which are often confused with those of Ptfm.
The closely related P. tritici-repentis, which causes similar spot
lesions, also lacked this intron. DNA sequence analysis of the ITS1 and
ITS2 spacer regions revealed only 1.6% divergence between the 2 forms.
Disease management involves the use of seed treated with fungicide, avoidance
of direct sowing on stubble without ploughing, and starting fungicidal
treatment according to local advice when symptoms occur on one of the last
3 barley leaves. When plants are severely attacked, applications of fungicide
should commence at the one node stage to delay possible disease outbreakref1,
ref2,
ref3,
ref4
=> tan spot of wheat commonly infects wheat
in the Canadian prairies. Resistance to tan spot is not widely dispersed
in the International Maize and Wheat Improvement Center (CIMMYT) germplasm,
but moderate resistance is known to occur (Rees and Platz, 1992). Some
newer CIMMYT lines, such as Milan, Attila, Corydon and Tinamou, and some
Chinese wheats and their derivatives, such as Luan, are also reported to
carry high to moderate resistance (Diaz de Ackermann and Kohli, 1998).
Tan spot is increasing in areas where reduced tillage practices are being
combined with stubble retention. CIMMYT has an ongoing project to search
for new and better sources of resistance to tan spot for these areas. The
fungus over-winters on infected wheat straw or stubble. Spores are dispersed
primarily by wind. Wheat is the primary host, but forage grasses and rye
are alternate hosts. Barley and oats are highly resistant to tan spot.
Ways to reduce tan spot include rotating between cereal and broadleaf crops,
such as oilseeds and pulses, planting disease-free seed or seed that has
been treated with a recommended fungicide, planting cultivars with known
resistance to one or more leaf spot diseases, and, if leaf spots are present
and rain is forecast, applying a registered foliar fungicide might be advisableref1,
ref2,
ref3,
ref4
=> apple scab is a serious disease causing maximum economic
loss. A sound forecasting and early warning system has been developed for
prediction of AS. Also, a judicious fungicide spray schedule has been devised.
Under high disease pressure, systemic fungicides performed better, while
under low disease pressure, ergosterol biosynthesis inhibiting (EBI) fungicides
were as good as protectants. Ascosporic inoculum produced by over-wintered
apple leaves could be substantially reduced by giving post-harvest applications
of Bavistin (0.1%) and EBI chemicals Penconazole (0.5%) and Flusilazole
(0.01%), as pre-harvest fungicidal sprays control scab during storage.
AS survives on infected plant parts, including fruits. Disease management
depends upon spraying with proper fungicides, at the proper time of application,
at the optimum doseref1,
ref2.
India produces all deciduous fruits, including pome fruits (apple and pear)
and stone fruits (peach, plum, apricot and cherry), in considerable quantity.
These are mainly grown in the northwestern Indian States of Jammu and Kashmir,
Himachal Pradesh and in the Uttar Pradesh hills. The North-Eastern Hills
region, comprising the States of Arunachal Pradesh, Nagaland, Meghalaya,
Manipur and Sikkim, also grows some of the deciduous fruits on a limited
scale. Due to introduction and adaptation of low-chilling cultivars of
crops like peach, plum and pear, they are also now being grown commercially
in certain areas of the north Indian plains. Out of all the deciduous fruits,
apple is the most important in terms of production and extent. Based on
previous evaluation of local cultivars, a program for breeding cider apple
(Malus domestica) cultivars was initiated in the SERIDA of Asturias
(NW Spain) in 1989 with 3 major aims: to improve the durable resistance
to diseases and pests of local cultivars, to obtain cultivars with no biennial
bearing and to improve fruit quality. To achieve the 1st objective, Asturian
cultivars with low susceptibility to scab were crossed with "Florina",
which carries the Vf gene for resistance to apple scab caused by Venturia
inaequalis and shows very low susceptibility to fire blight caused
by Erwinia amylovora
and resistance to the rosy apple aphid (Dysaphis
plantaginea). The 1st cross, performed in 1989, was "Raxao" x "Florina."
After greenhouse and nursery evaluation, 34 hybrids resistant to scab (the
presence of the Vf gene has been confirmed with molecular markers) and
low susceptibility to powdery mildew (Podosphaera leucotricha) were
pre-selected. After evaluation of these hybrids against the rosy apple
aphid, fire blight, apple scab and powdery mildew, as well as characterization
of their productivity and quality, 4 hybrids were selected and are in registry
at the present time. Numerous other crossings have been performed since
then and are in different phases of evaluation and selectionref.
Dothideomycetes et Chaetothyriomycetes incertae sedis
Botryosphaeriaceae
Botryosphaeria
Botryosphaeria
rhodina (a.k.a. Lasiodiplodia theobromae, Botryodiplodia
theobromae) is a pathogen that causes fruit spot on eggplant
(Solanum melongena). Other fungal pathogens infecting eggplant
are a leaf and fruit spot caused by Phoma sp., leaf spot caused
by Cercospora melongenae and fruit rot caused by Rhizopus stolonifer
=> citrus black spot disease, one of the most serious citrus
diseases affecting citrus production in South America, South Africa, Netherlands,
and Australia. Black spot affects all commercial citrus cultivars and is
particularly severe in Citrus
limon. The disease is particularly virulent late in the season,
and postharvest losses can also occur
=> sphaeropsis rot [SR] is a newly reported postharvest fruit
rot disease of d'Anjou pears and apple. First found on d'Anjou pear, it
was shown to be much more severe on apples. In one instance, 2% of the
apple fruit in storage bins was rotted by SR after several months of storage.
SR has been recorded on d'Anjou pear and on several apple varieties (Red
Delicious, Golden Delicious, Fuji, and Granny Smith). Surveys for diseases
of stored pears in Washington State in the late 1930s and in the past 60
years did not yield detailed data. 75 distinct fungal species belonging
to 22 genera are associated with fruit rots in stored pears but no Sphaeropsis
spp. were reported in the latter study. The SR fungus grows at -3-25°C,
does not grow at 30°C but survives at this temperature. Optimum temperaturefor
mycelial growth is between 15 and 20 deg C. Conidia germinate at 0 to 30
deg C, and a minimum wetness duration of 5-6 h is required for germination
at optimum temperature. Conidia can germinate at relative humidity as low
as 92%. SR causes twig dieback and cankers on apple and crabapple trees.
