The dry shoot disease of peach

Dead annual peach shoot with the leaves still attached and brown — The symptom that resembles nothing else: the annual shoot has died, but *the leaves did not fall* — they stayed brown and attached to it, inside a canopy that is otherwise growing normally. The flow was cut at a point lower down, and that is where the canker is.

Savvas Pastopoulos, Agronomist MSc — Pastopoulos Agronomics, Neos Mylotopos, Pella, Greece

Since 2021 the plain of Giannitsa, the most important clingstone peach producing district in the world, has been living through an epidemic that growers named themselves: the dry shoot. Dead annual shoots with the leaves hanging on them, buds that fail to break, and in heavy attacks cultivars that lose the entire crop. The cause is a fungus, Diaporthe amygdali. This article is the detailed picture of the disease — and it starts from the distinction that has cost the greatest number of wrong sprays in recent years: the dry shoot is not the blind shoot.

Units in this article Any rate given is per hectare. One hectare equals 10 Greek stremmata, the unit used in the Greek edition of this article.

The confusion that has to be settled first A blind shoot is a shoot that is alive, carrying buds that failed to break. It points to eriophyid mites and calls for an acaricide, in spring. A dry shoot is dead wood. It points to a fungus and calls for removal, burning and a fungicide, with the emphasis on autumn [8]. Two different problems, two different windows, two different product groups. They appeared in the district at roughly the same time and are discussed together — but the spray for one does nothing for the other.

2021the year the disease took epidemic form in Pella and Imathia

28.5%yield loss recorded in affected commercial orchards

45–63%reduction of cankers from AUTUMN sprays

10–28%reduction from SPRING sprays alone

~1 monthfrom infection to the first visible canker

608,688conidia from ONE pycnidium, at the optimum temperature

Contents

Why «dry shoot», and why the name matters
Dry shoot and blind shoot — the field distinction
The pathogen and its three names
The symptoms, in the order they appear
Fusicoccin — why the shoot collapses so fast
The disease cycle and its numbers
The entry points — why autumn decides the season
What the Greek data have shown since 2021
Cultivar susceptibility
Control — the cultural measures
Control — chemical
The table of confusions
The year's programme at a glance
Sources

1. Why «dry shoot», and why the name matters

The disease has at least five names in circulation: dry shoot in the orchard, Phomopsis in the Greek technical literature, constriction canker in the North American usage, twig canker and shoot dieback in the most recent Greek review [2], and TCSB — twig canker and shoot blight — internationally [4]. They are all the same disease.

The title of this article keeps the name growers use, because that is the name with which the problem will be described to the agronomist. The reason the names matter in practice is simple: a literature search under the wrong name returns nothing, and a conversation under the wrong name ends in the wrong product.

Two articles, one subject This article is the detailed treatment of the disease. Its place within the whole set of peach diseases and pests, together with the diagnostic tool that compares field symptoms against thirty-three causes, is in Peach diseases and pests. The other story — fruit deformation, bud drop and blind shoots — is covered in the peach fruit deformation disease, available in Greek only.

2. Dry shoot and blind shoot — the field distinction

The two problems appeared in Pella and Imathia almost simultaneously, are discussed together at every meeting, and the confusion has reached the point where acaricides are sprayed against a fungus and fungicides against a mite. The distinction takes a knife and ten seconds.

Criterion	Dry shoot	Blind shoot
The wood	Dead. Scraping the bark reveals brown, dry tissue	Alive. Scraping the bark reveals green, sappy tissue
The buds	Dead, along with the shoot carrying them	Dry, shrivelled, tightly appressed — but on a living shoot
The canker	Present, oval, centred on a bud or a leaf scar [5]	Absent. The shoot is uniform
The leaves	Brown, attached to the dead shoot	Normal or absent, with no necrosis
Under a lens	Black pycnidia on the lesion [5]	Nothing; possibly mites among the bud scales
Cause	The fungus Diaporthe amygdali	Eriophyid mites, associated with the viroid PLMVd [8]
Window	Autumn, around leaf fall	Spring, at bud break [8]
Intervention	Removal, burning, fungicide	Acaricide at the right time

The scraping rule Scrape the bark with a thumbnail or a blade, immediately below the point that failed to break. Green means blind shoot. Brown means dry shoot. Nothing else is needed to decide which of the two directions the orchard should take.

And a warning that follows from having both at once: heavy infestation by the deforming mite weakens and kills buds, and dead buds are exactly the entry point the fungus is looking for. It is one of the factors proposed to explain the intensity of attacks in Greek orchards [2]. The two problems are different, but one opens the door for the other.

