Bacterial canker of stone fruit, Pseudomonas syringae

A canker with gum exudation on sweet cherry caused by bacterial canker — Figure 1. A canker with abundant gum exudation on a sweet cherry scaffold limb.

Savvas Pastopoulos, Agronomist MSc — Pastopoulos Agricultural Ltd

Bacterial canker of stone fruit is a dangerous and destructive disease capable of causing serious loss of the orchard itself. It is caused by bacteria of the genus Pseudomonas. The pathogens attack the woody tissue of the tree in shoots, buds, scaffold limbs and trunks and move systemically through the xylem vessels. They cause extensive dieback of shoots and buds, and in young trees they can kill the whole plant in the form of an apoplexy. All stone fruits are susceptible, but sweet cherry, apricot and plum are the most sensitive species.

Contents

The pathogen — two bacteria, not one
The symptoms
The annual cycle and the points of entry
Frost is not a coincidence — the bacterium creates it
The predisposing factors
Differential diagnosis — what else looks like this
Cultivars and rootstocks
Management
Copper: which form, when, and why it fails
When to send a sample
Sources

1. The pathogen — two bacteria, not one

Two pathovars with different behaviour

Pseudomonas syringae pv. morsprunorum — found exclusively on Prunus species. It comprises two races, R1 and R2, originally recorded as the same pathovar; phylogenetic analysis showed, however, that they are distantly related and belong to different phylogenetic groups.
Pseudomonas syringae pv. syringae — has a much wider host range. It attacks sour cherry, peach, plum, soft fruit, and a great many weeds growing on the orchard floor.

Why this matters: because pv. syringae survives epiphytically on many other plants, the weeds in the rows and the neighbouring vegetation act as a permanent reservoir. A clean orchard does not guarantee a clean environment. It is also worth noting the correct spelling: morsprunorum, from mors (death) and prunorum (of the plums).

The bacterium lives on the tree without making it ill A point that changes how the problem is approached: colonisation can occur in any plant tissue without causing infection or symptoms. The bacterium lives epiphytically, as a normal inhabitant of the surface of leaves and shoots. Infection requires two things at the same time: a wound or natural opening, and wet conditions or standing water. Without a wound there is no disease, however high the population. The whole strategy comes down to this: the target is not the bacterium, it is the doors it comes in through.

2. The symptoms

The disease causes copious gum exudation at the point of attack (the canker). The affected wood turns dark brown, and at the margin of the lesion a dark line is sometimes visible.

At the start there is a small water-soaked spot at the point of attack, which within a short time can expand longitudinally and irregularly. The bark often splits and abundant gum is produced.

On the leaves the disease produces circular brown spots, which separate from the leaf and drop out, giving the familiar shot-hole symptom — similar to shot hole caused by Wilsonomyces.

Figure 2. Bacterial canker attack on the trunk of a young sweet cherry tree.

Gum on its own is not a diagnosis — and its colour is not enough either

In sweet cherry there are also non-infectious causes of gummosis: mechanical injury, sunscald, frost damage, attack by wood-boring insects, water stress. The descriptions in circulation are as follows:

Non-infectious gummosis: generally described as clear to amber.
Bacterial canker: the most characteristic symptom is a dark canker, sometimes accompanied by a reddish-brown exudate.

But care is needed over how much weight colour is given. The very source that gives the above description adds immediately that “diagnosis usually requires expert assessment or laboratory testing”. The colour of the gum is an indication, not a criterion: there is overlap between the two categories, and non-infectious gummosis is also described as dark amber.

The reliable criterion in the field is the knife, not the eye. The outer bark is scraped away beneath the gum, over a small area:

If the inner bark is still cream-coloured, the tissue is alive and the gummosis is due to a non-living cause — no intervention is needed.
If the inner bark is tan to brown, the tissue is dead and was most probably killed by a pathogen or a pest.

In bacterial canker specifically, the necrosis under the bark shows a distinct reddish-brown pattern affecting the vascular system, visible when bark and wood are cut tangentially with a clean, sharp knife. Finally, a feature that is rarely looked for: reddish lesions with a foul smell in the bark of the root are reported as indicative of P. syringae attack.

When the canker girdles the trunk If the lesion girdles the trunk or a scaffold limb, the tree above the canker shows no gum or canker at all. It shows chlorosis, small leaves, small fruit and general decline — a picture that looks exactly like water stress or nutrient deficiency. Many trees are “fertilised” and “irrigated” for years while their trunk is strangled. Before any change to the fertiliser programme, the check is made at the base of the trunk.

