Brown rot of stone fruit: cause, symptoms and control

Brown rot on ripe peaches. The ash-grey sporodochia cover the rotted area. The most instructive detail, however, is transmission by simple contact: the healthy fruit is infected by its neighbour, because the contact surface carries microcracks, a thinner cuticle and permanent moisture. This is why thinning is a plant-protection measure and not only a quality one.

Savvas Pastopoulos, Agronomist MSc, Pastopoulos Agronomics, Giannitsa, Pella, Greece

Brown rot is the most serious fruit disease of stone fruit and one of the leading limiting factors of fruit growing worldwide. This article is the complete guide: every species of the genus and which ones actually occur in Greece, the history of the disease from 1796 to the invasion of Europe by Monilinia fructicola, the temperatures and wetness hours as the studies measured them rather than as they circulate, latent infections, postharvest handling, and fungicide resistance with the Greek data. A table is included that separates brown rot from the twelve causes it is confused with.

1. Why brown rot is unlike any other rot

Brown rot is caused by fungi of the genus Monilinia and affects every commercial stone fruit, peach, nectarine, apricot, sweet cherry, sour cherry, plum, almond, as well as pome fruit: apple, pear, quince and medlar [2][3]. Greece holds fifth place worldwide in stone fruit production, after China, the United States, Italy and Spain, with the main regions being Thessaly, the Peloponnese and Western and Central Macedonia, the last being the most important [2].

It differs in four respects, and all of them make management harder.

First, infection occurs twice a year, with a different face each time. In spring it blights blossoms and young shoots. In summer it rots the fruit. These are not two diseases but one, and the first feeds the second. The number of conidia formed on an overwintered mummy is more than ten times greater than on a newly infected blossom [3].

Second, it infects without showing. The fungus enters the young fruit and remains dormant, in a latent infection, for weeks or months. It wakes when the fruit begins to ripen. The symptom seen in July may come from an infection that occurred in May.

Third, it continues after harvest, and that is where it costs most. Losses from postharvest rots are usually far more severe than those from preharvest infections [2]. In California, storage losses frequently exceed 30% and have reached 80 to 90%; in Spain, 59% has been recorded in certain years [3].

Fourth, its symptoms are not pathognomonic. Blossom blight is also caused by spring frost, by Botrytis and by Cladosporium. Twig cankers are also caused by Leucostoma, by Fusicoccum, by bacteria and by hail. Gum exudation is a general reaction of stone fruit to anything that disturbs them [2]. Section 9 provides a table for exactly this.

Sources: 1 2 3

2. History: from Persoon to the invasion by M. fructicola

Brown rot has been studied in Europe for more than 150 years, in North America for about 100, and more recently in Australia, New Zealand, China and Japan. The first authentic description of the fungus causing brown rot on fruit was published in 1796 by Persoon [1].

During the 19th century publications multiplied, and by the end of the century it had been established that two species occur in Europe, M. fructigena and M. laxa [1]. In North America the fungus was at first thought to be one of the two European species, and only later was it found to be different and given the epithet fructicola [1].

The sequence of events that concerns us

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3. The species of the genus, and which ones occur in Greece

The genus Monilinia belongs to the ascomycetes, order Helotiales, family Sclerotiniaceae, and comprises about 25 accepted species [41]. Of these, only four concern fruit growing. Their anamorphs are the corresponding deuteromycetes of the genus Monilia, hence both names are encountered [2].

The name comes from the Latin monile, meaning necklace: the conidia are formed in chains on hyphal branches, arranged like beads on a string [1].

The distinction matters in management. The two species do not behave alike:

• M. laxa is the stronger on blossom blight and twig blight, and is more frequent on almond and apricot [3].
• M. fructicola is clearly more destructive on the fruit, and more frequent on peach, nectarine and plum [3]. Its mycelium can remain concealed in newly set fruit until ripening begins [3].
• M. fructigena, unlike the other two, causes serious losses only when the fruit is wounded. This is why the most important measure against it is the control of fruit-boring insects [3].

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4. How the species are separated in the laboratory

Symptoms do not separate the species. No single morphological character is reliable on its own; separation is made by combining several [3]. Even so, atypical isolates of M. fructicola are misidentified as M. laxa and the reverse [1].

The table below follows the EPPO diagnostic protocol PM 7/18 [5], with additions from the literature.

The growth data refer to culture on PDA at 22 °C under a light and dark cycle with near-ultraviolet radiation of 320 to 380 nm [1][5]. Conidial dimensions are extremely variable and are influenced by environmental conditions and by the host [1].

The three characters that actually work

• The germ tube on water agar. It is measured in two different ways, both useful.
  • Distance to the first branching point. In M. laxa it is less than 60 µm. In M. fructigena and M. fructicola it exceeds 220 µm before branching [3].
  • Total length, at 18 hours and 25 °C. M. fructicola forms a single long unbranched tube of 750 to 900 µm, M. laxa a single but short, 150 to 350 µm, twisted one, while M. fructigena often forms two tubes per conidium [5].
  The values are more variable when conidia are taken directly from fruit.
• Anastomosis. In M. fructicola the germ tubes anastomose abundantly; in M. laxa rarely [1].
• Growth rate. M. fructicola grows about twice as fast as the other two [1].

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5. Quarantine status: what actually applies

This point is very often written incorrectly, so it is stated here precisely. There are two different regimes and they are not the same.

It has now been confirmed: the EPPO listing of everything the European Union regulates does not contain M. fructicola [7].

Sources: 6 7

6. The disease cycle through the year

Winter, where the problem starts

The pathogens overwinter in mummified fruit, on the tree or on the ground, in blighted blossoms and in twig cankers, as mycelium, conidia and pseudosclerotia [2]. These are not leftovers. They are next spring's factory.