3. The pathogen and its three names

The cause was identified in France in 1905 as Fusicoccum amygdali and kept that name for several decades, until it was renamed Phomopsis amygdali. In 2010, phylogenetic analyses of isolates led to its placement in the genus Diaporthe [2]. The current name is Diaporthe amygdali (Ascomycota, Sordariomycetes, Diaporthales, Diaporthaceae), with the two older names as synonyms.

That taxonomic history is why the literature looks thin when searched under a single name. In practice a complete search requires all three.

The host range is wide. Beyond peach, nectarine and almond — where it causes the most severe damage — the pathogen attacks plum, apricot and pear, and also avocado, walnut, grapevine and various ornamental species [2]. Its global distribution includes the United States, China, Japan and Uruguay, with the most severe attacks recorded in the Mediterranean basin — Spain, France, Italy and Greece [2]. In Greece its presence on peach has been formally recorded since 2006, in a report concerning fruit rot [7].

Sources: 2 7

4. The symptoms, in the order they appear

Stage 1 — The bud that did not open

The first symptoms are small, oval necroses around the buds on annual shoots. The bud fails to break and the shoot shows reduced flowering and reduced growth [2]. This is the stage that passes unnoticed, because one dead bud among dozens of healthy ones does not catch the eye.

Dead peach bud with a dark lesion around it on an annual shoot — The starting point of the disease, magnified. The bud is dead and dark, and the oval lesion is outlined around it. The fungus entered *here*: from the base of the bud, not from some wound along the shoot.

Stage 2 — The canker that girdles

In spring the necroses enlarge and extend laterally into elongated cankers 1 to 5 cm long [2]. They are brown or reddish-brown at first, then become sunken and take on a silvery colour. The international description is more precise about the shape: oval, reddish-brown cankers centred on a bud or a leaf scar, with a necrotic centre and a purple halo [5].

The canker enlarges until it girdles the shoot. From the moment the ring closes, everything above the canker is lost — hence the name constriction canker.

Cut annual peach shoot with a necrotic zone in the middle and living growth at the base — The same shoot, cut. The necrotic zone stops at a clean margin and the fruiting bodies of the fungus can be seen at its edge. Below the canker the shoot is still producing leaves normally — *the damage is local, its consequence is not*.

Stage 3 — The dead shoot with the leaves on it

The annual shoot dies entirely above the canker, and the leaves or fruit it was carrying stay attached to the dead shoot [2]. This is the symptom the grower sees from the road, and it is almost diagnostic on its own: on a tree that is otherwise growing normally, a brown shoot with its leaves hanging on it does not have many explanations.

Infected peach shoot with a necrotic section and healthy leaves at the tip — The intermediate stage, before the whole shoot dies: the necrosis has advanced along the shoot but the tip is still being fed. Within a few days, once the ring of the canker closes, these leaves too will turn brown without falling.

The character that separates Phomopsis from the other diebacks

The absence of gum Gum exudation is rarer in Phomopsis, whereas it is the rule in attacks by Monilinia, by Botryosphaeria and by Cytospora [1]. A dead annual shoot without gum, with an oval canker around a bud and with the leaves still on it, is Phomopsis until proven otherwise. The opposite picture — abundant gum at multiple points on a woody scaffold — points elsewhere.

The contradiction with the international literature is only apparent: on mature cankers, gum exudation from the necrotic tissue has also been observed [2]. The diagnostic element is not absolute absence, it is proportion: in Phomopsis gum is the exception, in the other diseases it is the rule.

Three infected peach shoots with dead buds along their length — Three shoots from the same orchard. The dead buds are not scattered at random — they follow one after another along the shoot, because all of them were infected in the same period, at the leaf fall of the previous autumn. Brown discolouration, not a drop of gum.

More rarely, on the fruit

On fruit the attack appears as brown cankers [1]. It is the rarest expression, but the first official record of the pathogen in Greece concerned precisely a rot of peach fruit [7]. In very severe attacks, researchers in China have reported the dieback of whole trees [1].

Sources: 1 2 5 7

5. Fusicoccin — why the shoot collapses so fast

Here lies the answer to a question every grower has: how a canker a few centimetres long kills an entire shoot within days. The mechanical explanation — that the canker girdles and cuts the flow — is correct but partial.

The complete genome of D. amygdali, published in 2025, showed that the fungus carries the entire biosynthetic gene cluster for fusicoccin [4]. Fusicoccin is a diterpenoid phytotoxin with a very specific action: it irreversibly activates the plasma-membrane proton pumps of the guard cells of the stomata. The result is that the stomata open and do not close again, the shoot loses water uncontrollably and the tissues collapse [4].

What this means in practice

First, it explains why the dieback extends beyond the point of infection: the toxin travels, the canker does not.