'Manchurian' crabapple trees are very susceptible to twig dieback and cankers
caused by this fungus. It also appears to be associated with dead bark
or twigs on trees. Fruiting bodies (pycnidia) of the fungus are often present
in diseased tissues on infected trees. The fungus primarily infects the
stem and calyx of fruit and causes stem-end rot and calyx-end rot, respectively.
SR inoculum is apparently present in the orchard. Disease management is
relatively simple. Cankers and diseased twigs with dieback symptoms should
be removed from orchards to reduce inoculum. For orchards with a high percentage
of crabapple trees as pollinizers, pruning diseased twigs is particularly
important to disease control. Research on chemical control of this disease
is currently in progressref1,
ref2
Sphaeropsis
malorum (the imperfect stage of Botryosphaeria obtusa (Bo))
is common on dead or moribund wood of a wide range of hosts. In North America,
Bo is reported to cause an important leaf spot, canker, and fruit rot of
apple (black rot or frogeye leaf spot of apple), while in England
and New Zealand it is chiefly a weak secondary pathogen associated with,
but not necessarily the primary cause of, leaf spots, cankers, and fruit
rots. It has been associated with various wood diseases of grapevines in
several viticultural regions of the world. Frequently, it is found on tissues
that have been damaged by physical factors or killed by primary pathogens.
This species can be distinguished from other Botryosphaeria spp.
by the large, dark brown, mostly aseptate conidia, and the distinctly annellate
conidiogenous cells. It is probable that the disease is caused by a complex
of species. Control of diseases caused by Bo is difficult, as information
on disease control, especially chemical control, is very limited. Currently,
there are no fungicides registered for use against Botryosphaeria
dieback in South Africa (Nel et al., 1999). France is one of the very few
countries in which a fungicide is registered for control of black dead
arm caused by Bo, B. dothidea, and, in some cases, B. stevensii.
Sodium arsenite is recommended and must be used under the same conditions
as for the treatment of Esca disease. Good sanitation practice, specifically
removal and burning of pruning debris, is recommendedref1,
ref2,ref3,
ref4.
Other species of Sphaeropsis infect citrus. Disease management basically
requires strict attention to sanitation in orchards and the use of an appropriate
fungicidal spray regimen.
=> maize ear rot in Spain, Israel
: disease incidence can range from 1-80% of ears, and test weights can
be reduced substantially. During the 1950s and early 1960s, maize ear rot
was the most common ear rot disease of corn in the Corn Belt of USA. Disease
management for maize ear rot includes crop rotation, conservation tillage
to reduce soil erosion, and planting of
maize cultivars with a range of maturity dates
=> black leaf streak disease / black sigatoka disease (BSD)
is the most damaging disease of banana worldwide. It decreases photosynthesis,
reduces fruit size and induces a premature maturation. It reduces leaf
area, decreases yields by > 50% and causes premature ripening, which downgrades
marketability of fruit. Unable to reproduce sexually, propagation depends
upon cloning, using shoots from trees. Consequently, all banana cultivars
are almost identical and are universally susceptible to the disease. According
to FAO data from 2003, bananas rank 4th behind rice, wheat, and maize in
worldwide production, measured in metric tons. Bananas and plantains (cooking
bananas) are staple food crops for millions of people who produce the fruit
in backyards and small plots in developing countries. The disease was 1st
reported in Fiji in 1963 but was probably well established in southeast
Asia and the south Pacific before that time. It was been reported in Honduras
in 1972 and now is reported from Mexico south to Bolivia and northwestern
Brazil and in the Caribbean region. It was reported in 1996 in Trinidad
and Tobago porobably introduced from Venezuela. In 1998 it was reported
in southern Florida, probably by introduction of infected suckers from
elsewhere. It can be found all over the world with the exception of the
Canary Islands, and its management and control have become a key concern
of commercial banana producers. Disease management of large plantations
is costly ($1000 per hectare), but is more costly in smaller plantations
that cannot apply fungicides by air. Small farmers usually opt for other
control measures of control such as removal of old infested leaves, intercropping
with disease-resistant crops and planting in partial shade, which slows
the development of the disease. Disease management involves application
of protectant fungicides or systemic chemicals such as the sterol biosynthesis
inhibitor, tridemorph, several sterol demethylation compounds, and systemic
compounds such as propiconazole, methoxyacrylate, and azoxystrobin. There
is a tendency for resistance or tolerance to systemic fungicides to be
developed over time, and this is being countered by use of broad-spectrum,
protectant fungicides such as the dithiocarbamates and chlorothanlonil.
There is an intensive international effort to develop resistant hybrids
for more long-term resistance to black sigatoka. Genetic engineering may
be a possible means of producing resistant planting stock for disease control,
but that will take some considerable time to effectref1,
ref2,
ref3,
ref4,
ref5,
ref6,
ref7,
ref8,
ref9
=> red band needle blight. A number of countries in the Northern
hemisphere, including the United Kingdom, France, and Canada are reporting
an upsurge in the severity and distributionref.
Milder and wetter weather conditions are partly to blame, as the spread
of this pathogen is favored under moist, warm, light, and sheltered conditions.
This disease has become particularly noticeable over the past 2 years and
has apparently been increasing in frequency for 5 to 6 years. In the 2002–2003
period, > 25% of the trees were suffering serious defoliation in the East
Anglia forest district, where large numbers of the highly susceptible Corsican
pine are planted. New Zealand and Australia have been coping with widespread
D.
pini infection for decades and have been quite successful in protecting
their pine forests. The fungus rarely kills the tree, but the percentage
of pine needles infected is directly proportional to loss of wood yield,
so D. pini can have a severe economic impact. One new approach that
could be fruitful is to genetically engineer trees that inactivate, remove,
or prevent synthesis of toxin dothistromin by the fungus, thought
to be the primary cause of disease and is structurally related to the potent
carcinogen aflatoxin. This similarity has enabled scientists to identify
and isolate key genes involved in the synthesis pathway. One option would
be to use non–toxin-producing strains as biocontrol competitorsref
with the toxigenic fungi in the field. Others include engineering trees
that express dothistromin-specific antibodies in the needles or targeting
destruction of the toxin in the plant tissue by enzymatic means. Another
approach is the deployment of toxin transporter genes into host plants.
