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7/28/2019 Fire Blight
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Introduction
Blight
Blight refers to a specificsymptomaffectingplantsin response to infection by
apathogenicorganism. It is simply a rapid and completechlorosis, browning, then death of
planttissuessuch as leaves, branches, or floral organs.
Fire blight
Fire blight is a common and very destructive bacterial disease of apples and pears. The disease
is so named because infected leaves on very susceptible trees will suddenly turn brown,
appearing as though they had been scorched by fire. As a result of this disease, blight susceptible
pear cultivars are no longer grown in many parts in the Midwest.
Damage and losses from fire blight on apple result from: death or severe damage to trees in
the nursery; death of young trees in the orchard; delay of bearing in young trees due to frequent
blighting of shoots and limbs; loss of limbs or entire trees in older plantings as the result of
girdling by fire blight cankers; and direct loss of fruit due to blighting of blossoms and young
fruit.
Fire blight may cause severe damage to many other members of the Rosaceae family. Quince,
crabapple, mountain ash, spirea, hawthorn, pyracantha, and cotoneaster are all susceptible.
Cultivars within some of these species are resistant.
Causal Organism
Fire blight is caused by the bacterium,Erwinia amylovora. The fire blight bacteria overwinter in
living tissue at the margins of cankers on the trunk and main branches.
Invasion
Invasion can occur directly through natural openings, such as lenticels and stomata, under
conditions of prolonged rain and high humidity. However, shoot infection more commonly
occurs through wounds created by sucking insects, such as aphids.
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Pear shoot with fire blight.
Symptoms and Signs
Symptoms of fire blight can be observed on all above ground tissues including blossoms, fruits,
shoots, branches and limbs, and in the rootstock near the graft union on the lower trunk.
Generally, symptoms of fire blight are easy to recognize and distinguishable from other diseases.
Blossom clusters and young shoots
Blossom symptoms are first observed 1-2 weeks after petal fall. The floral receptacle, ovary, and
peduncles become water soaked and dull, grayish green in appearance. Later these tissues shrivel
and turn brown to black. Similar symptoms often develop in the base of the blossom cluster and
young fruitlets as the infection spreads internally (Figure 2). During periods of high humidity,small droplets of bacterial ooze form on watersoaked and discolored tissues (see example on
fruit, Figure 7). Ooze droplets are initially creamy white, becoming amber tinted as they age.
Figure 2 Figure 7
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Shoot symptoms
Shoot symptoms are similar to those in blossoms but develop more rapidly. Tips of shoots may
wilt rapidly to form a "shepherd's crook" (Figures 1 and 3). Leaves on diseased shoots often
show blackening along the midrib and veins before becoming fully necrotic. Numerous diseased
shoots give a tree a burnt, blighted appearance, hence the disease name (Figure 4).
Figure 1 Figure 3 Figure 4
Advanced foliar symptoms
Infections initiated in blossoms and shoots can continue to expand both up and down larger
branches and limbs. Bark on younger branches becomes darkened and water-soaked (Figure 5).
At advanced stages, cracks will develop in the bark, and the surface will be sunken slightly
(Figure 6). Amber-colored bacterial ooze mixed with plant sap may be present on bark. Wood
under the bark will show streaked discolorations.
Figure 5 Figure 6
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Pear and apple fruits
Indeterminate, water-soaked lesions form on fruit surface and later turn brown to black. Droplets
of bacterial ooze may form on lesions, usually in association with lenticels (Figure 7). Severely
diseased fruits blacken completely and shrivel.
Pathogen Biology
Erwinia amylovora is a member of the family Enterobacteriacae. Cells ofE. amylovora are
gram-negative, rod-shaped, measure 0.5-1.0 x 3.0 mm, and flagellated on all sides (peritrichous)
(Figure 9). Physiologically,E. amylovora is classified as a facultative anaerobe. It grows on most
standard microbiological media and on several differential media. Optimum temperature for
growth is 27C (81F), with cell division occurring at temperatures ranging from 5 to 31C (41
to 88F). Identification ofE. amylovora isolates is based on biochemical and serological tests,
inoculation of immature pear fruits and apple seedlings, and DNA hybridization assays.