Second, it explains why water stress makes the picture worse. A tree that is already struggling to meet its own demand has no margin left for shoots with permanently open stomata.

Third, it shows where the research is heading: the authors propose double-stranded RNA gene-silencing strategies targeting the enzymes of the fusicoccin pathway, so as to reduce virulence without having to kill the fungus [4]. It is not an available technology today; it is, however, the reason the disease deserves attention beyond the spray tank.

Sources: 4

6. The disease cycle and its numbers

The fungus overwinters as mycelium inside the cankers on the twigs and as pycnidia on those cankers and on the dead shoots [1] [2]. The pycnidiospores are the inoculum that causes infection.

How the inoculum is released

When the ambient temperature is suitable — around 19 to 20 °C — the pycnidia absorb water from rain or from the atmosphere, swell, and pycnidiospores begin to emerge from the ostiole as dull white masses or narrow coiled tendrils — the cirrhi [2].

The pycnidiospores are slime spores: they are dispersed by rain water to nearby twigs. Wind makes a small but real contribution, carrying droplets in which spores are trapped [2]. Without rain there is no dispersal — and that is the key to the timing.

The temperature ranges

The Greek data for peach give the following [2]:

Process	Range	Optimum
Pycnidiospore germination and infection	5 to 37 °C	around 20 °C
Sporulation	0 to 37 °C	22 °C
Release of cirrhi from the pycnidia	—	19 to 20 °C
From infection to the first symptoms	—	about one month

Why summer gives a respite — and why it is not one High temperatures from late spring and throughout summer hinder the growth of the fungus and at the same time speed up the healing of the scars left by falling leaves and fruit, making infection harder still [2]. The reverse holds every autumn.

The practical conclusion has already been stated by the orchard itself: holdings in hot, dry situations in autumn show limited attack intensity [1]. That is not coincidence — it is the same phenomenon read from the grower's side.

The numbers from almond

The most complete quantitative study of the pathogen's biology was published in 2025 and concerns almond [3]. It is given here as an order of magnitude, with the host stated explicitly:

Mycelial growth: from 5 to 35 °C, with an optimum of 26.7 °C and a maximum rate of 13.89 mm per day.
Germination of α-conidia: from 5 to 35 °C. Above 15 °C and after 20 to 50 hours of incubation, germination reaches 100%. At 15 °C or below, with fewer than 20 hours, it stays at 0 to 20%.
Conidial production: from 11 to 33 °C, with an optimum of 21.6 °C and a maximum of 608,688 α-conidia per pycnidium.
Formation of mature pycnidia: from 11 to 28 °C, with an optimum of 16.5 °C. The fungus is therefore adapted to mature its fruiting bodies under cool conditions — late winter and early spring.
Leaf infection: a maximum of 62% at about 33 °C with 72 hours of wetness; a minimum of 12% at 28 °C with only 6 hours. Prolonged wetness is the decisive factor.
Lesion development on detached twigs: a maximum rate of 7.7 mm per day at 30 °C.

Putting the two together: the pycnidia mature in the cold (optimum 16.5 °C), the spores come out with the rain at 19 to 20 °C, and infection needs many hours of wetness. The Greek autumn and the Greek spring meet all three conditions at once.

The inoculum curve through the year

The only study that followed inoculum month by month for two years was carried out in New Jersey, sampling thirty cankers per cultivar every month from January 1997 to December 1998 [13]. Its findings:

Canker size follows a sinusoidal pattern: smallest in late winter and early spring, largest in late summer and early autumn.
Pycnidia per canker: from a mean of 94 in one year to 205–221 in the next — more than twice as many, depending on the season.
Proportion of pycnidia exuding cirrhi: from about 10% in winter to 70 to 80% in summer and autumn.
Conidia per canker: peaking between day 170 and day 210 of the year — that is, 19 June to 29 July — with 7.4 to 10.8 million conidia per canker. The lowest levels, 1.0 to 3.9 million, in December and January.

The counter-intuitive conclusion: inoculum is NOT the limiting factor

The authors conclude that the pathogen behaves as an r strategist: it produces copious inoculum through most of the year, and even the lowest winter levels are sufficient to cover both autumn leaf fall and spring bud break [13].

The implication is unwelcome but useful: in an orchard with a history of the disease, there is no level of sanitation that will starve the fungus out. What decides the epidemic is not how many spores are present, it is whether the environment allows infection — temperature and hours of wetness.

This does not make sanitation pointless. It means sanitation does not replace timing: it reduces dead wood and the foci within the orchard, but the season is won or lost on whether the spray is on the tissue when the rain window opens.