These transporters are normally used by the fungus to allow secretion into
plant tissue and to provide a self-protection mechanism against the effects
of its own toxin. A candidate dothistromin transporter has already been
isolated from D. pini that could be used in this way. Genetic modification
of trees is not necessarily the best option for disease management, but
in the long term, it may well be our detailed knowledge of the molecular
biology of the pathogen and its toxin that will provide the basis for sustainable
control
=> white leaf spot disease of dry
red kidney bean (Phaseolus vulgaris L.). Corresponding with
fungal growth, yellow, angular spots are observed on the upper leaf surface.
In older leaves, lesions coalesce, covering most of their surface, while
younger leaves are relatively free of symptoms. Heavily diseased plants
senesced faster and defoliated earlier than nonsymptomatic plants. Identification
of the pathogen is conducted by direct observation of infected plant tissues
with light andelectron microscopes. Conidia are hyaline, filiform, rounded
at their apex, and with no visible scar at their point of attachment to
the conidiophore. Conidia have one to 4 septa, were 57-68 mm
long, and approximately 2.4 mm in diameter.
Conidia are produced at the tip of colorless, short conidiophores that
emerge through stomata in groups of 5 or more.
Pseudocercosporella capsellae
Brassica juncea has advantages over B. napus including
more vigorous seedling growth, quicker ground-covering ability, greater
tolerance to heat and drought, and enhanced resistance to the blackleg
fungus, Leptosphaeria maculans. WLS survives on residues of infected
plants. Under favourable autumn and winter conditions, it produces wind-borne
conidia, which mainly cause leaf lesions. In turn, the conidia produced
in these lesions are carried by wind and rain to cause secondary spread
of the disease. WLS is also spread from infected seeds and from pieces
of infected debris present with the seed. Optimum temperatures for WLS
infection are 13-18°C, but high moisture levels are necessary for disease
development. WLS disease usually develops after periods of high rainfall.
It can be found in most plantings, but is not usually a cause of heavy
yield losses. WLS can cause complete loss of leaves in highly susceptible
varieties, with yield losses as high as 30% if the disease is severe. However,
losses are unlikely to exceed 5-10% with current Australian cultivars.
Nitrogen-deficient crops seem to be more severely affected by WLS. Disease
management is similar to that of blackleg which means using crop rotation
and good hygiene. Sow only cultivars expressing very high levels of resistance,
and practice crop rotation. All varieties recommended for sowing in Western
Australia have good adult plant resistance to blackleg. Canola fields should
be in a rotation for at least 3 years to allow diseased residues to decompose
and reduce the risk of ascospore infection. In recent years, some growers
have successfully reduced this break period, but there is increased risk
from this practice. If the seedling stage of crop development (cotyledon
to 1- or 2-leaf stage) coincides with heavy airborne spore discharges from
nearby stubbles, even adult resistant varieties can suffer substantial
damage. If there is no erosion risk, destroy crop residues after harvest
to reduce carryover of the fungus on infected
stems. Graze stubbles heavily to reduce fungus carryover. Canola should
be planted as far as possible from previous canola crops to reduce the
risk of infection by wind-borne ascospores. Do not plant in areas downwind
from old stubbles where the prevailing winds are likely to blow air-borne
sporesref1,
ref2,
ref3,
ref4,
ref5
=> fruit and leaf spot disease of citrus was the main disease
in western Kenya in the late 1990's. Application of various contact and
systemic fungicides (triazoles and copper) were useful
=> grapevine leaf spot in several genera of Vitaceae (Ampelopsis,
Cissus,
Parthenocissus)
and different species of Vitis are listed as hosts of Pv (Farr et
al., 1989). Pv has been found in Brazil, Europe, India, Japan, North America,
Korea, Pakistan, Saudi Arabia and South Africa (Ellis, 1971; Shin, 1997).
Pv was reported in Argentina on European grapevine (V. vinifera)
almost a century ago but no symptoms were described (Spegazzini, 1910).
Mummified fruits (dried fruits) remaining from the previous fruiting season
are the source of inoculum for the next crop season. Mummified fruit containing
fruiting bodies (perithecia and pycnidia) overwinter on ground and vines.
Fruiting bodies release spores which then infect nearby plants. Moisture
is a critical element in disease etiology. Disease management involves
use of preventative and curative fungicides, and removal of mummified fruitref.
Eurotiomycetes
Eurotiales
Trichocomaceae
mitosporic Trichocomaceae
Penicillium
Penicillium
allii, rather than P.hirsutum or P. viridicatum,
is the pathogenic species responsible for garlic crop losses during storage
due to blue mold in Argentina. This is the 1st report confirming P.
allii as a field pathogen of Allium sativum. The general problem
of correct diagnosis of Penicillium species on onions and garlic
is exemplified by this study. This plant disease in garlic is managed by
storing bulbs with a minimum of bruising, wounding, or insect damage. Prompt
curing of bulbs so the necks are dry and storing bulbs at temperatures
of 41°F (5°C) or less with low relative humidity minimizes disease
lossesref1,
ref2,
ref3,
ref4
=> powdery mildew of sugar
beet by Eg causes a serious fungal foliar disease resulting in sugar
yield losses of up to 30%. Eg occurs world-wide in all regions where sugar
beet is grown, and it also infects other edible beet crops, e.g. garden
beets, Swiss chard, and fodder beet. Eg infection of sugar beet is especially
damaging in arid climates, e.g. Mediterranean countries, the Middle East,
Idaho, Colorado, Nebraska and California. The host range of Eg is specific
to Beta species. Several powdery mildew fungicides are effective
if applied in a regular preventative program commencing with the 1st signs
of the fungus. Disease management depends upon the use of resistant cultivars,
applications of registered chemical fungicides in rotation to delay evolution
of resistant strains of Eg, crop rotation, removal of old plant debris,
and deployment of a single monogenic form of mildew resistance in lines
derived from Betamaritima. Sources of genetic resistance
to Eg are available in cultivated, and wild, Beta germplasm and
molecular markers developed linked to Eg, the only single major R gene
described so far, and also to quantitative trait loci (QTL). Production
of the perfect stage (teleomorph) of Pg and its over-wintering in western
Nebraska is cause for concern for sugar beet producers, especially in terms
of its survival as inoculum for long periods in soilref.
