May 21, 2001 Volume 10 No.10 Update on Pest Management and Crop Development
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CANTANKEROUS CANKER DISEASES |
(Cathy Heidenreich mcm4@nysaes.cornell.edu & Bill Turechek wwt3@nysaes.cornell.edu, Plant Pathology, Geneva)
Take a walk through almost any sweet cherry or peach orchard in New York and it quickly becomes obvious that something is wrong. Large open wounds oozing with amber colored gum, trees mangled from excessive pruning, and stumps of trees long since removed scattered throughout the orchard are a common sight in many New York orchards. In nearly all cases, this damage was caused by canker-causing pathogens. Canker diseases are an important production problem and account for significant losses of fruit-bearing surfaces where numerous infections occur or cankers are large. In New York, there are two major canker diseases, perennial canker (also known as Cytospora, Leucostoma, Valsa or fungal canker) and bacterial canker.
Perennial canker is the major canker disease responsible for the early decline and death of peaches in New York, and to a lesser extent, sweet cherries. Perennial canker is caused by fungi in the genus Leucostoma. In mature peach orchards, L. cincta is commonly found infecting nodes on 1 year-old shoots, leaf scars, and dead buds. It also causes a decline in sweet cherry. L. persoonii is most commonly isolated from peach and cherry pruning wounds. The two fungi have quite a wide host range, including other species within Rosaceae (the Rose family) and species outside of it. Some of their other hosts include: Sitka mountain ash, black, flowering, pin, sour and Japanese cherries, chokecherry, Damson, common, wild and cultivated plums, prunes, apricots, and golden willow.
Perennial canker symptoms on peach vary, depending on the infection location. Small twig infections are usually found around winter-killed buds or leaf scars. They appear as sunken discolored areas with alternating zonation lines. Infections at nodes appear 24 weeks after bud break and ooze amber gum unless the twig is killed. Branch or twig infections may develop leaf symptoms during the growing season. Leaves often turn yellow, droop, wilt and die. Dead twigs and branches, and canker margins become covered with pinhead-sized black structures coming out through the bark (Fig. 1).
These are pycnidial stroma and are the reproductive structures of the fungus. Under moist conditions, these structures exude flesh to orange colored tendrils (cirri), which contain thousands of spores (conidia). Main trunk and branch infections usually start in pruning wounds or winter-killed tissue. From these points of entry the cankers slowly expand and girdle infected trunks or branches. Small, weak shoots that develop in the centers of trees are especially susceptible. Cankers on the main trunk, older branches, scaffold limbs and in branch crotches are the most conspicuous evidence of the disease (Fig. 2).
These cankers are elliptical in shape and exude excessive amounts of amber colored gum. As cankers age, the gum becomes dark brown and the bark dries and cracks open, exposing the blackened dead tissue beneath.
During late spring and early summer, the active growth of the tree restricts canker enlargement. Often a callus ring is formed around the infection, preventing invasion of new tissue (Fig. 3).
However, when the tree goes into dormancy, the fungus becomes active again and continues to infect surrounding healthy tissue. This yearly alternation of callus formation and tissue invasion leads to a very evident canker with concentric callus rings. Trees under stressed conditions may have more diffuse cankers, as they are unable to produce callus rings in self-defense.
Bacterial canker is caused by the bacteria Pseudomonas syringae pv. syringae and Pseudomonas syringae pv. morsprunorum. The bacteria overwinter in bark tissue at canker margins, in apparently healthy buds and/or systemically in the vascular system. In the spring, bacteria multiply and emerge from their overwintering sites and are disseminated by wind and rain to blossoms and young leaves. In severe cases, infected buds emerge but are quickly "blasted" (Fig. 4).

Bacteria of both pathovars can live in an epiphytic phase (i.e., live on plant tissues without causing symptoms) on blossoms and leaves from bloom through leaf fall in autumn. P.s. pv. syringae can also live epiphytically on a variety of weed hosts. During the spring and summer, epiphytic bacteria or those from wound sites enter the host through leaf stomata, enabling them to endure adverse environmental conditions during warm and dry periods. Under cool and wet conditions, the bacteria multiply profusely and induce disease symptoms and/or replenish epiphytic populations. The bacteria may reach axillary buds by systemic spread from infected leaves through the petiole throughout the season. Cankers subsequently appear at the base of infected buds. Canker expansion slows during winter but resumes again in early spring. The bacteria typically enter tree limbs and the trunk through pruning wounds and/or sites of freeze injury in autumn and early winter (Fig. 5 shows a young canker; Fig. 6 an advanced canker).