Sources: 1 2 3 13

7. The entry points — why autumn decides the season

The pathogen is a weak one. It does not penetrate healthy, intact bark: it needs a wound or a natural opening in order to infect [2]. That weakness is also the grower's greatest opportunity, because it means managing the openings is managing the disease.

The entry points, in order of importance [2]:

The petiole scars at leaf fall. The most important by a wide margin. Every falling leaf leaves a fresh scar, and on an annual shoot the scars number in the dozens. They all open within a few weeks, exactly when temperature and rainfall are ideal.
The bud scars and their scales.
The scars left by flowers that were not fertilised.
The scars left by the drop of aborted fruitlets.
Micro-cracks in the bark caused by late or early frost.
Fruit scars in summer. June drop, thinning and harvest itself all leave scars. On a highly susceptible cultivar, 6% of the nodes examined after such events had become infected [6]. It is a small proportion, but it explains why the orchard is never entirely out of danger.

The size of what is at stake is clear from how far these infections can go: in a heavy attack up to 50% of a tree's shoots are affected [9]. These are not isolated shoots — this is half of next season's bearing surface.

What it costs, with figures

In affected commercial orchards in New Jersey, a quantitative survey over two consecutive seasons recorded yield losses of 28.5% and 21.0%. In severely infected orchards, 500 to 800 cankers per tree were counted [6]. In one treatment of the same study, the trees that were pruned averaged 640 cankers on 342 infected shoots [6].

These figures come from another country and another decade and do not transfer unchanged. They do, however, give the order of magnitude of the problem when it is left alone: this is not a disease that costs at the margin.

The key period, with a figure Trials in the United States showed that autumn sprays during leaf fall reduced cankers by 45 to 63% [6]. No other intervention of the year produces a difference of that size. The Greek recommendation turns it into a calendar: applications start at 10% leaf fall and continue up to the copper spray [8].

The practical consequence is unwelcome for anyone who plans crop protection only as far as the last harvest: the coming season is decided after the end of the season that is leaving. An orchard that closes with the last application in August leaves leaf fall uncovered.

A second, equally overlooked entry point is fresh pruning cuts. The removal of infected shoots must not be carried out before expected rainfall, precisely because fresh cuts are an entry point for the pathogen [2]. The right action at the wrong moment becomes the wrong action.

Sources: 2 6 8 9

8. What the Greek data have shown since 2021

The disease has been present in Greece for a long time and probably predates its recognition. For decades it was controlled without anyone knowing it: the preventive sprays aimed at other diseases, leaf curl first among them, kept it at low levels [1].

The timeline of the outbreak

2021. The problem first takes epidemic form, in peach orchards — clingstone above all — and almond orchards in Central and Western Macedonia and in Thessaly. The Plant Pathology Laboratory of the Aristotle University of Thessaloniki takes the initiative to study it [2].
2021, the sampling. Symptomatic twigs from orchards in the districts of Pella and Imathia; laboratory assessment establishes that in every case the cause was Diaporthe amygdali [2].
From 2021 onwards. The intensity of attack increases year by year [2]. On the plain of Giannitsa the picture deteriorates to the point where production falls dramatically on many holdings [1].
2026. The growing season takes explosive proportions, causing serious concern across the whole stone fruit sector [2].

The three explanations that have been proposed

Why did a disease that was manageable for decades become an epidemic? Three factors are cited [2]:

The withdrawal of thiophanate-methyl. This benzimidazole fungicide, applied for other targets, as a rule kept the intensity of the disease low without causing any particular concern about it. Its approval was not renewed in the European Union, with authorisations withdrawn by April 2021 [11] — that is, exactly the year of the first outbreak.
The susceptibility of the cultivars grown, especially the older clingstone ones.
The role of the deforming mite: heavy infestation by Eriophyes spp. weakens or kills buds, and dead buds serve as an entry point.

A field observation worth testing This particular outbreak does not appear to correlate directly with the weather of any given season, but with whether a susceptible cultivar is present on the holding [1]. It is a field observation, not an experiment — but it agrees with the laboratory susceptibility data of the next section, and if it is confirmed it changes the ranking of the measures: the cultivar before the spray.

Sources: 1 2 11

9. Cultivar susceptibility

This is where the Greek research produced the most directly usable result. In a recent study by the Plant Pathology Laboratory of the Aristotle University of Thessaloniki, the susceptibility of ten clingstone cultivars to the pathogen was assessed by artificial inoculation of twigs and measurement of wood discolouration fifteen days later [2].

Ranking	Cultivars
Highest susceptibility	Fortuna, VLG
Lowest susceptibility	Romea, Ferlot — with Ferlot described as resistant
Intermediate in the trial	Fergold, Katerina, Andros, Everts, IDF-A37, Fercluse

Recent experience from Greek orchards shows that the disease is particularly severe in clingstone peach orchards and specifically in orchards of older cultivars such as Andros and Katerina [2] — and these are precisely the cultivars in which the greatest destruction is recorded on the plain of Giannitsa, together with A37 [1].

