Bacterial canker of kiwifruit (Psa)

Kiwifruit leader with an extensive canker and bacterial exudate, March 2017. The reddish fluid running from the split in the bark is a dense suspension of living bacteria and is the main source of inoculum for the whole orchard in spring.

Savvas Pastopoulos, Agronomist — Pastopoulos Agronomic P.C.

Bacterial canker of kiwifruit is the most serious disease of the crop worldwide. It cannot be cured. Whatever is done, it is done before infection, and success depends on how well the biology of the pathogen is understood and how faithfully orchard hygiene is observed. This article draws on our published work of 2020 and on experience from the orchards of Giannitsa, northern Greece, from 2014 to the present, updated with the international literature, the current EU framework and the products currently approved in Greece.

1. What it is and why it differs from everything else

Bacterial canker of kiwifruit is caused by Pseudomonas syringae pv. actinidiae, referred to in the international literature and in everyday conversation among growers as Psa. It is a Gram-negative, obligately aerobic bacterium, occurring singly, in pairs or in short chains, and moving by one to three polar flagella [1].

Its difference from the familiar diseases is fundamental and needs to be understood before going further. In fungal diseases there are systemic fungicides that act curatively: a spray after infection can stop its progress within a window of some hours or days. With bacterial canker there is no curative intervention. Every available means is preventive and acts only on the plant surface or by preparing its defences. Once the bacterium is inside the tissues, no product reaches it.

The second essential difference is that Psa moves systemically within the plant, through the xylem vessels. It does not stay where it entered. It has been found a metre away from the point of initial infection within six months [1]. This changes cutting practice radically: when removing an infected shoot, the cut must be made well below, into apparently healthy tissue, because the visible canker is only the part of the infection that has had time to express itself.

The third difference is economic and explains why the world panicked. In Italy, between 2010 and 2012, more than 2,000 hectares of kiwifruit were uprooted or cut back. Estimated losses ran to €20,000 per hectare per year in production, €50,000 per hectare for the lost planting investment and €15,000 per hectare for destroying the plants to stop the spread, with orchard yield reductions of 10% to 50% [2].

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2. The pathogen and the four biovars

Psa was first isolated in 1984 in Japan and formally described in 1989 by Takikawa and co-workers. China followed in 1983 and Italy in 1992, where for sixteen whole years it caused no particular problems. In 2008 everything changed: the first major epidemic broke out in the Lazio region and spread immediately to northern Italy. In 2010 it appeared in France, Portugal and New Zealand, in 2011 in Spain, Australia and Chile, and in 2014 in Greece [1][2].

The reason the same bacterium was of no consequence for decades and then became a pandemic lies in its genetics. The pathogen falls into four groups, called biovars or pathotypes in the literature, differing radically in aggressiveness [10].

The fourth group was reclassified in 2015 as a separate pathovar, Pseudomonas syringae pv. actinidifoliorum, precisely because it was shown not to cause the same disease [11]. This has direct practical significance: leaf spots without cankers and without exudate do not automatically mean disaster. It may be the far milder actinidifoliorum, or even a completely different Pseudomonas species. This is why laboratory identification is not a luxury.

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3. Which plants it attacks, and how badly

The highest susceptibility is in Actinidia chinensis, that is, the yellow-fleshed cultivars. In New Zealand the cultivar Hort16A was literally flattened: within less than three years of the first detection, the disease had been found on more than 1,400 orchards, that is 52% of the country's total area, and by March 2014 on 11,084 hectares, that is 81% [2]. The country organised a coordinated national research response, with collaboration between ZESPRI, KVH, Plant & Food Research and the responsible ministries [17].

Actinidia deliciosa, to which the green-fleshed Hayward, Tsechelidis and Greenlight belong, is also attacked, but with less intensity [1]. Infection of the Greek cultivar Tsechelidis has been documented and published [18].

Three things from field experience that are not easily found in the books:

• Males are more susceptible than females and show symptoms earlier. In particular, males of the cultivar Matua are infected more easily than those of Tomouri [1]. In any survey, start with the pollinisers.
• The age of the orchard counts more than is generally assumed. Young plants, young shoots and young leaves are the most susceptible parts. A young orchard collapses, while a very old one shows symptoms only on the arms, without the central trunk being easily attacked, and goes on producing without a large reduction [1].
• The bacterium is not confined to kiwifruit. It has been isolated from plants of other genera, such as Alternanthera philoxeroides, Setaria italica and Paulownia fortunei [1]. The weed flora and the hedgerows around the orchard are not neutral.