Eg grows on the surfaces of leaves and stems. Older infected leaves
yellow and wither, and growth of heavily infected plants is diminished.
The disease is favored by moderate temperatures. Eg produces airborne spores
that facilitate spread of the disease. Moisture is not necessary for germination
and infection, and is actually detrimental to the fungusref1,
ref2
Leveillula
Leveillula
taurica causes severe disease on pepper,
aubergine, artichoke, and other vegetables in glasshouse and field production.
Disease management involves use of fungicides. Bicarbonate solutions are
also effective in reducing damage to leaves. Unfortunately, cultivars vary
in their disease susceptibility
Podosphaera
Podosphaera
phaseoli (Sphaerotheca phaseoli) => powdery mildew on cowpea
(Vigna sinensis L.), Phaseolus spp., and Rhynchosia volubilis
in Turkey. White, epiphytic mycelia and conidia, characteristic of a powdery
mildew, are present on leaves, stems, and inflorescences. The plant tissue
underneath the mycelial patches is purplish in colour. Mycelial growth
was amphigenous, thick, forming irregular white patches, sometimes effused
to cover the whole leaf surface and had a poorly developed nipple-shaped
single appressorium. Simple straight conidiophores (115-190 x 10-13 mm)
developed mostly singly from a hyphal cell, arising from the upper part
of mother cells, and having the basal septum at the branching point of
the mycelium with a sharp constriction. Each conidiophore has 3 to 8 barrel-shaped
conidia formed in a chain. Conidia with fibrosin bodies are 28-42 x 15-18
mm
in size and germinated below the shoulder by producing a simple germ tube.
Dark brown ascomata, found on leaves and stems as embedded in the mycelial
felt, are spherical, gregarious to subscattered and measured 85 to 105
mm
in diameter. Appendages (6 to 15) are myceloid, arising from the lower
half of the ascomata, brown, paler upward and 6 to 8 micrometers wide.
The ascomata contained single ascus (65-95 x 55-67
mm).
The ascus contained 8 ellipsoidal to ovoid ascospores (18-24 x 12-16 mm)
=> cucumber powdery mildew is 1 of the world's most widespread and
damaging cucumber diseases. Px consists of several races, some of which
attack all cucurbits, while others have a host range restricted to certain
types of cucurbits. 997 cucumber (Cucumis sativus L.) accessions
from the U.S. National Plant Germplasm System (NPGS) collection were tested
for resistance to powdery mildew. Plants were evaluated and classified
for their resistance to Px. 3 susceptibility grades were used: susceptible
(S), intermediate (I) or resistant (R). 94 of 977 accessions (9.6%) contained
at least 1 I or R-type plant and 17 of the 20 most-resistant accessions
originated in Asia. Disease management depends upon use of resistant cultivars
and application of both systemic and protectant fungicides, alternating
among systemic fungicides in at least 2 chemical classes and including
a protectant fungicide in at least every other application. Resistant varieties
are being developed and are becoming an increasingly important component
of management programs. There is the danger, however, that strains may
develop which could overcome the genetic resistance of some cultivarsref1,
ref2,
ref3.
Oidiopsis
taurica Salmon (Syn. Oidiopsis sicula Scalia) is usually
found in its imperfect form, Oidiopsis taurica [Ot]. It was identified
as the causal agent of a powdery mildew disease occurring on distinct Allium
species in Brazil. This disease was initially observed in plastic house
and field-grown garlic (Allium sativum) and leek (A. porrum)
accessions in Brasilia (Federal District) and in field-grown and greenhouse
onion (A. cepa) cultivars in Belem do Sao Francisco (Pernambuco
State) and Brasilia, respectively. Typical Ot symptoms consisted of chlorotic
areas on the leaf surface corresponding to a fungal colony. These lesions
turn to a brownish color with the progress of the disease. Fungal morphology
was similar to that described for Ot. Endophytic mycelium emerging through
estomata, light pale conidia were dimorphic (lanceolate primary conidia
and somewhat cylindrical secondary conidia), fibrosin bodies were absent,
conidia formed predominantly single (not in chains), and appressoria were
non-lobed. Its sexual stage, Leveillula taurica (Lev.) Arnaud, was
not observed. Inoculations were performed with the Ot isolates from distinct
Allium
hosts. These isolates were also pathogenic to sweet pepper and tomato,
indicating an apparent absence of host specialization. One bunching onion
(A. fistulosum) accession was not infected by Ot, suggesting that
this species might carry useful resistance alleles to this pathogen. This
is the 1st formal report of a powdery mildew disease on species of the
genus Allium in Brazil. Ot might become important on these vegetable
crops, especially in hot and dry areas such as those in the Central and
Northeast regions of Brazil. Genetic resistance is not well documented,
but susceptible tomato cultivars are available. Since Ot also infects other
hosts (e.g., eggplant (Solanum
melongena) and tobacco, weed hosts such as nightshade), scouting
of these hosts can be helpful to identify potential sources of inoculum.
Chemical control is targeted at eradication of existing infections and
protection of healthy tissues. Once disease is detected, the 1st sprays
should be aimed at eradication. These are usually followed by sprays for
protection. Eradicant sprays should be applied as soon as symptoms are
first observed since early control is critical. Monitor and rotate the
types of compounds used to avoid development of fungicide resistance in
the powdery mildew population. Among the compounds registered for use are
azoxystrobin, chlorothalonil, bicarbonates, cupric hydroxide, sulfur, and
paraffinic (horticultural) oilsref1,
ref2,
ref3,
ref4.
Helotiales
Dermateaceae
Neofabraea
Neofabraea
alba (Na) (a.k.a. Pezicula alba; anamorph: Phlyctema
vagabunda) There are many fungal pathogens affecting apple worldwide.
With regard to those in Washington State, 4 species of the genus Neofabraea
are known to cause bull's eye rot (BER) of apple. Na is the main
pathogen causing BER in continental Europe, and also has been reported
as a minor disease of apple in eastern North America
Neofabraea
malicorticis causes anthracnose canker / bull's-eye rotracnose
canker of apple trees and is found principally in the more humid areas
of the Pacific Northwest (PNW). It is an aggressive pathogen able to infect
sound wood directly
Neofabraea
perennans causes perennial canker of apple trees. The pathogen
requires wounds to infect the wood, and the fungus survives in cankers
by infecting injured tissue at the border of old cankers.