How this table should be read The trial used artificial inoculation and measures how fast discolouration advances within fifteen days. It does not measure what will happen in an orchard with natural inoculum, natural entry points and natural weather. «Resistant» does not mean «unaffected», and no cultivar in the table is exempt from the cultural measures. It does mean, however, that in a new planting in a district with a history of the disease, the choice of cultivar is a crop-protection decision and not only a marketing one.

Sources: 1 2

10. Control — the cultural measures

Control rests entirely on prevention. There is no curative intervention for a shoot that has already been girdled by a canker: the part above the canker is dead and does not recover. Whatever is done, is done for the next shoots [1].

A. Removal and destruction of the inoculum

This is the most important measure, and it is the precondition for all the others. No chemical intervention can succeed unless the inoculum has been cleared first [1].

All year round, not only at winter pruning. The pathogen is maintained and dispersed from the pycnidia on the infected shoots; removal must continue throughout the year [2].
The cut is made 10 centimetres below the lesion, in healthy wood [8]. The canker extends invisibly within the tissues before it shows on the surface.
Destruction by burning. Prunings are not left stacked at the edge of the orchard — there the pycnidia go on maturing and releasing spores.
Disinfected tools, with frequent disinfection during the work [2] [8].
Never before rain. Removal must not be carried out before expected rainfall, because fresh cuts are an entry point [2].

How much removal actually delivers — and why it is not enough on its own In the three-year New Jersey trial, removing the cankers by pruning in September reduced disease incidence by 42% in one year but had no effect in another [6]. The authors attribute this to the fact that the test trees were surrounded by heavily infected, unsprayed trees: wind and rain brought inoculum in from next door.

Two conclusions follow. First, removal is a measure that pays off at the scale of a whole block, not on individual trees inside an infected orchard — exactly as with bait spraying against the olive fruit fly. Second, it does not replace the spray: fungicides protect the shoot irrespective of where the inoculum comes from, removal does not.

B. Pruning as a humidity measure

Beyond removal, pruning helps to reduce humidity levels around the tree, creating an environment less favourable to the fungus [2]. Proper aeration of the canopy through summer pruning is a basic control technique [1].

C. Fertilisation — in both directions

Neither too little nor too much Both a shortage of nitrogen and excessive nitrogen fertilisation affect the susceptibility of the shoots to attack [2]. The second is the commoner in practice: on holdings where untimely or excessive fertiliser has been applied, infection is favoured because of the excessive, soft growth [1]. The aim is not minimal fertilisation — it is appropriate fertilisation, following analysis and on-site assessment.

D. Irrigation — the trunk and the canopy stay dry

Avoiding wetting the tree during irrigation limits the spread of the fungus, while drip irrigation, which keeps the potential infection sites dry, makes infection harder [2]. Any overhead irrigation in a risk period is the equivalent of artificial rain on the pycnidia.

E. Confirming the diagnosis

Twig cankers are not a pathognomonic symptom: several fungi and bacteria produce a similar picture — Cytospora spp., Monilinia spp., Botryosphaeria spp., Leucostoma spp., Valsalia spp., and other species of the genus Diaporthe [1] [2] [10]. Where there is doubt, samples are sent to the Benaki Phytopathological Institute for identification of the pathogen and for guidance [1].

Sources: 1 2 8 10

11. Control — chemical

Chemical control is, and remains, the most effective way of managing the disease [2]. There are two conditions, however, and both concern timing.

First condition: preventive, not curative

Applications must be preventive and concentrated in the periods that are decisive for infection [2]. A spray applied after symptoms appear is spraying cankers that were created a month earlier.

Second condition: two seasons, with autumn first

The period of leaf fall in autumn is the most dangerous and requires cover of the shoots against the scars that are created. The pre-blossom sprays in spring are also critical, protecting the new growth as it begins to emerge [2].

The effectiveness of the autumn applications is far more decisive, since preventing cankers from autumn infections reduces the inoculum available in spring. Combined applications in both seasons are therefore recommended, with priority given to autumn [2].

