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BACTERIAL GALLS AND CANKERS
CANKERS-3rd pathogen
Pseudomonas syringae and Canker A General view:
The pathogen:
The gram-negative plant-pathogenic species Pseudomonas syringae is comprised
of at least 50 pathovars that can be distinguished by their host ranges. Many P.
syringae pathovars also contain several races characterized by their avirulence on
different host cultivars. Genetic control of host specificity at the race-cultivar
level, and possibly the pathovar-host species level, is conditioned by “gene-forgene” interactions between avirulence genes in the pathogen and the
corresponding resistance genes in the plant. In the last 2 decades, a number of
pathogen avirulence genes, as well as the corresponding host resistance genes,
have been cloned and identified. Resistance gene products, regardless of whether
they encode resistance to viral, bacterial, fungal, nematode, or insect pathogens,
share similar structures and with few exceptions contain a leucine-rich repeat
region, suggesting a conserved mechanism(s) for pathogen recognition and signal
transduction events. In contrast, avirulence gene products share little sequence
similarity, although it is well known that bacterial avirulence gene products, along
with other virulence factors collectively termed effectors, are injected into the host
cell via the specialized type III secretion system (TTSS) that is conserved among
plant and animal pathogens. The P. syringae effectors are designated Avr
(avirulence) or Hop (Hrp outer protein) according to a recently adopted
nomenclature system. P. syringae effectors collectively are important to
virulence, and increasing evidence suggests that these proteins are involved in
suppression of host defense responses in compatible interactions with host plants.
(Joadar et al 2005)
Two related bacteria, Pseudomonas syringae pv. syringae van Hall and P. s. pv.
morsprunorum (Wormald) Young et al., can cause bacterial canker. Both
pathogens affect sweet cherry, sour cherry, plums and prunes in Michigan and the
neighboring province of Ontario, Canada. Disease outbreaks are sporadic and
more frequent on sweet cherry than on sour cherry. P. s. syringae is found on
peach in the southeastern United States.
The host-specific bacterium that causes canker and decline of European hazelnut
was originally described as Pseudomonas syringae pv. avellanae (19,21). Further
evidence obtained from fatty acids methyl ester analysis, whole-cell protein
profiles, and sequence comparisons of the 16S rRNA gene changed the
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designation to P. avellanae . In 1999, based on DNArelatedness studies (i.e.,
genomospecies) of P. syringae and related species, P avellanae was included in
the genomospecie 8, together with P syringae pv. theae. Subsequently, it has been
shown that P syringae pv. actinidiae might also be included in this genomospecies
. P avellanae strains have hrp genes encoding for the harpin proteins that are
involved in the elicitation of the hypersensitivity reaction in leaf tissues.
A less destructive bacterial disease of European hazelnut, causing limited twig and
branch wilting, has recently been found in other areas of European hazelnut
cultivation in Italy. The pseudomonads associated with this disease resemble P
syringae pv. syringae. Unlike P. avellanae, these P syringae pv. Syringae like
isolates do not cause cankers and rarely result in tree mortality. When leaf scars of
European hazelnut were artificially inoculated with the two pathogens, P
avellanae caused extensive twig dieback even at low inoculum levels, whereas P.
syringae pv. syringae-like strains caused dieback to a lesser extent and only at the
highest inoculum doses. .(Scortichini 2002)
Pathogen Diversity
Diversity within P avellanae strains was initially examined by biochemical and
nutritional tests, fatty acid methyl ester analysis, and whole-cell protein profiles.
These analyses indicated a high degree of similarity among strains isolated in
Greece and central Italy. However, Italian isolates lose fluorescent pigment
production on King's medium B after subculturing, whereas isolates from Greece
do not.
Subculturing of P. avellanae on nutrient sucrose agar (NSA) supplemented with
7% instead of 5% sucrose and incubated at 30 deg C, or subculturing 30-day-old
colonies on NSA, resulted in the appearance of clear, waterdrop-like colony
variants. These variants did not induce the hypersensitivity reaction in tobacco
leaves. This colony type was occasionally observed on NSA during isolation of P
avellanae from wood and bark. These colonies would sometimes revert to the
wild-type colony morphology of P avellanae upon further subculturing
Genetic variability among P avellanae strains was determined by plasmid analysis
and repetitive polymerase chain reaction (PCR) using ERIC, BOX, and REP
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primer sets. P avellanae strains from Greece were clearly differentiated from those
of Italy by the selective amplification of approximately 300- and 800-bp fragments
using ERIC primers. Similarly, monoclonal antibodies raised toward cell wall
polysaccharides of strains isolated in Greece and central Italy clearly differentiated
two serotypes.