Figure 9 Figure 10
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Disease Cycle and Epidemiology
Disease Cycle
Overwintering
Erwinia amylovora overwinters in a small percentage of the annual cankers that were formed on
branches diseased in the previous season. These overwintering sites are called holdover
cankers. As temperatures warm in spring, the pathogen becomes active in the margins of
holdover cankers. Free bacterial cells are released onto the bark surface, sometimes as visible
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ooze. Insects attracted to the ooze (e.g., flies) or rain disseminate the bacteria from the canker to
blossoms.
Floral epiphytic phase
Stigmas, which are borne on the ends of the style, are the principal site of epiphytic colonization
and growth byE. amylovora. During the floral epiphytic phase, the ultimate population size that
the pathogen attains is influenced by temperature, which regulates the generation time of the
pathogen, and by the number of blossoms in which the pathogen becomes established, which is
facilitated by pollinating insects, honey bees in particular. Under ideal conditions, stigmas of
each flower can support ~106
cells of the pathogen.
Primary infection in flowers
Blossom blight is initiated when cells ofE. amylovora are washed externally from the stigma to
the hypanthium (floral cup). On the hypanthium, E. amylovora gains entry to the plant through
secretory cells (nectarthodes) located on the surface. In pear, the importance of blossom blight is
expanded further by the tendency of this species to produce nuisance, secondary or rattail
blossoms during late spring and early summer, long after the period of primary bloom.
Secondary phases
This includes shoot, fruit, and rootstock blight. These phases are usually initiated by inoculum
produced on tissues diseased as a result of blossom infection. Wounds are generally required
byE. amylovora to initiate shoot and fruit blight. Insects, such as plant bugs and psylla, create
wounds on succulent shoots during feeding. Strong winds, rain, and hail can create numerous,
large wounds in host tissues. Infection events induced by severe weather are sometimes called
trauma blight. Rootstock blight of apple can result from shoot blight on water sprouts or from
internal translocation ofE.amylovora from infections higher on the tree.
Canker expansion
Both primary and secondary infections can expand throughout the summer, with the ultimate
severity of an infection being dependent on the host species, cultivar, environment, and age and
nutritional status of the host tissues. Young, vigorous tissues and trees are more susceptible to
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fire blight than older, slower growing tissues or trees. Similarly, trees that have received an
excess of nitrogen fertilizer, and therefore are growing rapidly, are more susceptible than trees
growing under a balanced nutrient regime. Rates of canker expansion also can be enhanced by a
high water status in a tree caused by excessive or frequent irrigation or poorly drained soils.
Canker expansion slows in late summer as temperatures cool and growth rates of trees and
shoots decline.
Epidemiological models
Blossom blight is sporadic from season to season owing to the requirement for warm
temperatures to drive the development of large epiphytic populations. Several epidemiological
models (e.g., COUGARBLIGHT, MARYBLYT) predict the likelihood of blossom blight
epidemics based on observed climatic conditions (Figure 11). The models work by identifying
the periods conducive for epiphytic growth ofE. amylovora on blossoms before infection occurs,
and thus are used widely to aid decisions on the need for and timing of chemical applications.
Blossom blight risk models accumulate degree units above a threshold temperature of 15.5
(60F) or 18C (64F). Data on rain or blossom wetness during periods of warm weather are also
used in the models to indicate more precisely the timing and likelihood of blossom infection.
Other temperature-based models predict the time to symptom expression after an infection event
(i.e., the length of the incubation period) based on heat unit sums. These models are used to timeorchard inspections and/or pruning activities.
Figure 11
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Disease Management
Effective management of fire blight is multi-faceted and largely preventative. The grower must
utilize a combination of sanitation, cultural practices, and sprays of chemical or biological agents
to keep the disease in check.