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4. The disease cycle through the year

The pathogen is active all year round, but behaves entirely differently by season. Understanding this cycle means understanding when to intervene.

The practical conclusion is that infections and canker formation happen earlier than most people assume, late in autumn or in winter, while the exudate seen in February is the consequence of infections that took place months before [1]. Anyone starting protection in spring has already lost half the battle.

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5. The symptoms, season by season

First phase: the exudates, winter and early spring

From the cankers, the pruning cuts and the buds of infected shoots, a viscous fluid is secreted, initially white and later red or brick-coloured. On buds there is usually a single drop hanging, and the bud often dies [1].

Canker on the trunk of a young plant with the characteristic red exudate running downwards. Note the split in the bark along the canker: beneath it the vascular tissues are discoloured brown.

In the canker area there is a brown discoloration of the vascular tissues beneath the epidermis, as well as a red discoloration of the lenticels [1]. That second sign is a useful diagnostic marker that many people walk past.

Second phase: the leaves, May to August

Asymmetric necrotic spots appear, small at first, surrounded by a yellow halo. The halo is caused by the toxins the bacterium produces, phaseolotoxin or coronatine depending on the biovar [1]. In periods of heavy rainfall the spots enlarge, coalesce and kill larger areas of the leaf.

The classic leaf symptom, photographed with the light behind. The spots are angular and asymmetric, bounded by the veins, and surrounded by a clear yellow halo. Shooting against the light is the easiest way to see the halo in the field.

One finding should govern behaviour: there is a strong correlation between the number of infected leaves in spring and summer and the number of cankers that will appear the following winter [1]. The leaves are not merely a cosmetic problem. They are a forecast.

If rain or high relative humidity prevails before flowering, the young buds are attacked too. The sepals turn brown and flower drop may follow [1].

Third phase: the dieback

At the end of the second phase the infected shoots dehydrate and wilt completely. If the infection is on the trunk of a young tree, the plant dries from the point of infection upwards, while vigorous growth emerges low down, below the point of infection [1]. This frantic production of suckers from the base while the top dies back is one of the most characteristic pictures of the disease at an advanced stage.

Extensive canker along a leader, with dark wet exudate. The section beyond the canker has already lost its vitality. The removal cut must be made well below the visible boundary, because the bacterium has gone ahead inside the vessels.

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6. How it spreads and where it enters

The short answer is: by every possible route. The detail matters, because each route of spread corresponds to a measure that can be taken.

Bees deserve detail, because they are often underestimated. Researchers found that the bacterium survives on bees for up to two weeks, and that it is transferred even to hive bees that never visited an infected plant [9]. The origin of hives brought in for pollination is therefore a plant health matter, not only a beekeeping one. The same applies to artificial pollination with purchased pollen.

From personal observation in the Giannitsa orchards: the common house fly moves over the wet exudate of the cankers, becoming a carrier and transferring the bacterium to other plants [1].

As regards entry points, the bacterium enters through leaf stomata, broken trichomes, lenticels of the woody tissues, flowers, and every wound: pruning, hail, frost or harvest [1]. The plant, in other words, is full of open doors.

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7. Temperature and weather: when infections happen

Here is the key to spray timing. The optimum temperature for development and infection in new shoots is 12 to 18 °C [3][2]. Temperatures above 20 °C do not favour further infection, and from 25 °C symptoms are entirely restricted and the plant forms callus tissue over the cankers [1][2].

This explains why the disease is a problem of spring and autumn and not of summer, and why autumn is more dangerous than it looks: temperatures fall back into the critical window exactly at the time when harvest is creating wounds.

Wind, rain and hail are not merely means of transport: they simultaneously create the wounds through which the bacterium enters. This is why the New Zealand recommendation explicitly includes a spray after a serious wind, rain or hail event [4].

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8. Pruning wounds

This section deserves more attention than any other, because it overturns a very widespread belief.

At Plant & Food Research in New Zealand an experiment was carried out precisely to answer the question how long a pruning cut stays susceptible. Young Hort16A vines were pruned at different intervals, from 0 to 64 days before artificial inoculation. Inoculation was with a 10-microlitre drop of a suspension of 10⁹ bacteria per millilitre, placed on the exposed cut surface.