P. avellanae is easily differentiated from P. syringae pv. syringae strains obtained
from European hazelnut by fatty acid methyl esters and sodium dodecyl
sulfatepolyacrylamide gel electrophoresis (SDSPAGE) protein analysis (32,35) or
molecular techniques (Amplified rDNA Restriction Analysis, repetitive-PCR) (35)
(Fig. 5). In addition, all P avellanae strains lack the syrB gene, whereas most of
the P syringae pv. syringae strains from hazelnut have this gene encoding for the
production of phytotoxins (i.e., lipodepsinonapeptides). Genetic variability was
also found among many P. syringae pv. syringae strains isolated from diseased
trees within one region of European hazelnut cultivation in Italy (Campania,
Piedmont, Sicily, and Sardinia). These strains were genetically different from
those of the other regions.(Scortichini 2002)
Symptoms of The Disease:
Symptoms in general are most obvious in spring and include limb dieback with
rough cankers and amber-colored gum. There may also be leaf spot and blast of
young flowers and shoots. The sour sap phase of bacterial canker may not show
gum and cankers, but the inner bark is brown, fermented, and sour smelling.
Flecks and pockets of bacterial invasion in bark occur outside canker margins.
Frequently, trees sucker from near ground level; cankers do not extend below
ground. The disease attacks most parts of the tree .Cankers on trunks, limbs and
branches exude gum during late spring and summer. Leaves on the terminal
portions of cankered limbs and branches may wilt and die in summer or early
autumn if girdled by a canker. Occasionally, large scaffold limbs are killed. Leaf
and fruit infections occur sporadically, but they can be of economic significance in
years with prolonged wet, cold weather during or shortly after bloom. Leaf spots
are dark brown, circular to angular, and sometimes surrounded with yellow halos.
The spots may coalesce to form large patches of dead tissue, especially at margins
of leaves, or the centers of the necrotic spots may drop out, resulting in tattered
leaves. Infected leaves may abscise during midseason. Lesions on green cherry
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fruit are brown with a margin of wet or water-soaked tissue . The affected tissues
collapse, leaving deep, black depressions in the flesh, with margins becoming
yellow to red as lesions and fruit age. On fruit stems, lesions are elliptical and
brown with watersoaked margins.
nfected leaf and flower buds may fail to open in spring, resulting in a condition
referred to as "dead bud.' Small cankers often develop at the bases of these buds.
Other infected buds open in spring but collapse in early summer, leaving wilted
leaves and dried-up fruit. If blossom infection occurs, whole blossom clusters
collapse as infection spreads into the fruit-bearing spurs. Blossom blight and spur
blast are most.(Jones-west Virginia University REF23)
Predisposing Factors:
Environmental factors can play a significant role in increasing the susceptibility
for example European hazelnut to P avellanae. Spring frosts often occur in valleys
of central Italy where hazelnuts are grown. Surveys conducted in orchards where
bacterial canker and decline was prevalent revealed that symptoms were more
severe on trees located at the bottom of small valleys where frost was more likely
to occur . During March and April, temperatures in these valleys dropped to lows
of -1 to -5C, sometimes on consecutive days, during bud swell. These spring frosts
can cause longitudinal cracks to form along the branches and trunk that are
subsequently colonized by P avellanae dispersed from oozing cankers by rain and
wind.
Soils of volcanic origin with pH values <5.0 are present in some areas of central
Italy. Acidic soils can increase the susceptibility of fruit tree species to
pseudomonads. In addition, the current agronomical techniques adopted in central
Italy include the use of soil acidifying nitrogen fertilizers. Also for the P
avellanae-C. avellana pathosystem, a low pH accompanied by a high content of
aluminum in the soil (>20%) and in tree roots (>600 mg kg-'), in the absence of
adequate calcium, can increase the susceptibility of the tree . Acidic soils are also
present in northern Greece where P avellanae has eliminated the cultivation of
European hazelnut. (Scortichini 2002)
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Disease Cycle:
The bacteria can survive from one season to the next in bark tissue at canker
margins, in apparently healthy buds and systemically in the vascular system.
