Introduction Blight

Blight refers to a specific symptom affecting plants in response to infection by

a pathogenic organism. It is simply a rapid and complete chlorosis, browning, then death of plant tissues such 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

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

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 of E. 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 of E. 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

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 by E. 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 of E. 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 by E. 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 of E. 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 of E. 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 time orchard inspections and/or pruning activities.

Figure 11

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

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 bacterium Pseudomonas 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

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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