Bacterial canker attack on a sweet cherry trunk — Figures 3, 4. Trunk lesions caused by bacterial canker.

Canker and gummosis on a trunk — Figures 3, 4. Trunk lesions caused by bacterial canker.

Video. Bacterial canker attack in the field.

3. The annual cycle and the points of entry

As the temperature rises in summer the tree reacts and produces callus tissue, while at the same time the bacteria become inactive; in winter, however, the infections start again.

In spring, with the rains, the bacterium emerges from the cankers and is dispersed onto the leaves and shoots. It enters through the leaf stomata and causes the leaf spotting. In autumn and winter the bacteria attack the shoots through leaf scars, pruning cuts and hail wounds, causing the dieback.

Two peaks a year — and the autumn one is usually forgotten

The bacterial population is not constant. It follows a defined curve:

Overwintering: it survives inside the cankers and inside the buds. These two sites are the main source of inoculum for the following season.
Spring: the population increases after bud break, and symptoms develop in spring and summer.
Late summer: the population declines.
Autumn: there is a second peak of infection, with the cooler and wetter conditions.

The optimum temperature range for infection is 15–25 °C combined with moisture. This is therefore not a disease of hard winter or of extreme heat — it is a disease of the transitional seasons. Autumn leaf fall, which leaves tens of thousands of fresh scars per tree at exactly the moment the rains begin, is the most underestimated point in the year.

The commonest point of entry in young trees is not where it is looked for

In the records of recent years, most infections in new plantings were associated with the heading cut made at planting in spring — that is, the short cut of the young tree to establish the training system — when that cut was wetted by irrigation water at cool temperatures.

Other documented entry points: frost damage or thermal injury to the trunk, wounds from animals and rodents, mechanical injury from machinery, and fresh leaf scars — whether from natural fall in autumn or from hand removal of leaves at the base of newly planted trees. The practical conclusion for planting is simple: heading cuts and sprinkler irrigation do not coincide in cold, wet weather, and the trunks of young trees are protected.

4. Frost is not a coincidence — the bacterium creates it

Ice nucleation: the bacterium that freezes the tree

This is the most misunderstood mechanism of the disease. P. syringae produces a protein that acts as an ice nucleus (ice nucleation activity, INA). The bacterium can form ice inside the plant cell itself.

The consequence is twofold and vicious: a plant carrying a large population of INA bacteria freezes at a higher temperature than it would freeze without them. In other words, frost becomes damaging earlier. And the wounds the frost creates are exactly the doors the bacterium itself needs in order to enter.

The bacterium therefore manufactures the very wounds through which it will invade. That is why, internationally, the disease is most severe precisely in the areas of high frost risk, and why a large part of its management worldwide has turned towards frost management rather than bactericides. Reducing the epiphytic population before the spring frosts brings a double benefit.

5. The predisposing factors

The disease rarely strikes healthy, balanced trees. It strikes trees that are already stressed by something else.

Biotic factors

Viruses and phytoplasmas — a weakened tree, easier establishment.
Verticillium — found in combination with P. syringae in the same trees.
Leucostoma (Cytospora) — a second canker on the same tree.
Nematodes — see the box below.

The nematode–bacterium complex: the experiment that proved it

The ring nematode Mesocriconema xenoplax feeds on the fine absorbing roots and predisposes Prunus species to bacterial canker. In experiments on sandy soil, peach trees became seriously diseased only when both were present — the nematode and the bacterium. If either one was missing, serious disease did not develop.

The mechanism is attributed to reduced nutrient uptake and to a change in the carbon-to-nitrogen ratio within the plant, which leaves it vulnerable. Practical consequence: in an orchard with recurrent bacterial canker, particularly on light, sandy soils, a soil nematode analysis is worth doing. Spraying copper alone addresses half the problem.

Abiotic factors

Winter frosts and late spring frosts — the strongest factor.
Alkaline soils and calcareous layers that restrict root development.
Nutrient deficiencies and water stress.
Extreme heat, which leaves the tree weakened going into the autumn infection period.
Poor drainage and a high water table, which keeps water in contact with the trunk.

6. Differential diagnosis — what else looks like this

The symptoms are not pathognomonic, since the same symptoms are produced by other diseases as well, such as Cytospora and Botryosphaeria.