Bacteria multiply within these overwintering sites in the spring and are
disseminated by rain to blossoms and to young leaves. Bacteria of both pathovars
can live in an epiphytic phase on the surface of symptomless blossoms and leaves
from bloom through leaf fall in autumn. After leaves abscise in autumn, the
bacteria may enter the tree through fresh leaf scars. Outbreaks of bacterial canker
are often associated with prolonged periods of cold, frosty, wet weather late in the
spring or with severe storms that injure the emerging blossom and leaf tissues.
Freezing can predispose the tissue to infection, but infection depends on the
presence of wet weather during the thawing process. Free water on leaf surf'aces
and high relative humidity are required for at least 24 hours before significant leaf
infection can occur following violent storms. Symptoms appear about 5 days later
at temperatures between 70 and 80 degrees F. .(Joens-WestVirginia University
REF 23)
MANAGEMENT
Problems with bacterial canker can be minimized at planting by carefully selecting
the planting site, choosing the least susceptible rootstocks, and following
recommended cultural practices regarding pruning and fertilizing. Bacterial canker
tends to mostly affect weak trees, so any management practice that improves tree
vigor (e.g., lighter, more frequent irrigation, improved tree nutrition, nematode
management, etc.) will help to reduce the incidence of this disease. Delayed
pruning may help. Lovell nectarine rootstock is usually more tolerant than others.
In plum, prune, trees planting trees that are budded or grafted about 32 inches
above the root crown can help suppress bacterial canker infections. Bacterial
canker tends to mostly affect weak trees, so any management practice that
improves tree vigor (e.g., lighter, more frequent irrigation, improved tree nutrition,
nematode management, etc.) will help to reduce the incidence of this disease.
Trees on Lovell peach rootstock are more resistant than others; those on plum
rootstocks are most susceptible. Delayed pruning may help.
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In light sandy soils and some heavy soils, successful control has been achieved
with preplant fumigation for nematodes. Application of copper during dormancy
has not been shown to protect against bacterial canker.
However in Apricot, bacterial canker tends to affect mostly weak trees, so any
management practice that improves tree vigor (e.g., lighter, more frequent
irrigation, improved tree nutrition, nematode management, etc.) will help reduce
the incidence of this disease.
Delayed or summer pruning may help. Of the rootstocks commonly used for
apricots in California, trees planted on peach appear to be the least susceptible to
bacterial canker, possibly because it has greater tolerance of the ring nematode;
peach rootstock is followed in susceptibility by apricot, Myrobalan, and Marianna
2624, which is the most susceptible. Copper sprays applied at the beginning and
end of leaf fall have been tried with highly variable results.
In cherry, Delayed pruning may help. Of the rootstocks commonly used for
cherries in California, Mahaleb is the most tolerant of bacterial canker, Colt is
moderately susceptible, and Mazzard is susceptible. Copper sprays applied at the
beginning and end of leaf fall have given variable control.
But in almond ,consequently, management of this disease should focus on
preventing conditions that predispose trees to the disease.

Before planting, properly sub-soil the orchard to break up hard-pan areas.
When replanting an orchard, fumigate the soil before planting to reduce ring
nematode populations.

Trees planted on Marianna 2624 and peach-almond hybrid (Hansen)
rootstocks are very susceptible to bacterial canker. Of the rootstock that are
somewhat resistant to the disease, Lovell rootstock produces trees that are more
tolerant than those growing on Nemaguard.



Maintaining proper nutrition, particularly nitrogen, is important.
Recent studies have shown that a foliar application of 100 lb/acre of low
biuret urea before leaf drop significantly reduces canker size in infected trees.
Annual nematicide treatments in October can help reduce disease severity.
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In light, sandy soils and in some heavy soils, control has been achieved with
preplant fumigation for nematodes. Application of copper during dormancy has
not been shown to protect against bacterial canker.
Organically Acceptable Methods
Cultural controls are acceptable for use in an organically certified crop.
Control:
The disease is troublesome on some sweet cherry cultivars but not others. Schmidt
and Windsor are susceptible and often severely damaged. Hardy Giant is very
susceptible-this cultivar should be avoided. Copper-containing compounds may be
of limited value for the control of bacterial canker because strains of P. s. syringae
resistant to copper are common in orchards with a history of copper usage. Also,
copper injures most stone fruit crops. Even on the more tolerant crop species, it
becomes more injurious as applications are repeated.(REF23 -West Virginia
University)
The way in control in the hazelnuts bacterial canker caused by Pseudomonas
syringae pv. avellanae may be a good example for controlling the disease in
several hosts, effective control of bacterial canker and decline of hazelnut is
difficult. The production of disease-free nursery plant material is very important.