Because cherries are vulnerable to winter injury, bacterial canker is particularly a problem in New York where winter injury is common. Canker expansion at these sites is similar to that described for axillary bud infection.
Disease Management. Since canker symptoms are often indistinguishable, these two diseases are often confused with each other, particularly on sweet cherry. Moreover, an infection initiated by one of the pathogens often predisposes a tree to infection by the other; as a result, these two diseases can often be found together on the same tree. This, however, is much more common on sweet cherry than peach or nectarine. How best to tell them apart? The presence of pimply pycnidia on the margins of perennial cankers or along the length of infected wood is probably the best clue, but is not always reliable, as pycnidia are not formed in all cases.
Although these two diseases are caused by pathogens on opposite ends of the biological spectrum (i.e., one is caused by fungi, the other by bacteria), disease management tactics are similar for both. Remember, both attack weak, injured, or dying trees. Thus, any practice or event that weakens or injures a tree, such as freeze injury, pruning cuts, and poor nutrition, promotes infection by these pathogens. Reduction of mechanical and winter injuries and other stresses will help to reduce your chances of infection. Pruning wounds are most susceptible to infection early in the dormant season, but spring pruning cuts may also become infected. There are no fungicides registered specifically for Leucostoma control, and those applied for peach leaf curl and brown rot control give only minimal reduction in perennial canker infections. Fixed-copper compounds are recommended for bacterial canker control; however, the optimum timing and effectiveness of copper compounds is not fully understood. (We are limited to when we can apply copper due to the phytotoxic effects.) Current label recommendations call for one autumn application "before heavy rains begin" and another at late dormant. A third application is also labeled for use shortly after harvest in orchards where disease is severe, but is sometimes discouraged due to the phytotoxic effects of copper.
The other important factor to consider in disease management is to reduce the amount of inoculum or disease pressure in and around your orchard. Pruning out cankers removes the source of disease for new cankers within your orchard, and eliminating wild hosts around the periphery of your orchard reduces disease pressure from outside sources. Sanitizing pruning instruments between cuts will reduce the chance of spreading disease through pruning cuts. The bottom line is that there are no silver bullets. Disease management is accomplished though a combination of well-timed horticultural and disease sanitation practices. The following checklist provides guidance to help minimize damage due to canker diseases.
Establish new plantings at a distance and upwind from old cankered blocks.
Plant on sites with deep, well-drained soils and good air drainage to minimize winter injury.
Removal of wild Prunus species in hedgerows adjacent to sweet cherry orchards will help to reduce inoculum.
Nursery stock should not be too large (11/16 caliper or smaller), and should be planted without delay upon receipt to minimize additional stress.
Plant only disease-free nursery stock. Inspect trees before planting. Cut out any small cankers on lateral branches, removing at least 10 cm of healthy tissue below the canker before planting.
Train to promote wide crotch angles, which will help reduce winter injury and breakage.
Prune trees to open centers, eliminating small, weak shoots.
Annual pruning should be done in June or July when trees are active. This allows pruning cuts to heal quickly. Prune if possible during warm, dry weather. Avoid leaving pruning stubs.
All cankers should be pruned from trees and burned, buried or removed far from the orchard to reduce inoculum sources.
Prune cankered limbs well below visible canker, avoid pruning in early spring and fall when bacteria are most active, and sterilize pruning tools before pruning healthy trees.
Control oriental fruit moth, peachtree borer, brown rot and peach leaf curl diseases to reduce points of entry for the fungus. This is particularly important during the establishment years! Use wire tree guards to prevent rodent damage.
The area around the base of young trees should be kept free from weeds and trash. This helps keep the trunk and crown dry and potentially reduces epiphytic populations of P. s. pv. syringae.
Promote tree vigor! Use balanced nitrogen fertilization with adequate potassium. Do not over-fertilize late in the season, as this delays winter hardening. Avoid water stress.
White latex paint applied to the southwest sides of trunks and lower scaffold limbs may help to reduce winter injury (sunscald).