The result: the plants were infected at every pruning time. Seven weeks after inoculation, characteristic necrotic spots developed on inoculated and non-inoculated shoots for all pruning times. There was no statistically significant effect of time [6].

The first signs of infection appeared on shoots inoculated within 24 hours of cutting, about five weeks after inoculation: death of the terminal bud, failure of leaves to expand and rapid collapse of the shoot [6]. Five weeks of silence, in other words. By the time the symptom is visible, the infection is already a month old.

An equivalent risk applies to every other mechanical wound, such as girdling [6].

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9. Fertilisation and irrigation: the two mistakes that get paid for

Pruning time and nitrogen fertilisation, in rate and in form, are the two most critical management points in the field [2]. This is not a vague good-practice recommendation. It is a specific mechanism.

Nitrogen

Excessive nitrogen fertilisation produces vigorous, tender growth, which is precisely the most susceptible tissue for infection. At the same time, dense growth reduces ventilation and light within the orchard, creating the high relative humidity that favours the pathogen [1]. The fertiliser therefore works twice in the disease's favour: it makes susceptible tissue and a favourable microclimate.

Water

Excessive irrigation contributes to excessive growth and to high relative humidity within the orchard [1]. The irrigation programme must aim at a balance between growth and cropping, not at maximum growth.

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10. Diagnosis and what to do with a suspected case

There are other Pseudomonas species that attack kiwifruit and cause similar symptoms. Many symptoms attributed to Psa turn out to come from other, far more harmless pathogens [1]. Identification is done only by a specialist laboratory.

In Greece, identification is carried out by the bacteriology laboratory of the Benaki Phytopathological Institute [1][16]. Internationally, molecular methods are used: rep-PCR, 16S rDNA sequencing, duplex-PCR, nested PCR/RFLP and quantitative real-time PCR [2].

Surveys must be targeted by season: late February and March, look for cankers with red exudate; in April and May, and through the summer, look for leaf spots [1]. The Benaki Phytopathological Institute has issued guidelines for macroscopic inspection [16].

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11. What changed in the legal framework

Today Pseudomonas syringae pv. actinidiae is listed as a Regulated Non-Quarantine Pest (RNQP) in Annex IV of Regulation (EU) 2019/2072, in Parts D and M, in relation to propagating material of ornamental plants and to fruit plants and propagating material of the genus Actinidia [12].

What the change means in practice. The move from "quarantine" to RNQP does not mean the problem has been downgraded. It means the Union has recognised that the pathogen is already established and that regulation shifts from eradication to control of the quality of propagating material. In practice, the weight falls even more heavily on what is planted: the material purchased must come with the prescribed certificates, and the nursery has a clear obligation.

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12. Copper

Copper remains the most important preventive means. It acts on the bacterial cell wall: it forms complexes that destroy the cell's proteins and disrupt enzyme function, killing the bacterium [1][4].

How effective it actually is

The classic experiment by Serizawa and co-workers, in 1989, on seven-year-old vines in Japan, with three applications at seven-day intervals, gave the following:

Source: Serizawa and co-workers, 1989, as cited in the review by Jeyakumar and co-workers [4]. The antibiotics are quoted only for comparison of efficacy. The use of antibiotics for plant protection is prohibited in Greece and in the European Union [1][4].

Note the figure: copper reduces symptoms by roughly two thirds, not to zero. It is a tool for reducing pressure, not a shield.

When it is applied

Based on New Zealand experience, the recommendations place copper sprays immediately after winter pruning, at bud break, and two and four weeks later, preferably ahead of a significant rain event. Post-bloom sprays are recommended only in high-risk situations, that is after a serious wind, rain or hail event. Applications follow after harvest and at leaf fall, so that the bacterium cannot enter through harvest wounds or leaf scars [4].

Max and co-workers stress that the sprays after harvest and during winter are the most important for limiting infections, since these also disinfect the wounds of human origin [1].

The two problems with copper

First, resistance. Copper-resistant Psa strains have been reported, with minimum inhibitory concentrations from 2.25 to 3.0 mM [4]. Nakajima and co-workers showed that the genetic basis of copper resistance is similar to that of P. syringae pv. tomato [5]. The mechanism consists of three different systems, and additional genes conferring maximum resistance have also been identified [4]. The same researchers have also shown streptomycin resistance, through genes analogous to strA and strB.