Pathogen	How it is distinguished
Bacterial canker P. syringae	A canker with no clear margin, expanding longitudinally with an irregular outline. Reddish-brown gum. Internally a reddish-brown necrosis pattern in the vascular system, visible when bark and wood are cut tangentially with a clean, sharp knife.
Cytospora canker Leucostoma cinctum	The canker has a clearly defined margin. On its surface, minute, pimple-like structures — the pycnidia — are visible, inside which the spores are produced. It is the most reliable macroscopic distinguishing feature.
Little cherry disease and X-disease LChV-1/2, phytoplasma	These also give small fruit and decline, but with an uneven picture: on the same limb, ripe fruit of normal size coexists with small, yellow, unripe fruit. In bacterial canker the small fruit are uniformly small and uniformly coloured throughout the affected limb or tree.
Shot hole W. carpophilus	It also produces holes in the leaves, but the spots are regular and circular and are accompanied by small cankers on the shoots without gum.

And a reminder It is entirely possible for one tree to have more than one disease at the same time. Finding one does not rule out the other — and often one is the reason the other developed.

7. Cultivars and rootstocks

Resistant cultivars are planted in the wet sites. For example: the sweet cherries Tsolakeika and Grace Star are fairly susceptible to infection and are not recommended for wet, heavy ground.

The international ranking — and what it says about rootstocks

All cultivars and all rootstocks become infected. The differences are of degree, not of absolute immunity.

Susceptible cultivars: Sweetheart, Bing, Staccato, Royal Ann (Napoleon), Van. Particularly susceptible is Coral Champagne.
With higher resistance: Corum, Regina, Moreau, Lambert, Sam.

Rootstocks: Mazzard and Colt appear more resistant, while the more dwarfing rootstocks are more susceptible — Gisela 6 and Krymsk 5 are named explicitly.

And one point that concerns spread within the orchard: the bacterium is transmitted by grafting and moves systemically. Vigorous rootstocks have a greater likelihood of natural root grafting between neighbouring trees, and therefore of carrying the bacterium from tree to tree, compared with dwarfing and semi-dwarfing ones.

8. Management

The disease has no curative chemical treatment. Control is achieved through preventive measures:

The seven measures

Planting material free of the bacterium.
Removal every year, at pruning or earlier, of all affected shoots back to healthy tissue, and painting of the wounds with copper.
Regular winter sprays with copper products, particularly during leaf fall and before and after pruning — not onto green growth. Painting of the trunks with Bordeaux mixture.
Pruning during dry periods, when there is no rain.
Planting resistant cultivars in the wet sites.
Ionic, gluconate and other coppers in summer — their effectiveness remains under investigation.
Products based on antagonistic bacterial strains can be used in summer.

Two techniques that are not widely known in Greece

Cauterisation of the cankers. A method documented since 1976: the canker on the scaffold limbs is cauterised with a portable gas torch. The treatment is applied in spring. It works because the bacterium is located at the margin of the canker, in a zone that the heat reaches, while the woody tissue withstands it.
Whitewashing the trunk. In new plantings of susceptible cultivars, protecting the trunk with white paint — together with a double drip line so that water does not touch the trunk — is recorded as a best cultural practice. It reduces thermal injury and the cracks caused by sharp temperature swings, which are precisely the points of entry.

The pruning shears: what the data show Disinfecting tools is sound practice and should not be abandoned. It is worth knowing, however, where the risk actually lies: mechanical transfer on pruning tools does not appear to be a major risk — unless the equipment comes into direct contact with fresh gum and the conditions are favourable, that is cool and wet. The primary risk is not the tool; it is the cut itself, left open in wet and cool weather. That is why the rule “prune in dry weather” carries more weight than the rule “disinfect the shears” — and both together are the right answer.

9. Copper: which form, when, and why it fails

Not all coppers are the same against this bacterium

This is among the most practical and least known findings. In comparative trials on sweet cherry twigs:

Copper hydroxide (divalent copper, Cu²⁺) is the documented choice for winter sprays.
Copper oxides (monovalent copper, Cu⁺) proved ineffective at controlling the disease.

Given that many programmes rely on copper oxide because of its cost, the finding deserves attention. The recommendation stands: for bacterial canker, copper in the hydroxide form.

Source: Torres, R. and Latorre, B. 2009. Efectividad de compuestos a base de cobre en el control de Pseudomonas syringae pv. syringae en ramillas de cerezo. Resúmenes Jornadas Agronómicas, Chile. The trial is cited and evaluated in Sallato, B., Grove, G. and Johnson, A., Bacterial canker in Washington sweet cherries, WSU Extension FS366E, which also carries the recommendation to use fixed copper in the hydroxide form for winter sprays. Note: this is a conference proceedings publication, not a peer-reviewed journal paper; the finding is clear but comes from a single series of trials.