N. malicorticis and N. perennans are considered a single
species in Europe, whereas they have been regarded as distinct species
in North America. A putative new species, yet to be described, has been
recorded in Australia. It was recently recorded in a phylogenetic study
of Neofabraea spp. causing tree cankers and apple BER. It was represented
by one isolate from Nova Scotia, Canada, and one from Portugal. An undescribed
species also has been identified recently in a molecular study in Australia.
Another fungus, Cryptosporiopsis perenanns, causes similar chronic
diseases of apple wood and fruit, respectively. Any factor that produces
excess succulent growth -- such as high nitrogen fertilization or overirrigation
-- or that weakens the tree increases the severity of perennial canker.
Disease management involves removal of branches containing cankers, which
helps to reduce inoculum of Neofabraea spp. and Cryptosporiopsis
malicorticis in the orchard. Ziram (zinc bis(dimethyldithiocarbamate),
applied within 2 weeks before harvest is recommended for control of BER
in the Pacific Northwest. Any practice that helps to maintain trees in
a healthy vigorous condition is critical for controlling the canker phase
of the disease. Cankers generally develop only on stressed or weakened
trees. Prune trees annually and maintain a balanced fertility program based
on soil and foliar nutrient analysis. Cankers generally develop rapidly
on winter-injured trees. The use of fungicides combined with good sanitation
is beneficial for controlling the fruit rot phase of these diseases. Fungicides
are not effective for controlling the canker phase of the disease on weakened
trees. Commercial apple producers should consult the appropriate agencies
for current information on recommended fungicides. Postharvest controlled
atmospheres (CA) are used increasingly to supplement good refrigerated
storage practices. In CA-controlled storage, a beneficial combination of
reduced oxygen levels and increased carbon dioxide concentrations in the
atmosphere are being combined with refrigerationref1,
ref2,
ref3,
ref4,
ref5,
ref6
=> Botrytis blight or gray mold (GM) is a fungus disease infecting
many herbaceous annual and perennial crops. GM can be particularly damaging
under continuous rainy, drizzly weather conditions for several days. The
host range of GM is extensive (asparagus, bean, beet, crucifers, cucurbits,
eggplant,
grape, lettuce,
onion,
pepper,
potato,
tomato,
turnip, and others). If cool, overcast conditions predominate, the disease
progresses and a fuzzy grey mold develops. If conditions are warm and sunny,
only ghost spots remain without any further disease progression. Cool,
wet weather exacerbates disease expression. Fungicides can be used to prevent
the spread of infectionref1,
ref2,
ref3,
ref4,
ref5.
Botrytis blight of peanut is a late-season disease that generally occurs
in cool, wet weather. Infected tissues rapidly develop a water-soaked,
brown appearance and are frequently covered by a greyish-brown mold. Although
all currently planted varieties are susceptible to Botrytis blight, NC
17 appears to be highly susceptible to this disease. In the USA, Botrytis
blight occurs predominantly in certain areas of West Texas. Symptoms of
this disease closely resemble Sclerotinia blight. Disease management is
best accomplished by harvesting in a timely fashion and avoiding plant
injury so as to reduce symptom incidence and severityref1,
ref2.
=> mango blossom rot : there is one reference indicating that
Botrytis
cinerea causes the disease in India. Another important disease of mango
called blossom blight can be responsible for up to 94% losses depending
on the cultivar. This disease is caused by a series of fungal pathogens.
Although the cultivars "Awase" and "Alfonse" were found to be moderately
susceptible and "Hendy Bezra" even less susceptible, specific fungicidal
sprays are the accepted and widespread method of controlref1,
ref2,
ref3.
There are different varieties available in Andhra Pradesh state of India
: table varieties are Banganapally (Benishan) Totapari, Neelum, Dashehari,
Langra, Kesar; juice cultivars are Peddarasam, Chinnarasam, Cheukurasam,
Navaneetham and Panakalu; and pickle varieties are Jalal, 2C Amani, Rajapuri,
Royal Special, Bobbili Punasa, and Baramasi.
=> brown rot (BR) is a major pathogen on stone fruits (peaches,
cherries, plums, prunes, nectarines, and apricots) and wine grapes ( in
Vitis
vinifera) in France and China, affecting blossoms, fruit, spurs,
and small branches : depending on weather conditions, can cause extensive
crop losses. BR is most important on fruits just before ripening and during
and after harvest. Under favorable conditions for disease development,
the entire crop can be completely rotted. Peaches not kept in cool storage
may rot in 2 to 3 days. Management of Mf is usually not a problem on early
maturing cultivars. Application of fungicide sprays to reduce blossom and
twig blight help minimize loss to ripe fruit rot at harvest. Removal of
remaining fruit from trees soon after harvest will help reduce inoculum
the following spring. Disease management involves use of phytosanitary
measures (removal and destruction of rotted fruit, mummies, and neglected
trees as possible inoculum sources); pruning of cankers during the
dormant season; and insect control to avoid insects that feed on
punctured or bruised fruit in the orchard or during harvesting and packing.
Fruit should be cooled and refrigerated (as close to 0°C as possible)
immediately after harvestref1,
ref2.
The fruit of the crop plant peach, Prunus persica, is susceptible to the
disease brown rot both on and off the tree. Other species of Monilinia
are known to rot peaches in Hungary, so this is not the first report of
brown rot. The significance of the observation has to do with the fact
that the pathogen is included in the EPPO A2 list of quarantine organisms
for Europe. It was detected for the 1st time in Europe in 2001 (in France)ref1,
ref2,
ref3,
ref4,
ref5
=> Sclerotinia blight [Sb] is a destructive mid-to late-season
disease of peanuts. 1st discovered on peanut in Virginia in 1971, it subsequently
spread to North Carolina, Oklahoma, and Texas. Sm survives in soil as sclerotia
(resistant seed-like structures) and attacks plants near the soil line.
Sm occurs worldwide, primarily in cool, moist regions. Its host range includes
canola, sunflower, bean, sweet potato, cole crops, and soybean. In Oklahoma,
yield losses in experimental plots infested with Sb ranged from 7% to 80%.
Spread of the disease is limited because Sm does not Sm produce airborne
spores during the cropping season. Sclerotia are the major means of long-distance
movement. Sm is seedborne and is found as a contaminant in soils cropped
by peanut. Infection by Sb can be very damaging and is difficult to control.