Second, phytotoxicity and accumulation. Excessive use causes copper to accumulate in the soil and selects for resistant strains [1]. Cases of phytotoxicity with leaf curling and chlorosis have been reported [1][4]. In addition, Goodwin and McBrydie reported that applying copper products during pollination significantly affected yield [4].

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13. Copper resistance in the Pella region

The copper section noted that resistant strains have been recorded internationally. The Greek study shows how far the phenomenon has advanced in this particular region. The findings, using Cazorla's criterion which classes as resistant any strain with a minimum inhibitory concentration above 0.8 millimolar:

The last figure is the most worrying. In more than one in four of the Mylotopos strains, copper does not kill the bacterium even at 400 micrograms per millilitre [19].

What the field showed

The same work tested products in two commercial kiwifruit orchards, in fourteen-year-old plantings, over two years, with all products at 2 millilitres per litre [19]:

• The copper products did not fully control the disease. IONIC CONCENTRATED COPPER, MAGNA BLUE and CUPROFIX ULTRA failed to control Psa, which the researchers attribute precisely to the resistance they had measured. In the second orchard, indeed, no treatment reduced spots per leaf in the first year, and only in the second year did the copper products show some reduction.
• The defence activators performed. BION, with acibenzolar-S-methyl 50%, MICONIC, NUTRI BIOCLEAN and the experimental BAR significantly reduced symptom severity. The percentage of infected leaves was significantly reduced by BION, MICONIC and NUTRI BIOCLEAN in both years.
• None eliminated the disease. The researchers are clear: the products reduced symptom severity, they did not remove it.

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14. Plant defence activators

The second category consists of products that do not kill the bacterium but activate the plant's systemic acquired resistance, known as SAR. They induce the production of defensive metabolites, so that the plant is prepared when the pathogen arrives [1].

The main active substance internationally is acibenzolar-S-methyl, known as ASM. It belongs to the benzothiadiazoles and mimics the action of salicylic acid, which the plant itself produces in response to infection [1][2]. On the basis of glasshouse experiments, ASM is considered one of the most effective activators for improving kiwifruit tolerance to Psa [2].

In Greece today it is not ASM that is on the market for kiwifruit but two other activators, COS-OGA and laminarin. The currently approved products should be checked in the approvals database [15], because approvals change. Those approvals are valid in Greece only; in every other country the corresponding national register applies.

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15. Biological products

The third category comprises antagonistic microorganisms and their products. The approach is not new in agriculture, having been applied since 1929, but for Psa it is a field of active research [1].

The combination that outperforms its parts

De Jong and co-workers, in 2019, examined the combined use of ASM with the fungus Aureobasidium pullulans strain CG163 [8]. The results in reducing leaf symptoms:

The combined application therefore returned more than either did separately [1][8]. The message is that no single means is sufficient and that the strategy has to be combinatorial.

Trichoderma at the root

Hill and co-workers, in 2015, worked with endophytic Trichoderma strains isolated from the roots of healthy vines in areas of high Psa presence. These fungi colonise the surface and the interior of the root, release metabolites and induce systemic resistance [7].

The striking finding: a single inoculation with Trichoderma early in the plant's development had a significant effect on health and survival, and established a strong endophytic community in the root that contributed to Psa control even when the plants were older [7]. At the end of the trials, the roots of inoculated plants contained significantly more Trichoderma strains than the controls.

In practice: the moment of planting is an opportunity that does not return. Inoculating the young plant in the nursery or in the planting hole pays for years.

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16. Annual protection programme

Putting all of the above together, the annual programme takes the following shape. It is a framework for thinking, not a recipe: timing is adapted to the region, the cultivar and the course of the weather, and is finalised by an agronomist.

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17. Managing an orchard that is already infected

If the orchard is positive, the objective changes: entry is no longer being prevented, the aim is to limit spread and keep the orchard productive.

Staff hygiene

• Entry and exit with hygiene measures observed, always with clean clothing and footwear.
• Disinfection whenever staff move from one orchard to another.
• Use of protective equipment, gloves and head covering, and thorough hand washing after work.

Machinery and materials

• Thorough disinfection with alcohol or 10% bleach solution.
• Movement of plant material out of the holding is prohibited, except for harvested fruit.
• The pathogen survives in the soil for a long period; anything that comes into contact with it, tools and bins, must be sterilised [1].