Timing — and the absolute limit

Winter sprays: at leaf fall and during dormancy, with emphasis before and after pruning.
Before bloom: copper; internationally, a combination with the antibiotic kasugamycin is also reported, which is not approved in the European Union for this crop.
After full bloom, copper is not applied. This is an absolute limit, both for phytotoxicity and for the pollen.

The four reasons copper fails Copper control is in practice erratic: it works in some seasons and not in others. Four causes are documented — (1) copper-resistant strains, which have been recorded alongside antibiotic resistance, (2) poor coverage of the tree by the spray, (3) wrong timing and (4) very high disease pressure within the orchard. The first three are within the grower's control. When copper is not working, the problem is usually not the product but the coverage and the timing.

10. When to send a sample

In cases of doubt about the pathogen causing the symptoms, a sample should be sent for analysis to the Benaki Phytopathological Institute, or to the corresponding national diagnostic laboratory. Bactericides must always be used in accordance with the label instructions.

When laboratory testing is genuinely worth it

When the canker has no clear margin but no pycnidia either — that is, when it cannot be separated from Cytospora.
When there is general decline with small fruit and no visible canker, in which case little cherry disease and phytoplasma also have to be ruled out.
In a new planting with tree losses, where the question “did it come with the material or was it infected here?” has financial consequences.
When an orchard has a recurrent problem despite correct copper sprays — in which case a soil nematode analysis is requested at the same time.

11. Sources

Sallato, B., Grove, G. and Johnson, A. — Bacterial canker in Washington sweet cherries. WSU Extension Publication FS366E, Washington State University. Main source for the annual cycle, the points of entry, cultivar and rootstock susceptibility, cauterisation, trunk whitewashing and the differential diagnosis.
Cherry (Prunus spp.) — Bacterial canker. Pacific Northwest Plant Disease Management Handbook. Source for the four reasons copper fails and for copper resistance.
Characterization of the pathogenicity of strains of Pseudomonas syringae towards cherry and plum. Source for the distinction between pv. syringae and pv. morsprunorum and for races R1 and R2.
Kennelly, M.M., Cazorla, F.M., de Vicente, A., Ramos, C. and Sundin, G.W. 2007. Pseudomonas syringae diseases of fruit trees: progress toward understanding and control. Plant Disease 91:4–17.
Lindow, S.E., Arny, D.C. and Upper, C.D. 1978. Distribution of ice nucleation-active bacteria on plants in nature. Applied and Environmental Microbiology 36:831–838. The foundational paper on ice nucleation.
Influence of ring nematode infestation and calcium, nitrogen and indoleacetic acid applications on peach susceptibility to Pseudomonas syringae pv. syringae. Phytopathology.
Influence of Nemaguard and Lovell rootstocks and Macroposthonia xenoplax on bacterial canker of peach. The experiment showing that both organisms are needed for serious disease.
Plant-parasitic nematodes in pome and stone fruit orchards. WSU Tree Fruit.
Spotts, R.A., Wallis, K.M., Serdani, M. and Azarenko, A.N. 2010. Bacterial canker of sweet cherry in Oregon — infection of horticultural and natural wounds, and resistance of cultivar and rootstock combinations. Plant Disease 94:345–350.
Torres, R. and Latorre, B. 2009. Efectividad de compuestos a base de cobre en el control de Pseudomonas syringae pv. syringae en ramillas de cerezo. Source for the difference between copper hydroxide and copper oxide.
Gummosis of stone fruits — Utah State University IPM Pest Advisories. Source for the knife test: cream inner bark means a non-living cause, tan means tissue killed by a pathogen.
Gummosis on Prunus (cherry) — University of Tennessee, Department of Plant Sciences.
Hawkins, J.E. 1976. A cauterization method for the control of cankers caused by Pseudomonas syringae in stone fruit trees. Plant Disease Reporter 60:60–61.
Mgbechi-Ezeri, J., Porter, L., Johnson, K.B. and Oraguzie, N. 2017. Assessment of sweet cherry (Prunus avium L.) genotypes for response to bacterial canker disease. Euphytica 213:145.
Control of bacterial canker in stone fruit trees by chemical and biological products. Agronomy 13(4):1166.
Benaki Phytopathological Institute — submission of samples for laboratory identification.

Disclaimer This text is informative and educational in character. It does not replace an on-site agronomic assessment, nor does it constitute a prescription for the application of plant protection products. No trade names are given; the choice is made on the basis of the authorisations in force in the country concerned — in Greece, those of the Ministry of Rural Development and Food. Approvals of active substances, doses and pre-harvest intervals change and differ between countries and crops; the label instructions always apply. Pastopoulos Agricultural Ltd accepts no liability for the use of the above information.