The best way to avoid the disease is to prevent the introduction of latently infected
plants. Monitoring of orchards for early disease symptoms is essential. Inspections
should preferably be made during spring and summer with the aim detecting
wilting twigs and branches. Infected plant parts must be removed from the orchard
and should be burned. In case of completely wilted trees, the roots and suckers
also must be removed. Pruning and/or sucker removal should be avoided during
humid periods. After a branch is cut, it is advisable to seal the wound with wax or
Bordeaux mixture. It may take several years to eradicate the pathogen in severely
damaged orchards.
Taking into consideration that P. avellanae mainly lives inside the plant, the
efficacy of copper-based compounds, the only chemicals allowed in Italy for
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controlling bacterial disease, is rather low. However, a combination of agronomic
techniques and applications of copper-based materials at key times can partially
manage the disease. As a general rule, farmers apply copper-based chemicals
immediately after pruning, spring frost, hail, windy storms in early autumn, and at
the beginning and middle of leaf drop, to reduce the possibility of wound
colonization by the bacterium. Orchards having very acidic soils require lime
application to increase the soil pH. It is also very important to control the
Scolytidae by using chromotropic traps
Chemical Control
Bactericide applications have no reliable effect on bacterial canker and their use is
not recommended. Preplant fumigation for nematode control reduces the severity
of bacterial canker in newly planted orchards. Nematodes stress trees, which
predisposes them to bacterial canker. The benefits of preplant soil fumigation for
control of bacterial canker usually last only a few years; in some areas only limited
improvements in disease control occur following soil fumigation.
Following planting, if bacterial canker occurs in an orchard, apply nematicide
around all trees in the affected area of the orchard on a yearly basis until the trees
are 8 years old.
Some Previous Studies:
1- Pectate lyase (PL) is an important tissue-macerating enzyme, which can be
produced by a wide variety of phytopathogenic bacteria, especially those capable
of causing soft rot, such as Erwinia and Pseudomonas. The PL produced by softrotting P. viridiflava and P. fluorescens is usually found as a single protein with a
pI at 8.5 or higher (Liao et al. 1988). The PL produced by E. chrysanthemi,
however, exists in four or five isozymic forms, with pIs ranging from 4.3 to 9.0
(Van Gijsegem 1989). Because of their pathological importance, the PLs and the
genes (pels) coding for these enzymes have been extensively investigated and
reviewed (Py et al. 1998). In addition, the three-dimensional structure of two E.
chrysanthemi PLs (PLc and PLe) in relation to their enzymatic function has been
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determined and elaborated (Heffron et al. 1995; Henrissat et al. 1995; Yoder and
Jurnak 1995).
Since a vast majority of P. syringae strains or pathovars cause diseases in the form
of necrosis or canker, they usually have a weaker ability in producing pectic
enzymes, such as PL and polygalacturonase (PG). PL is a glycosidase that cleaves
α-1,4 glycosidic bonds between uronic acid residues in polygacturonate or low
methoxylated pectin by β transelimination. By comparison, PG is an enzyme that
cleaves α-1,4 glycosidic bonds by hydrolysis. Production of PL or PG by several
pathovars of P. syringae has been previously reported (Hildebrand 1971; Bashan et
al. 1985; Longland et al. 1992; Magro et al. 1994). However, the results presented
earlier were often varied with the methods tested. For example, Magro et al.
(1994) reported the detection of two PLs in the culture filtrate of P. syringae pv.
glycinea by the overlay enzyme activity staining technique. However, a diagnostic
pectate gel assay conducted by Hildebrand (1971) predicted the production of PG
instead of PL by P. syringae pv. glycinea. By using a cloned pel gene from P.