Disease management basically depends upon preventing movement of contaminated
soil to clean areas. Farm implements coming off contaminated soils should
be washed thoroughly to remove soil and straw. A combination of cultural
and chemical management practices will usually provide adequate control.
New resistant cultivars have been developed recently by USDAref1,
ref2,
ref3,
ref4.
=> Cylindrocladium black rot (CBR) was first found in 1965 in
peanut in southwest Georgia and subsequently spread to Florida, in Alachua
and Columbia counties. In the mid 1980s CBR was found in peanut in the
panhandle section of Florida. Since 1975, CBR has been found in alfalfa,
clovers, and soybean. Other crops reported to be susceptible to CBR are
cowpea, bean and blueberry. Yield losses from CBR in some infested peanut
fields in Florida have exceeded 50%. CBR has become a limiting factor for
production of peanut in some fields in the panhandle area, particularly
in Santa Rosa County. In general, CBR appears to be gradually increasing
in severity in peanut throughout the peanut-producing areas of Florida.
Management of CBR includes avoidance of susceptible crops, a crop rotation
of 4-5 years, elimination or reduction of weeds such as hairy indigo (Indigofera
hirsuta), beggarweed (Desmodium purpureum ) and coffeeweed (Sesbania
exaltata). Soils should be well drained. Phytosanitary measures such
as removal of soil and plant debris from tractor tires and implements before
moving them to non-infested fields is advised. Some peanut cultivars possess
low levels of resistance to CBR. Chemical control for CBR in peanut has
provided some control. In Virginia, North Carolina, and to a limited extent
in Georgia, preplant fumigation with metam-sodium has been used successfully,
particularly if fumigation is coupled with use of a resistant variety.
In Florida, CBR has been suppressed in peanut by means of post-plant sprays
of approved fungicides at mid-seasonref1,
ref2,
ref3.
=> Fusarium head
blight (FHB), also known as scab or tombstone, is a disease
of wheat, barley, oats and other small cereal grains and corn. It is caused
by several Fusarium species, primarily Gibberella zeae, Gibberella
avenacea, Fusarium culmorumandMicrodochium
nivale. FHB causes severe production losses worldwide and may be
as high as 50%. It is a major cereal disease in Manitoba, Saskatchewan
and Alberta. Scab can cause significant yield and quality damage, as well
as toxicoses in animals and humans. Damage due to scab in the USA was estimated
to be more than USD one billion in 1993 and USD 500 million in 1994. In
China, the estimate is that scab may affect up to 7 million ha, and 2.5
million tons of grain may be lost in epidemic years. Diseases related to
fusarial mycotoxin in humans have been reported in China, India and Japan,
whereas in animals, diseases have been reported in numerous parts of the
world. FHB-infected kernels often contain a mycotoxin called deoxynivalenol
(DON), also known as vomitoxin. It is a very mild mycotoxin. When present
at high enough levels in the diet (>2 ppm), it causes a reduced feed intake
in swine. DON is of limited concern to cattle producers because it is metabolized
extensively in the rumen. DON belongs to a family of mycotoxins called
tricothecenes. Tricothecenes are protein inhibitors, and it has been speculated
that animals fed high levels of tricothecenes may have a weakened immune
system. owever, DON is a very mild toxin compared to other tricothecenes.
It is also extensively metabolized, poorly absorbed and rapidly cleared
from tissues and fluids in ruminants. There is no evidence to support depressed
immune function, even in pigs, which are much more sensitive to DONref1,
ref2,
ref3,
ref4,
ref5,
ref6,
ref7,
ref8.
These Fusarium species are all asexual forms that produce only conidia.
The sexual stage is Gibberella zeae. Scab-infected wheat seed that
is planted may develop root rot as well. These Fusarium fungi are ubiquitous
and unfortunately can also cause a seedling blight and stalk, ear, and
root rot of corn. A major concern is the presence of several important
mycotoxins that can be produced in grain affected by scab. These toxins
are produced by growth of the Fusarium fungi in the kernels, and
ingestion of them can cause vomiting, nausea, dizziness, diarrhea, and
muscle spasms in non-ruminant animals. Highly sensitive laboratory tests
are currently used to detect mycotoxin contamination in grain. Thus, the
chances of toxic compounds getting into human food is almost nil. The problem
arises when farm livestock are fed uncleaned scabby wheat, oats or barley.
> 3% scabby kernels in feed may be poisonous to hogs. Hogs fed > 10% scabby
grain may vomit and refuse to eat the grain mixture. Cattle, sheep and
mature poultry are much less susceptible to the mycotoxins. These toxins
are quite stable and may remain in grain stored indefinitely. Disease management
involves crop rotation with legumes or other non-cereal crops; planting
only seed that has been thoroughly cleaned and treated with recommended
fungicides; using deep plowing to completely cover crop residues so as
to reduce head-blight infections; and planting less-susceptible wheat cultivars
where possible
=> potato dry rot => infection of wheat and barley is epidemic in USA and is increasingly
becoming a threat to the world's food supply due to recent outbreaks in
Asia, Canada, Europe, and South America. Crop quality and yield have been
adversely impacted. A major effect of Fg infection in cereals is contamination
of seeds with trichothecene and estrogenic mycotoxins, making them unsuitable
for food or feed. In Brazil, soybean crop residues in fields under conservation
tillage have been found to be heavily infested with Fg. Although the fungus
also reportedly grows on living soybean stems and seeds, many consider
the fungus non-pathogenic to soybean. Recent surveys of soybean seed grown
in Brazil also revealed infection by Fg. Fg strains from Brazilian soybean
seed consistently caused pod rot and root rot disease on all soybean varieties,
under all conditions tested. These same strains also caused FHB in wheat.
Farmers who use a soybean/wheat crop rotation should be aware of a potential
build-up of strains that infect both wheat and soybean, reducing the usefulness
of the rotation. Brazilian strains, which also produce a novel mycotoxin
known as 3-acetylnivalenol, have not yet been found in the USA In
Argentina, a range of wheat cultivars are known to be infected by Fgref
Fusarium
solani f. sp. cucurbitae (Fsc) causes necrotic lesions affecting
the stem near the ground, eventually resulting in girdling of the stem.