How much each season counts — the figures

The three-year field trial in two commercial New Jersey orchards, with seven to eight sprays in autumn during leaf fall and four to five in spring from bud break to full bloom, at intervals of about ten days, gave the clearest answer available in the literature [6]:

Programme	Disease control
Autumn only (7–8 sprays at leaf fall)	45 to 63%
Spring only (4–5 sprays, bud break to bloom)	10 to 28%
Autumn and spring, chlorothalonil	46 to 71% — the best in the trial
Autumn and spring, captan	46 to 69%
Autumn and spring, azoxystrobin	41%
Autumn and spring, myclobutanil	28 to 44%
Canker removal by pruning	42% in one year, no effect in another

The finding that changes the spray budget Adding the spring applications on top of the autumn programme improved control by only 0 to 8% [6]. The reason is that the autumn sprays, by preventing canker formation, reduce the inoculum that would have been available in spring — so the spring sprays find less work to do.

In other words: if the budget stretches to one programme only, it is the autumn one. The reverse — spring without autumn — delivers a third of the effect. In the final year of the trial, however, earlier spring sprays performed appreciably better, an indication that part of the infection occurs before bud break [6].

What the trials of the active substances show

The withdrawal of thiophanate-methyl raised the question of how effective the remaining approved fungicides are. A recent study by the Plant Pathology Laboratory of the Aristotle University of Thessaloniki, using protective applications followed by artificial inoculation of annual shoots, showed that among the active substances assessed dithianon gave the highest efficacy, followed by triazole fungicides such as difenoconazole and tebuconazole [2].

The Greek practical recommendation to growers turns the above into a programme: alternating applications from 10% leaf fall up to the copper spray [8].

Two points where the literature disagrees — and they need saying

First, the benzimidazoles. The Greek reading attributes part of the outbreak to the withdrawal of thiophanate-methyl [2]. The American trials point the other way: benomyl gave only 28% control in the field, and in a detached-shoot assay benomyl and thiophanate-methyl gave no control at all [6]. The explanation that reconciles the two is that thiophanate-methyl probably held the disease down indirectly — through the applications made for other targets and the general cover they provided — rather than through strong activity against this particular pathogen. That is a hypothesis, not a proof, and it deserves testing under Greek conditions.

Second, the sulphur products. In the same detached-shoot assay, sulphur, lime sulphur and iprodione gave no control, while chlorothalonil protected 78% of the shoots and the triazole bitertanol 89% [6]. Lime sulphur is included in the Greek alternation [8] — useful for other targets in the same season, but it should not be treated as the backbone of the programme against dry shoot.

A check before every purchase — and a note on what these names mean

The active substances named above come from experimental trials and are not a recommendation for application. The approval situation changes, and an approval always concerns a specific crop and a specific target.

Before any intervention, the database of approved plant protection products [12] should be checked for the current approval in peach, the rate, the maximum number of applications and the pre-harvest interval. Those approvals are valid in Greece only; readers elsewhere must follow their own national register.

Rotation of modes of action is not optional. One of the three products named is multi-site and two belong to the same mode-of-action group — a strategy resting entirely on the triazoles is a strategy that will be exhausted.

Sources: 2 8 12

12. The table of confusions

The pairs most often confused in the field, and the one character that separates them.

Looks like	But is	The character that separates them
Dry shoot	Blind shoot from mite	Scraping the bark. Brown and dry means fungus; green and sappy means mite. In the second case there is no canker.
Dry shoot	Fungal gummosis (Botryosphaeria)	The gum. Gummosis gives multiple exudation points on woody scaffolds; Phomopsis gives a canker on an annual shoot, with gum rare.
Dry shoot	Brown rot twig blight	Brown rot starts at the flower and moves down the pedicel; the dead flowers stay on the cluster and there is usually abundant gum.
Dry shoot	Bacterial canker	The bacterium gives brown internal discolouration beneath the bark descending from the canker, and irregular angular holes in the foliage. Phomopsis gives black pycnidia on the lesion.
Dry shoot	Frost damage	Frost strikes uniformly within a height band across the whole orchard and all at once. Phomopsis is scattered shoot by shoot and develops gradually.
Dry shoot	Capnodis or collapse from the root	There the whole tree or a scaffold dies back, starting at the crown. In Phomopsis individual annual shoots die within a healthy canopy.

13. The year's programme at a glance

Period	What is happening	What is done
Summer	High temperatures hinder the fungus and speed the healing of scars	Summer pruning for aeration. Removal of infected shoots — this never stops. Irrigation that does not wet the tree
Late summer	Inoculum reaches its maximum; the pycnidia are loaded	Mapping of the orchard. No removal before expected rain
10% leaf fall	The most critical moment of the year. Dozens of scars per shoot, temperatures at the optimum, rainfall	Applications begin. Alternating products, repeated at each new wave of leaf fall and after rain
Complete leaf fall	The infection period closes	Copper. The first cankers are already clearly visible — this is where the pressure for the coming season is assessed
Winter	The fungus overwinters as mycelium in the cankers; the pycnidia mature in the cold	Winter pruning with the cut 10 cm below every lesion. Removal and burning. Tool disinfection
Pre-blossom	New growth starts; bud-scale scars and flowers open fresh entry points	Pre-blossom spray. Less decisive than the autumn one, but not optional in an orchard with a history
Spring	The cankers enlarge; the dead shoots with the leaves on them appear	Recording of intensity by cultivar. Removal whenever the weather allows. What is visible now was infected last November