viridiflava (Liao et al. 1992) or P. syringae pv. lachrymans (Bauer and Collmer
1997) as a probe, only a single pel gene was detected in two different P. syringae
pv. glycinea strains examined
To clarify the confusion about the pectolytic property of P. syringae, Liao et al
decided to re-examine this property on a sensitive pectate agar medium designated
SSP (Liao et al. 1999) and to clone and characterize the pel gene from a
nonpectolytic strain of P. syringae pv. glycinea. Unlike the earlier reports
mentioned above, none of the 23 strains of the P. syringae pathovars glycinea,
phaseolicola, tagetis, tomato, and syringae examined in this study exhibited
pectolytic activity in vitro. However, we found that homologous pel sequences
could be detected in the genomes of several nonpectolytic pathovars of P.
syringae, including glycinea, phaseolicola, and tagetis. The primary objective of
this study was to determine why pel-containing P. syringae failed to exhibit
pectolytic activity and to produce a detectable amount of PL.(Liao et al 2006)
2- Janjusevic et al 2006 Studied the protein AvrPtoB from Pseudomonas syringae
which translocated into plant cells, where it inhibits immunity-associated
programmed cell death (PCD). The structure of a C-terminal domain of AvrPtoB
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that is essential for anti-PCD activity reveals an unexpected homology to the Ubox and RING-finger components of eukaryotic E3 ubiquitin ligases, and we show
that AvrPtoB has ubiquitin ligase activity. Mutation of conserved residues
involved in the binding of E2 ubiquitin-conjugating enzymes abolishes this
activity in vitro, as well as anti-PCD activity in tomato leaves, which dramatically
decreases virulence. These results show that Pseudomonas syringae uses a mimic
of host E3 ubiquitin ligases to inactivate plant defenses.
3- In 2004 Masami et al Studied the nucleotide sequence and organization of
copper resistance genes from Pseudomonas syringae pv. actinidiae. As Known
the copper containing bactericides have been used to control bacterial canker of
kiwifruit, caused by Pseudomonas syringae pv. actinidiae. However, the efficacy
of copper has been reduced by the occurrence of copper-resistant strains. Analysis
of the DNA sequence of a cluster region containing the copper-resistance genes
from P. syringae pv. actinidiae suggested the presence of three possible different
systems for copper resistance: copper-trapping, copper-efflux and copper-transport
systems. Transposon insertional inactivation analysis indicated that the coppertrapping system was essential for copper resistance (Masami et al 2004)
4- Kamiunten et al studied the characterization of ISPsy2 and ISPsy3 as a newly
identifeied insertion in Pseudomonas syringae pv. eriobotryae which causes
stem cankers on loquat trees. It harbors a 52-Mdal plasmid involved in its
virulence. In our previous paper6), they reported the cloning and sequence of the
virulence gene psvA on a 52-Mdal plasmid. Sequence analysis of the upstream
region flanking the psvA gene revealed the presence of an insertion sequence (IS)
5-like element. Insertion sequences are mobile bacterial DNA elements capable of
mediating various DNA rearrangements such as transposition, deletion,
inversion and cointegration. The psvA gene was also detected in the genomes of
gall-inducing P. s. pv. dendropanacis and P. s. pv. myricae6). The G+C content
of the psvA gene region is about 50%, which is relatively lower than that of P.
syrigae 59-61%, suggesting that the psvA gene is probably horizontally transferred
into P. syringae. If the IS5-like element was an active transposable element, this
IS5-like element located adjacent to the psvA gene could have something to do
with the horizontal transfer processes of the psvA gene, as was suggested for the
transfer of the IAA biosynthesis genes. In there study, they have demonstrated
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that this IS5-like element is indeed able to transpose frequently into a trap vector
of transposable elements, PSHI1063, in P.s.pv. eiobotryae. We thus designate it as
ISPsy2. We have also identified another new IS element, ISPsy3 transposed into
pSHI1063 in P. s. pv. eriobotryae. The two new active insertion sequences, ISPsy2
and ISPsy3, were isolated from Pseudomonas syringae pv. eriobotryae, the causal
agent of stem cankers of loquat trees. ISPsy2 is 1194-bp long, has 16-bp imperfect
terminal inverted repeats, and generates a 4-bp target site duplication upon
insertion into the selective cartridge of the entrap vector pSHI1063. The nucleotide
sequence of ISPsy2 is completely identical with that of the previously identified
IS-like element located adjacent to the virulence gene psvA of Pseudomonas
syringae pv. eriobotryae NAEG. The single open reading frame of ISPsy2 encodes
a 323-amino-acid protein that has similarity to the transposase of the IS5 subgroup
of the IS5 family. is 1507 bp in length, does not duplicate its target sequence,
GAAC, and presents The ISPsy3 belonging to the IS91 family an 81% sequence
homology with IS801 in P. s. pv. phaseolicola. The transposase of ISPsy3
possesses the conserved amino acid motifs found in the rolling-circle replication
protein. Southern blot analysis indicated that multiple copies of ISPsy2 and ISPsy3
are present in the genomes of P. s. pv. eriobotryae and some of the other P. s.
pathovars tested.( Kamiunten et al 2002).