Communication with the authorities

Notifying the authorities is not optional and is not against the grower's interest. It is an obligation, and at the same time the only route to reliable identification and to a coordinated regional response.

• The regional plant protection service. The first point of contact for any suspected case. The service collects the sample and forwards it for identification [1].
• Benaki Phytopathological Institute, Bacteriology Laboratory. The competent laboratory for official identification of the pathogen in Greece. It has also issued the guidelines for macroscopic inspection [1][16].
• The Ministry of Rural Development and Food. It has issued good-practice orchard hygiene guidelines for protecting kiwifruit holdings, which must be followed without deviation [1]. The same database is where the currently approved products are checked [15].

Organising the orchard

• Perimeter signage prohibiting entry to those without business there.
• Regular and thorough inspection of every plant at the stages when symptoms appear.
• Immediate destruction of confirmed cases on the spot, without movement.

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18. What to retain

This disease is not beaten with a spray. It is beaten with a system: clean propagating material, strict hygiene, correct pruning timing, rationalised nutrition and irrigation, regular inspection, and sprays based on the weather forecast rather than the calendar. It demands a thorough knowledge of the pathogen's biology and regular monitoring of weather conditions, so that the dangerous periods are correctly anticipated [1].

19. Sources

The numbers in the text refer to the list below.