The five things that really count

Scrape the bark before any decision. Dry or blind shoot — it determines whether a fungicide or an acaricide is bought.
Autumn decides the season. Sprays at leaf fall reduced cankers by 45 to 63%.
Clean before spraying. No intervention succeeds while the pycnidia stay in the orchard.
The cultivar is a crop-protection decision. In a new planting in a district with a history, it counts for more than any product.
No removal before rain. The fresh cut is an entry point.

14. Sources

The numbers in the text refer to the list below.

[1] Pastopoulos, S. (2023). Phomopsis in peach. Georgia – Ktinotrofia 5/2023 (in Greek). The basis of this article; full text. Source for the outbreak from 2021 on the plain of Giannitsa and in the cultivars Katerina, Andros and A37, for the observation that gum exudation is rarer in Phomopsis than in Monilinia, Botryosphaeria and Cytospora, for the observation that the outbreak correlates with cultivar susceptibility rather than directly with the weather, for the limited intensity in hot dry situations in autumn, for the link between excessive fertilisation and infection, for the priority of clearing the inoculum over any chemical intervention, and for sending samples to the Benaki Phytopathological Institute.
[2] Karaoglanidis, G. (2026). Twig cankers and shoot dieback of stone fruit — an emerging threat to peach and almond growing in Greece. Georgia – Ktinotrofia 4/2026, pp. 52–55 (in Greek). Professor of Plant Pathology, School of Agriculture, Aristotle University of Thessaloniki. Full text. Source for the taxonomic history of the pathogen and its placement in the genus Diaporthe in 2010, for the 2021 sampling by the Plant Pathology Laboratory of the Aristotle University in Pella and Imathia with D. amygdali identified in every case, for the host range, for the temperature ranges of 5–37 °C with an optimum around 20 °C for germination and infection and 0–37 °C with an optimum of 22 °C for sporulation, for the 19–20 °C release of cirrhi, for cankers 1–5 cm long and the one-month incubation, for the entry points and the role of leaf fall, for the assessment of ten clingstone cultivars with Fortuna and VLG as the most susceptible and Ferlot as resistant, for the highest efficacy of dithianon followed by difenoconazole and tebuconazole, for the link between the outbreak and the withdrawal of thiophanate-methyl and the attacks by Eriophyes spp., and for the cultural measures.
[3] Francia, C., Lázaro, E., Novellón, M., Ramón-Albalat, A., Beluzán, F., Vicent, A., Berbegal, M. & Armengol, J. (2025). Biology and epidemiology of Diaporthe amygdali: understanding how environmental factors influence fungal growth, sporulation, infection and lesion development on almond. Frontiers in Plant Science 16:1717223. Full text, open access, peer reviewed. Source for every quantitative figure in section 6 — mycelial growth 5–35 °C with an optimum of 26.7 °C and 13.89 mm/day, germination of α-conidia up to 100% above 15 °C after 20–50 hours, production of up to 608,688 α-conidia per pycnidium with an optimum of 21.6 °C, formation of mature pycnidia 11–28 °C with an optimum of 16.5 °C, leaf infection of 62% at 33 °C with 72 hours of wetness, and a lesion growth rate of 7.7 mm/day at 30 °C. The data concern ALMOND and are given as an order of magnitude.
[4] Turco, S., Brugneti, F., Cardacino, A. & Mazzaglia, A. (2025). Harnessing genomics of Diaporthe amygdali for improved control of peach twig canker and shoot blight (TCSB). Plants 14(19):2960. Full text, open access, peer reviewed. Source for the complete fusicoccin biosynthetic gene cluster in the pathogen's genome, for the mode of action of the toxin — irreversible activation of the plasma-membrane proton pumps of the guard cells, permanent stomatal opening, uncontrolled water loss and tissue collapse — and for the proposed direction of double-stranded RNA gene silencing.
[5] Michigan State University, Integrated Pest Management — Fusicoccum canker (constriction canker). Full text of the page. Source for the morphology of the cankers: oval, reddish-brown cankers centred on a bud or a leaf scar, a necrotic centre with a purple halo, girdling and dieback of the shoot above the canker, and black pycnidia on the lesion.
[6] Lalancette, N. & Robison, D.M. (2002). Effect of fungicides, application timing, and canker removal on incidence and severity of constriction canker of peach. Plant Disease 86(7):721–728. Full text. A three-year field trial in two commercial New Jersey orchards. Source for 45 to 63% control from autumn sprays against 10 to 28% from spring sprays, for the 71% achieved by chlorothalonil and 69% by captan applied in autumn and spring, for the 41% of azoxystrobin and 28 to 44% of myclobutanil, for the improvement of only 0 to 8% from adding spring applications to the autumn programme, for the 42% reduction from canker removal in one year only, for yield losses of 28.5% and 21.0% and 500 to 800 cankers per tree, for the 6% of nodes infected through fruit scars in summer, and — through the review it contains — for the detached-shoot assay in which benomyl and thiophanate-methyl, together with sulphur, lime sulphur and iprodione, gave no control, while chlorothalonil protected 78% and bitertanol 89% of the shoots.