5- Bacterial canker and blast of stone fruit trees, caused by Pseudomonas syringae
pv. syringae, affects all commercially grown Prunus species in California
including peach (Prunus persica), European plum and French prune (P.
domestica), Japanese plum (P. salicina), sweet cherry (P. avium), apricot (P.
armeniaca), and almond (P. dulcis). Losses can result from a direct reduction in
yield due to cold-induced blast or death of buds and flowers or from tree decline
and death due to the development of cankers in branches and major scaffold limbs.
P. syringae pv. syringae is unique among most P. syringae pathovars in its ability
to cause disease in over 180 species of plants in several unrelated genera. Strains
of P. syringae pv. syringae are identified on the basis of biochemical and
nutritional tests and symptom expression in host plants. In many cases, strains of
P. syringae that are found infecting a previously unreported host and are
biochemically similar to P. syringae pv. syringae strains have been placed in this
pathovar without establishment of a common host range.
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The relationship between P. syringae pv. syringae strains infecting Prunus species
and strains that infect other crops such as tomato, cereals, citrus, and kiwi fruit is
unknown and needs to be elucidated. Biochemical tests are not reliable for
differentiating strains at or below the pathovar level, and pathogenicity tests in
greenhouses are not reliable indicators of natural host preferences. Peach seedlings
and cowpea leaves were found to be susceptible to P. syringae pv. syringae strains
from various hosts. There is, however, evidence of host specificity among P.
syringae pv. syringae strains infecting beans and grasses based on the results of
pathogenicity tests.
Molecular analysis of genomic variability has been used to differentiate and
classify bacterial strains below the level of species. Analysis of restriction
fragment length polymorphisms (RFLP) of the chromosomal DNA of P. syringae
strains detected differences between and within the pathovars . More recently,
enterobacterial repetitive intergenic consensus (ERIC) sequences and repetitive
extragenic palindromic (REP) sequences, which are short repetitive DNA
sequences with highly conserved central inverted repeats that are dispersed
throughout the genomes of diverse bacterial species, have been used to design
universal PCR primers that generate highly reproducible, strain-specific
fingerprints that can differentiate bacterial strains below the level of species or
subspecies.
Little et al 1998, made a study the objective of it was to identify and characterize
strains of P. syringae pv. syringae isolated from various Prunus species and other
plant hosts by using pathogenicity testing and RFLP and ERIC-PCR analyses.
(Little et al 1998)
6- Field trials were conducted during 1982-85, to develop a comprehensive spray
program for the control of bacterial canker (Pseudomonas syringae pv, syringae)
of apricot and cherry. Five spray schedules were evaluated as measures to reduce
disease levels. Copper hydroxide at 2.5 g/L in water was applied to apricot, and
bordeaux mixture at 6 g copper sulfate + 8 g hydrated lime/L in water was applied
to cherry, during autumn, winter and pre-bloom spring. The effectiveness of
copper sprays in reducing epiphytic populations of the pathogen during postbloom spring was also tested. Copper hydroxide was applied to apricot, and a
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foliar copper nutrient and copper hydroxide were applied to cherry at low
concentrations. Most spray schedules tested significantly (P<0.05) reduced canker
incidence relative to controls. Excellent control of epiphytic populations of the
pathogen on apricot and cherry was achieved with copper sprays applied at postbloom in spring. A spray schedule consisting of 2 autumn, 1 winter and 2 prebloom spring sprays with copper hydroxide on apricot or bordeaux mixture on
cherry was successful in reducing canker (>67% reduction) and is recommended
for control of the disease. Two applications of copper hydroxide at 1.0 g/L in
water in post-bloom spring considerably reduced (>9 1 %) epiphytic populations
(P. syringae pv. syringae) on apricot and cherry leaves. Later sprays are
recommended for use in combination with the autumn-winter-spring (pre-bloom)
spray schedule, especially under excessively wet and cool weather conditions in
spring (Wimalajeewa et al 1991)
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