Left: A classic bacterial canker symptom showing cankers and gummosis of woody tissue. Right: Bacterial canker on a scaffold George Sundin
Bacterial canker, caused by Pseudomonas syringae pvs. syringae (PSS) and morsprunorum, is an important disease of sweet cherry, tart cherry, apricot, and other stone fruit. Symptoms include blossom blast and spur dieback, leaf and fruit lesions, cankers with associated gummosis of woody tissue, loss of scaffold limbs, and overall decreased fruit yields.
This disease is most problematic in sweet cherries, and epidemics often occur in conjunction with cold, frost-prone weather in the spring. Of the two bacterial canker pathogens, PSS is the most virulent. PSS is the predominant pathogen on sweet cherry in Michigan and represented approximately 62% of the pathogenic Pseudomonas isolates we recovered in a recent two-year survey of Michigan orchards.
The most important factor regarding bacterial canker is that the PSS pathogen is an opportunistic pathogen. This means that trees must be weakened or predisposed to infection for disease to occur. There are four main factors that can predispose trees to PSS infection:
• reduced soil fertility, with nitrogen levels most critical
• nematodes in the soil
• low soil pH
• frost injury
Researchers in California, led by Dr. Bruce Kirkpatrick, have shown that canker lengths on inoculated peach trees receiving supplemental nitrogen fertilization were significantly reduced compared with nonfertilized trees. Regarding nematodes, populations of the lesion nematode in Michigan soils and the pin nematode in California soils are associated with an increased incidence of bacterial canker. Trees planted on nematode-free fumigated sites typically are more resilient to bacterial canker. The nematodes may predispose trees to infection by altering tissue nitrogen levels. When soil pH falls below 5.5, this benefits the PSS pathogen, and this may also involve alterations in nutrient uptake. These first three predisposing factors affect the general health of trees and, in combination with PSS infection, lead to the overall decline of orchard blocks. The fourth factor, frost injury, can result in a much more active phase of canker infection due to the association of the PSS bacterium with frost-injured tissues as discussed under “Ice formation” below. Risk to cherries
Sweet cherry trees infected with bacterial canker are at high risk of being killed by this disease due to the endophytic nature of the infection and systemic movement of the pathogen in woody tissue. In young trees, this can mean death of the tree and, in older trees, loss of scaffold limbs. Endophytic PSS populations can be established in a number of ways. One method is through leaf scar infection in autumn at leaf drop, which results in internal migration and colonization of dormant buds. Bacterial populations are typically high on symptomless leaves in autumn, and conditions at leaf drop (wind and driving rain) favor dissemination of bacteria to leaf scars. Colonized buds can remain apparently healthy over the winter or can be killed by the pathogen, leading to the dead bud symptom which is typically associated with canker formation. In either case, colonized buds provide pathogen inoculum for the next season.
PSS can only infect trees through wounds or natural openings; however, this can include pruning wounds and other natural wounds such as cracks in bark. From a disease standpoint, the timing of pruning is best when the pathogen is inactive, either when trees are dormant or in midsummer. Systemic invasion of shoots following blossom infection can also occur. In the spring, PSS populations that overwintered in dormant buds provide the primary inoculum for epiphytic blossom colonization. Cold, wet weather then favors increases in PSS populations on blossoms; these populations are a particular problem because frost injury to blossoms causes wounds that provide an easy entry for the pathogen. Ice formation
Unfortunately, PSS cells also contribute to frost injury because most PSS strains are ice nucleation active. Ice nucleation activity is a trait whereby PSS cells can catalyze ice formation at temperatures only slightly below freezing. Pure water can supercool significantly below 32°F without freezing. The presence of ice-nucleation–active PSS cells, however, enables ice to form at temperatures of approximately 28°F or below. Once ice is formed, it rapidly propagates through sensitive tissue such as blossoms. The severity of frost damage plays a critical role in the occurrence of subsequent bacterial canker infection.
Ice formation initiated by PSS is dependent upon temperature and the number of cells present. At 28°F, approximately one in 1,000,000 PSS cells freeze. At 27°F, one in 10,000 cells freeze, and at 25°F and below, one in 10 cells freeze. Sweet cherry blossoms in Michigan typically harbor relatively large PSS populations on the order of 200 to 80,000 cells per individual blossom. Thus, these populations are large enough that orchard exposure to temperatures of 27°F or below during bloom can result in large-scale damage. Luckily, frost events below 27°F are rare and so frost damage is usually sporadic and typically results in the killing of small numbers of flowers without associated PSS infection. However, on May 22, 2002, a hard radiational frost occurred in northwest and west central Michigan with sustained temperatures of 26°F over an 11-hour duration. This freeze event and resulting injury was followed by widespread wood invasion, canker formation, and death of trees. Few control options
Thus, when these type of freeze events happen, they can be devastating. A major limiting factor is our ability to effectively reduce populations on blossoms. The only bactericide registered for bacterial canker management is copper, which is of limited use because sweet cherry trees are susceptible to copper phytotoxicity following bud break in the spring. Copper sprays have been traditionally applied during leaf drop in an attempt to reduce leaf scar infection, and as dormant sprays prior to bud break in an attempt to reduce pathogen populations either on the surface of cankers or emerging from dormant buds. Relatively high rates of copper (2 pounds metallic copper per acre) can be used at these timings. If the trees have broken dormancy and are in the prebloom stage (bud swell through white bud), copper rates should be reduced to 25% of the dormant rate, but we have found that knockdown of PSS populations only lasts for a few days. The development of copper resistance in PSS can be a factor, but we have found that currently this is not a serious problem in Michigan.
Bacterial canker may be the most difficult tree fruit disease to manage due to the lack of effective chemical controls and the susceptibility of many important varieties. Improving tree health may reduce long-term decline from this disease.