[7] First report of Phomopsis amygdali causing fruit rot on peaches in Greece. Plant Disease 90(12):1551. Abstract used. Documentation that the pathogen is recorded in Greece on peach, the first official report concerning fruit rot. The taxonomy has since been revised to Diaporthe amygdali.
[8] Greek Interbranch Organisation of Peach (2026). Clarifications on dry and «blind» shoots in peach — control guidance for growers (in Greek). Full text of the bulletin. Source for the official distinction between dry and blind shoots — the first caused by the fungus with infection at leaf fall, the second by eriophyid mites associated with the viroid PLMVd and expressed in spring — for the cut ten centimetres below the lesion and burning, for tool disinfection, and for alternating applications from 10% leaf fall up to the copper spray. The guidance and the approvals behind it are valid in Greece only.
[9] Luo, C.-X., Schnabel, G., Hu, M. & De Cal, A. (2022). Global distribution and management of peach diseases. Phytopathology Research 4:30. Full text, open access, peer reviewed. Source for the ranking of the disease among the most important peach diseases worldwide and for infection of up to 50% of a tree's shoots in a heavy attack.
[10] Adaskaveg, J.E., Schnabel, G., Ritchie, D.F. & Förster, H. — Common preharvest diseases of peach and nectarine caused by fungi and bacteria: biology, epidemiology and management, chapter 12, CABI. Full text of the chapter. Source for the general epidemiology of stone fruit cankers and for the differential diagnosis from Cytospora, Monilinia and Botryosphaeria.
[11] Commission Implementing Regulation (EU) 2020/1498 on the non-renewal of approval of the active substance thiophanate-methyl. Source for the date by which authorisations were withdrawn, 19 April 2021.
[12] Database of approved plant protection products (in Greek), from the register of the Greek Ministry of Rural Development and Food. The only authoritative source for what is permitted in peach in Greece today, at what rate, with what maximum number of applications and with what pre-harvest interval. Valid in Greece only.
[13] Lalancette, N. & Robison, D.M. (2001). Seasonal availability of inoculum for constriction canker of peach in New Jersey. Phytopathology 91(11):1109–1115. Full text. Two years of monthly sampling of thirty cankers per cultivar, 1997 and 1998. Source for the sinusoidal pattern of canker size, for 94 against 205 to 221 pycnidia per canker between the two years, for the proportion of pycnidia exuding cirrhi rising from 10% in winter to 70 to 80% in summer and autumn, for the peak in conidia between day 170 and day 210 of the year at 7.4 to 10.8 million per canker and the minimum of 1.0 to 3.9 million in December and January, and for the conclusion that the pathogen behaves as an r strategist and that inoculum availability is not the limiting factor of the epidemic.

Disclaimer

This text is informational and educational and does not replace an on-site agronomic assessment, nor is it a prescription for the application of plant protection products. Identification of the disease from symptoms is probabilistic: twig cankers are not a pathognomonic symptom and definitive identification requires laboratory examination.

Plant protection products are used only under the approvals of the Greek Ministry of Rural Development and Food (ΥΠΑΑΤ) and in accordance with their label: approved crops, rates, maximum number of applications, re-entry intervals and pre-harvest intervals. Those approvals are valid in Greece only and do not apply in other countries; readers elsewhere must follow their own national register. The active substances named describe the results of experimental trials and are not a recommendation for application.

For any foliar spray: application to trees carrying fruit may cause fruit marking and leaf scorch. A trial on a limited number of trees is required first, with the same product and the same rate, followed by 5 to 7 days of observation before any general application. Spraying is done in late afternoon or early morning, never in a heatwave and never on foliage under water stress.

Any intervention is made at the user's own responsibility, following an on-site assessment by a licensed agronomist. Pastopoulos Agronomics accepts no liability for damage or loss of production arising from the application of the above information without individual technical guidance.