• [1] Pastopoulos, S. (2020). Bacterial canker of kiwifruit — an update on the progress of the disease in Greece (in Greek). Georgia – Ktinotrofia, issue 8/2020:32–37, AgroTypos. Source for the progress of the disease in Greece since 2014, the timing of the phases in the Giannitsa region, the differential susceptibility of males and females, the behaviour of old orchards and the personal observations 2014–2020.
• [2] Donati, I., Buriani, G., Cellini, A., Mauri, S., Costa, G. and Spinelli, F. (2014). New insights on the bacterial canker of kiwifruit (Pseudomonas syringae pv. actinidiae). Journal of Berry Research 4(2):53–67. Source for the Italian economic figures (€20,000, €50,000 and €15,000 per hectare), the spread in New Zealand (1,400 orchards, 52%, 11,084 hectares, 81%), infection through leaf scars, the role of pruning time and nitrogen fertilisation.
• [3] Serizawa, S. and Ichikawa, T. Epidemiology of bacterial canker of kiwifruit 4. Optimum temperature for disease development of new canes. Annals of the Phytopathological Society of Japan. Source for the optimum temperature for development and infection in new shoots, 12 to 18 °C.
• [4] Jeyakumar, P., Anderson, C.W.N., Holmes, A. and Miller, S. Optimising copper sprays on kiwifruit: a review. Fertilizer & Lime Research Centre, Massey University, and PlusGroup Horticulture Ltd, New Zealand. Source for the Serizawa 1989 results (control 44.1%, copper 15%, antibiotics 4–7%), the copper spray programme, the 2.25–3.0 mM minimum inhibitory concentration in resistant strains, the three resistance systems, the effect of copper products on pollination, and the ZESPRI reservation about biologicals.
• [5] Nakajima, M., Goto, M. and Hibi, T. (2002). Similarity between Copper Resistance Genes from Pseudomonas syringae pv. actinidiae and P. syringae pv. tomato. Journal of General Plant Pathology 68(1):68–74. Source for the genetic basis of Psa copper resistance and its similarity to the tomato pathovar.
• [6] Vanneste, J.L. (ed.). Proceedings of the 1st International Symposium on Bacterial Canker of Kiwifruit (Psa), Mt Maunganui, New Zealand. Acta Horticulturae 1095, ISHS. Plant & Food Research paper on the risk of summer pruning. Source for the 0 to 64 day experiment: infection at every pruning time with no statistically significant difference, inoculation with 10 microlitres of a 10⁹ bacteria per millilitre suspension, first symptoms about five weeks later.
• [7] Hill, R., Stark, C., Cummings, N., Elmer, P. and Hoyte, S. (2015). Use of Beneficial Microorganisms and Elicitors for Control of Pseudomonas syringae pv. actinidiae in Kiwifruit (Actinidia spp.). Acta Horticulturae 1095:137–144, ISHS. Source for the endophytic root Trichoderma, the effectiveness of a single inoculation early in development, and the establishment of a strong endophytic community that also acts in older plants.
• [8] De Jong, H., Reglinski, T., Elmer, P., Wurms, K., Vanneste, J.L., Guo, L.F. and Alavi, M. (2019). Integrated Use of Aureobasidium pullulans Strain CG163 and Acibenzolar-S-Methyl for Management of Bacterial Canker in Kiwifruit. Plants 8(8):287. Source for the 75% symptom reduction with the combination, against 55% with ASM alone and 40% with CG163 alone.
• [9] Pattemore, D.E., Hoyte, S.M., McBrydie, H.M. et al. (2011). Survival of Pseudomonas syringae pv. actinidiae and P. s. pv. syringae bacteria on honey bees and in beehives. Plant and Food Research report to Zespri Group Ltd, Ref: VI1255. Source for the survival of the bacterium on bees for up to two weeks and its transfer to hive bees that never visited an infected plant.
• [10] Chapman, J.R., Taylor, R.K., Weir, B.S., Romberg, M.K., Vanneste, J.L., Luck, J. and Alexander, B.J.R. (2012). Phylogenetic relationships among global populations of Pseudomonas syringae pv. actinidiae. Phytopathology 102(11):1034–1044. Source for the division of global Psa populations into biovars and their phylogenetic relationships.
• [11] Cunty, A., Poliakoff, F., Rivoal, C., Cesbron, S., Fischer-Le Saux, M., Lemaire, C., Jacques, M.A., Manceau, C. and Vanneste, J.L. (2015). Characterisation of Pseudomonas syringae pv. actinidiae (Psa) isolated from France and assignment of Psa biovar 4 to a de novo pathovar: Pseudomonas syringae pv. actinidifoliorum pv. nov. Plant Pathology 64(3):582–596. Source for the reclassification of Psa 4 as a separate pathovar causing leaf symptoms only, without cankers.
• [12] Commission Implementing Regulation (EU) 2019/2072 of 28 November 2019, establishing uniform conditions for the implementation of Regulation (EU) 2016/2031 as regards protective measures against pests of plants. Source for the listing of P. syringae pv. actinidiae as a Regulated Non-Quarantine Pest (RNQP) in Annex IV, Parts D and M, for Actinidia propagating material.
• [13] Commission Implementing Regulation (EU) 2020/885, as regards measures to prevent the introduction into and the spread within the Union of Pseudomonas syringae pv. actinidiae. Source for the replacement of Implementing Decision (EU) 2017/198 and for the requirements concerning live pollen and Actinidia plants for planting.
• [14] EPPO Global Database — Pseudomonas syringae pv. actinidiae (PSDMAK), EPPO Datasheet. Source for the current categorisation of the pathogen and its global distribution.
• [15] Greek Ministry of Rural Development and Food — Plant Protection Products Database. Data retrieved 20 August 2026. Source for the products approved in Greece on kiwifruit targeting bacterial infections, the active substances, rates and pre-harvest intervals.
• [16] Benaki Phytopathological Institute — Guidelines for macroscopic inspection for Pseudomonas syringae pv. actinidiae (in Greek). Source for the inspection, sampling and identification procedure in Greece, and for the role of the bacteriology laboratory.
• [17] NZ Psa Research — Collaboration between ZESPRI, KVH, Plant & Food Research, MPI, MSI and the NZ industry. Source for the organisation of New Zealand's national research response to the epidemic.
• [18] Balestra, G.M., Renzi, M. and Mazzaglia, A. (2011). Occurrence of bacterial canker caused by Pseudomonas syringae pv. actinidiae in kiwifruit plants of cv. Tsechelidis. Journal of Plant Pathology 93. Source for the documented infection of the Greek cultivar Tsechelidis.
• [19] Thomidis, T., Pagoulatou, M.G., Alexandridis, E., Mpalantinaki, E. and Goumas, D.E. (2025). Copper Resistance in Pseudomonas syringae pv. actinidiae Strains from the Prefecture of Pella, Northern Greece, and a Comparison of the Effectiveness of Several Commercial Products to Control. Agriculture 15(2):157. Source for the copper resistance of the 22 Psa strains from Mylotopos, Pella (100% growth at 200 μg/mL, 9.1% at 400 μg/mL, 18.2% resistant subpopulations, 27.3% with MBC above 400 μg/mL), for the failure of copper products to control the disease in the field, and for the significant symptom reduction by the defence activators BION, MICONIC, NUTRI BIOCLEAN and BAR.