Plants become wilted and die rapidly during mid-season. The decay at the
base of the stem is soft and mushy. Fruit lesions begin as small corky
cracks that develop into sunken necrotic lesions. Internal tissue near
the site of infection becomes off-color and corky. Fruit decay results
in a firm, dry rot. A PCR-based technique has been devised to determine
genome variability between Fsc isolates of Fsc isolates races 1 and 2.
Fusarium crown and foot rot occurs sporadically in most areas, and disease
severity is dependent on soil moisture and inoculum density. Because the
fungus survives in the soil for only 2-3 years, a 4-year rotation is usually
adequate for disease control. Planting fungicide-treated seed is also effective
in reducing the incidence of disease initiated from infected seed. Additional
measures would include use of resistant or tolerant cultivars if available
and cleaning of farm machinery and tools so as to prevent soil-borne spread
of the pathogen. A PCR-based technique has been devised to determine genome
variability between Fsc isolates of races 1 and 2ref1,
ref2,ref3
=> sudden death syndrome (SDS) of soybean
: Initially, the cause of SDS was elusive, with mechanical, cultural, environmental
and biological factors all considered possible. Early studies involving
soil fumigation indicated that the origin was biological. Subsequent work
in Arkansas and Mississippi proved that SDS is caused by a strain of the
common soil fungus Fusarium solani (FS-A). This result has been
confirmed by work in Indiana and Missouri and is now generally accepted.
Although FS-A is the primary organism associated with SDS, other pathogens
may also be involved in disease development. The most studied of these
is the soybean cyst nematode (SCN).
Mississippi researchers found that while SCN is not required for severe
SDS to occur, SCN at sufficient levels exacerbates foliar symptoms, leading
to early and severe SDS. This finding is important, since the disease's
timing and severity, relative to soybean development, determines how severely
the yields are reduced. In addition to SCN, other soybean pathogens (foliar
and root/stem infecting) are being studied for their potential role in
SDS development. Preliminary data suggest that any stress factor (biological,
mechanical or environmental) may magnify SDS symptom expression and cause
SDS-affected plants to deteriorate earlier and
die prematurely. Other conditions that affect SDS severity are planting
date and nematode injury. Early planted soybeans generally suffer more
injury than those planted later. The positive correlation between soybean
cyst nematode injury and SDS severity was noted by some of the first researchers
to study the disease. While the presence of H. glycines tends to
exacerbate problems with SDS, it is not required for successful establishment
of F. solani f. sp. glycines in its host. The best way to
avoid SDS in future cropping is to avoid early
planting, plant early to mid-season varieties, and plant varieties
in SDS-prone fields which are not highly susceptible to SDS. True resistance
to SDS is not yet available. However, avoiding planting highly susceptible
varieties will usually help by delaying disease onset until the later stages
of crop development. Roots of plants are
infected and become diseased during the vegetative stages of plant
development. Then, typically as plants enter the pod development stages,
foliar symptoms are expressed as a result of foliar sensitivity to one
or more plant toxins produced by the fungus in diseased root tissue. In
extreme cases, plants can die prematurely, with yields being dramatically
impacted. In some years (such as 2004), plants will show symptoms early
and later recover, with no impact on crop yield. In most years the response
is somewhere in the middle of these 2 extremes. SDS is characterized by
a rotting of the primary and secondary root system and a subtle brown discoloration
of the stem tissue immediately inside the green exterior. Leaf symptoms
that start as yellow spots and blotches between the veins of upper leaves
(usually), leading to large areas of brown tissue between the veins, and
eventual defoliation of the leaflets, but not the petioles. Abortion of
flowers and young pods is common. Symptoms usually develop first in hot
spots in fields of varying shapes and sizes. Entire fields may eventually
become involved in severe instances, but even then, there are typically
areas in fields where the disease is more severe than in others. At this
time, there is nothing that can be done to make the disease less or more
serious. The die is cast, as it were. SDS is in a race against time with
the crop. If the crop reaches the R5-R6 stage before the disease is severe,
then the yield prognosis will be excellent. Serious disease prior to the
R5 stage, however, can result in substantial yield reductions. Typically
the earlier the onset of serious SDS, the greater the impact will be on
crop yieldref1,
ref2,
ref3,
ref4.
SDS has reached epidemic proportions in North and South America during
the past decade. It causes interveinal foliar chlorosis and necrosis leading
to defoliation of the leaflets but not the petioles. A molecular diagnostic
test to rapidly detect and distinguish the 2 SDS pathogens is being developed
by USDA scientists. Results of this study are important to plant pathologists,
plant breeders and quarantine officials who need to know that soybean SDS
is caused by at least 2 different pathogens. Factors affecting SDS include
the choice of cultivar, planting date, growth state at the time of infection,
and field environment. Selection of soybean varieties that are the most
resistant to SDS is crucial to maintaining a healthy soybean crop.
Disease progress is reduced in mid-May through early June plantings, compared
to those in early May, most likely because soil is warmer and drier in
later plantings than in earlier plantings. Crop rotation on a regular regimen
also lessens disease severityref1,
ref2
=> coffee wilt disease (CWD) / tracheomycosis / vascular wilt disease
occurred sporadically in Africa but in the last decade or so it has become
virulent, sweeping across Cameroon, the Congo and into Uganda. According
to the Uganda Coffee Development Authority (UCDA), CWD mainly affects the
native, lowland robusta variety and, since 1993, it has destroyed over
12 million plants. Uganda also grows arabica coffee, which constitutes
only 10% of production, grows mainly in the highlands, and is unaffected
by CWD. The entire plant is affected. Disease management was confined to
burning uprooted plants, but the development of wilt-resistant coffee cultivars
will be a major step in alleviating shortages due to CWDref1,
ref2.
=> potato dry rot [DR]. DR usually
causes extensive tissue decay and collapse, and large holes are common
in tubers. The amount of DR due to decay in storage depends upon the amount
of fungus in the soil, the extent of mechanical damage to tubers during
digging and harvesting, and on the susceptibility of the potato variety.