Cultivars
Selection of a resistant cultivar is the most effective method of controlling fire blight. In apple,
for example, some cultivars exist that are moderately resistant to the disease (e.g., Red and
Golden Delicious). For pears, cultivar choices are more limited because superior horticultural
traits (e.g., taste, storage, and marketing qualities) have been difficult to combine with higher
levels of disease resistance. In recent years, fire blight has become more common in apples
because the spectrum of cultivars grown commercially has expanded and shifted toward those
with greater susceptibility to the disease (e.g., Braeburn, Fuji, Gala, Pink Lady). With this shift
has come the recognition that popular dwarfing rootstocks for apple, Malling 9 and 26, are
highly susceptible to fire blight. Dwarfing rootstocks with resistance to fire blight are being
developed and evaluated (e.g., the Geneva rootstock series from Cornell University). Many
ornamental cultivars also show high levels of fire blight resistance.
Elimination of overwintering inoculums
Vigilant sanitation through the removal of expanding and overwintering cankers is essential for
control of fire blight in susceptible cultivars. Removal of overwintering ("holdover") cankers is
accomplished by inspecting and pruning trees during the winter.
Prevention of blossom blight
Prevention of blossom infection is important in fire blight management because infections
initiated in flowers are destructive and because the pathogen cells originating from blossom
infections provide much of the inoculum for secondary phases of the disease, including the
infection of shoots, fruits, and rootstocks. Management actions to suppress blossom blight target
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the floral epiphytic phase. Sprays of antibiotics, streptomycin or oxytetracycline, have effectively
suppressed blossom infection in commercial orchards. (Figure 12)
Figure 12
Copper compounds also are effective but not used widely because copper can be phytotoxic to
the skin of young fruits.E. amylovora has become resistant to streptomycin in some production
areas, limiting the effectiveness of this chemical. Non-pathogenic, bacterial epiphytes sprayed
onto blossoms can preemptively suppress fire blight by colonizing the niche (stigmatic surface)
used byE. amylovora to increase its epiphytic population size. The bacteriumPseudomonas
fluorescensstrain A506, is registered and sold commercially for this purpose (BlightBan A506).
Mid-season suppression of established infections
In summer, established infections are controlled principally by pruning. Effective control
through pruning requires that cuts are made 20-25 cm (8 to 10 inches) below the visible end of
the expanding canker (Figure 13) and that between cuts the pruning tools are disinfested with a
bleach or alcohol solution to prevent cut-to-cut transmission. Repeated trips through an orchard
are necessary, as some as infections are invariably missed and others become visible at later
times (Figure 14). Prunings harboring the pathogen are usually destroyed by burning (Figure 15).
Figure 13 Figure 14 Figure 15
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Selected References
1.Baker, K. F. 1971. Fire Blight of pome fruits: The genesis of the concept that bacteria can be
pathogenic to plants. Hilgardia 40:603-633.
2.Beer, S.V. 1990. Fire Blight. pages 61-63 in: Compendium of Apple and Pear Diseases. Jones,
A.L., and Aldwinckle, H.S. (eds.). APS Press, St. Paul, MN
3.Johnson, K.B., and V.O. Stockwell. 1998. Management of fire blight: A case study in
microbial ecology. Annu. Rev. Phytopathol. 36: 227-248.
4.McManus, P. and V. Stockwell. 2000. Antibiotics for plant disease control: Silver bullets or
rusty sabers? APSnet feature
article:http://admin.apsnet.org/publications/apsnetfeatures/Pages/AntibioticsForPlants.aspx
5.Smith, T.J. 1998. Principles of Fire Blight Control in the Pacific
Northwest.http://www.ncw.wsu.edu/treefruit/fireblight/principles.htm
6.VanderZwet, T., and S.V. Beer. 1995. Fire Blight - Its Nature, Prevention, and Control: A
Practical Guide to Integrated Disease Management. U.S. Dept. Agric., Agricultural Information
Bull. No. 631.
7.Vanneste, J.L. (ed.) 2000. Fire Blight: The disease and its causative agent,Erwinia amylovora.
CABI Publishing, Wallingford, UK.
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