Growers are advised to treat seed pieces with a recommended fungicide prior
to planting, to make certain that tubers go into clean and disinfected
storage bins, to handle treated seed with clean, disinfected equipment,
to harvest tubers during cool dry weather, and to prevent bruising during
harvesting, handling and grading operations. Note that F. graminearum
was reported on soybean in Brazil last year (2004)ref1,
ref2,
ref3
=> Fusarium yellows (FY) or wilt of sugar beet has been
reported from the Red River Valley of Minnesota and North Dakota, given
the opportunity for propagules of the fungus to be distributed on windborne
soil aggregates and by physical movement of soil on farm equipment. Disease
management utilizes certified seed of Fusarium wilt-tolerant or
resistant varieties, if available, treatment of seed or furrow with recommended
fungicides to delay initial infection of seedlings by Fusarium spp.
and other soil-borne pathogens, manage irrigation to eliminate moisture
stress to the developing plant, avoid excess water which may deprive roots
of oxygen, and dispose of sugar beet tare soil to avoid introduction of
FY propagules (or new races) into the fieldref1,
ref2
=> Fusarium wilt of canola is a disease that has only recently
been discovered in western Canada, and little is known about the host/pathogen
relationship. Canola varieties differ in disease susceptibility, and one
of the first priorities has been to determine the amount of genetic resistance
currently available in commercial canola cultivars. Varieties, inoculated
with Fusarium oxysporum f. sp conglutinans, at the seedling
stage in a greenhouse were classified as susceptible or resistant. A majority
of varieties are resistant. Management of this disease should be possible
by simply screening susceptible cultivars. In addition, field results from
locations with natural incidence of fusarium wilt have correlated well
with results from this artificial inoculation procedure, providing some
validity to this method of testing. The fact that infected cultivars can
be readily detected in fusarium-infested field plots will assist research
in disease managementref
=> Panama disease (PD) / Fusarium wilt of banana.
Banana and plantain are the most important agricultural products in the
tropics, with annual production of over 100 [million] metric tons. Ladyfinger
bananas are a special type of banana. Of the various pathogens encountered
in the tropics PD is the most significant. PD was considered a major
threat to banana production in the 1940s-1950s, but planting of a PD-resistant
banana known as the Gros Michel was a breakthrough. Over time, Gros Michel
was replaced by the 'Cavendish-type' cultivar, which has remained in production
to date. Recently a new variant of FOC, tropical race 4 (TR4), has been
responsible for the Southeast Asian outbreaks. Unlike subtropical outbreaks
that affect cold-stressed Cavendish in Australia, the Canary Islands, and
South Africa, TR4 affects Cavendish in the absence of predisposing factors.
Although it is found only in Southeast Asia, TR4 continues to spread in
that region. The great fear is that FOC will spread to the Americas and
Africa, where it could have a great impact on production of export bananas
and plantains that normally resist PD. TR4 poses a serious threat to a
multibillion-dollar industry and the food stability of millions of poor
farmers. In another development, phylogenetic work on FOC has revealed
that it has had at least 3 independent evolutionary origins. Different
clades of the pathogen are distantly related, and one is more closely related
to members of another forma specialis, F. oxysporum f. sp. melonis,
than to other FOC clades. There are 4 races of the PD pathogen: Race 1
attacks Ladyfinger, Sugar and Ducasse bananas but not Cavendish; Race 2
attacks Bluggoe and Blue Java, but not other banana varieties; Race 3 attacks
only
Heliconia and is not a problem on bananas; and Race 4 attacks
nearly all varieties of bananas, including the main commercial Cavendish
variety. Effects range from reduced yields to death of the plants. The
soil remains infested indefinitely so that only resistant varieties can
be grown on that site in the future. These effects create costs for production.
Disease management involves prompt detection and destruction of infected
plants, which cannot be cured. Strict quarantine regulations have to be
employed to prevent spread of infected material to clean areas through
movement of soil, water or plant materials. Foremost among preventive measures
is exclusion, supported by a general awareness of the characteristic external
and internal symptoms of Panama disease, so that reporting can take placeref1,
ref2,
ref3
=> Fusarium wilt of tomato, caused by 3 races is
one of the most important diseases of tomato. Races 1 and 2 are distributed
worldwide, whereas race 3 has amore limited geographic distribution with
no report thus far in Brazil. 7 Fol isolates were obtained from wilted
tomato plants of race 1 and 2-resistant hybrids 'Carmen' and 'Alambra'
in Venda Nova do Imigrante (State of Espirito Santo), Brazil. Results of
virulence assays using a set of race differential cultivars showed that
'Ponderosa' were susceptible to all races, 'IPA-5' was resistant to race
1, 'Floradade' was resistant to races 1 and 2 and 'BHRS-2,3' was resistant
to race 3. All isolates were highly virulent to 'Ponderosa', 'IPA-5' and
'Floradade' and were able to infect only a few plants of 'BHRS-2,3'. An
additional virulence test was conducted including the same set of cultivars
plus Lycopersicon pennellii 'LA716'. Identical results were obtained
with L. pennellii displaying an extreme (immune-like) resistant
response. These results indicated that all 7 isolates could be classified
as Fol race 3. This new Fusarium wilt might became an economically important
disease, since race 3-resistant cultivars adapted to Brazil are not yet
available. This is the 1st formal report of race 3 in Brazil, extending
the geographical range of this pathogen. Fol can be introduced into new
growing areas via contaminated seeds. The presence of race 3 in geographically
isolated tomato-growing areas in Brazil could be the result of either pathogen
introduction via contaminated seeds or the occurrence of an autochthonous
(indigenous) race 3 isolate. In fact, recent results indicate that new
race 3 isolates could have originated from genetic changes in the local
populations of native Fol isolates. Additional studies employing molecular
fingerprinting systems and/or vegetative compatibility groups with a world-wide
collection of Fol isolates could provide some indication of whether this
pathogen is endemic to Venda Nova do Imigrante or if it was introduced
and, if so, from which geographical area. This new Fusarium wilt might
became an economically important disease since race 3-resistant cultivars
adapted to Brazilian conditions are not yet available. In addition, screening
trials searching for new sources of resistance seems to be necessary, since
the genetic plasticity associated with selective pressures due to the use
of race 3 resistant cultivars might cause the establishment of new pathogenic
races of this fungus. These screening trials are already under way in Embrapa
Hortalicas, and new resistance sources have been found. Management strategies
for Fol include disinfestation of the soil and planting material with fungicidal
chemicals; crop rotation for several years, but Fol is long-lived; plantin
and plant immunology