In Spanish peach orchards, mummies on the tree were the main source of primary inoculum, and more than 90% of the isolates from them were M. laxa. The number of mummified fruits correlated with postharvest rot, with airborne conidia and with latent infections [15].

Cherry, after harvest. Five mummified fruits still hang on the same spur, next to pedicels that emptied normally. They are not a leftover of the past season: they are the primary inoculum of the next one, placed centimetres from the buds that will flower. The one on the right already has the grey, dry look of sporulation. Winter pruning is the cheapest intervention of the year against them, and the only one that needs no product.

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7. The sexual stage: apothecia and ascospores

The main diagnostic feature of the Discomycetes is the apothecium: a cup- or disc-shaped fruiting body on a slender stalk, arising from pseudosclerotia inside mummified fruit partly or wholly buried in the soil. Its inner surface is lined with thousands of asci, each containing eight single-celled ascospores, interspersed with sterile hyphae. Ascospore discharge produces a visible white cloud above the apothecium [1].

The question that concerns the grower is simple: does this matter in my orchard? The answer, for Europe, is probably not.

For Greece no record of apothecium formation was found in the literature consulted, neither in Greek research papers nor in extension material. That wording is exact: no record was found, not that anyone has demonstrated their absence. Across Europe in any case the perfect stage is considered rare. EPPO describes it as rarely seen in M. fructigena and M. laxa [6], while M. laxa is explicitly reported as not known to produce apothecia [43].

The absence of apothecia does not mean that sexual reproduction is ruled out. In M. fructicola comparative genomics finds signatures that arise only after a sexual cycle, so sexual reproduction is considered frequent in that species [4]. That is genomic evidence, not a field observation. For the grower the conclusion is unchanged: the inoculum that matters is up in the tree.

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8. Symptoms, organ by organ

Fungi of the genus Monilinia attack all above-ground parts of the plant: blighting of blossoms and fruitlets, spots and necrosis on leaves, cankers and blighting on shoots, and fruit rot [2]. The root is not attacked.

Apricot. The blighted flower clusters have remained on the shoot and their leaves dried with them without falling. This "they do not fall" is the character that separates brown rot from frost: frost drops the dead blossoms, brown rot holds them, because the mycelium has already passed into the pedicel and the wood. Beside them, this season's new growth is entirely healthy, the infection is discrete, cluster by cluster.

The same infection at limb scale. The left limb has lost its entire row of flower clusters, which dried and remained on the wood; the right one, a few centimetres away, carries a normal crop of green apricots. The difference is neither the cultivar nor the spray programme: it is the microclimate at the moment of bloom. The limb that stayed wet for more hours was infected; its neighbour was not. Every dead cluster will keep the mycelium inside the shoot until next spring.

The special case of the young fruitlet

Blossom infection does not always stop at the blossom. When a flower cluster is infected after fruit set, the mycelium passes into the newly formed fruitlet, and that fruitlet turns brown and mummifies while its neighbours continue normally.

Sweet cherry, the most instructive snapshot of the disease. On the same spur there coexist healthy green cherries, a bunch of blighted flowers still attached with their stamens visible, and one brown mummified fruitlet. That single fruitlet is the problem: it will stay there until harvest and will sporulate in every wet period, a few millimetres from cherries that are ripening. Removing it by hand at green thinning costs seconds.

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9. Diseases that can be confused with brown rot

The list of causes is not theoretical: it comes from the pathogens actually isolated from rotted peaches in Imathia and Pella over two consecutive seasons [18], supplemented with the abiotic causes and the cankers that the Benaki Institute names as the commonest confusions [2].

Each row is a pair that is confused in practice, with the one character that separates them.

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10. Temperature and wetness hours: what was actually measured

This is where the substance of management lies, and where most of the wrong numbers circulate. Brown rot needs two things at once: a suitable temperature and a wet surface. The second is the one that is underestimated, and it is the one that differs radically between blossom and fruit.

Cardinal temperatures

Wetness hours, the table that matters

The commonest error is transferring a number from one organ to another. The data differ for the blossom, for the fruit and for sporulation on cankers.

How quickly cankers sporulate, the winter table

Twig cankers are the principal overwintering site in well-managed orchards, where mummies are removed with winter pruning [13]. How easily they wake is shown below, as the percentage of cankers that sporulated.

Percentage of peach twig cankers with visible sporulation of M. fructicola, by temperature and wetting duration, 1991 data [13]. Of the 480 cankers examined that year, 31% sporulated within 72 hours, most of them associated with blighted blossoms and pedicels. The following season was far milder: in 1992 the corresponding average was 6.3%, on cankers from trees sprayed the previous season. The figures in the table are therefore the upper bound, not the average.

The incubation period

How long the symptom takes to appear after infection, on cherry blossoms infected by M. laxa, in days:

Time from infection to each necrosis stage, on cherry blossoms [10]. Infections can occasionally abort, if the infected petals or calyx abscise before the pedicel becomes diseased [10]. For field assessment the recommended stage is the one where less than one third of the pedicel is necrotic, because it cannot be mistaken for frost damage [10].

On the fruit, incubation is far faster: 48 to 72 hours to visible rot on ripe peach, under wet conditions and 20 to 25 °C [1]. The next generation of conidia forms about seven days after the initial infection [3]. The figure of 36 hours to the first fruiting structures is quoted in the Greek literature [2] but could not be verified in any accessible primary study.

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11. Latent infections

This section explains why in some seasons everything was done correctly and the crop still rotted.

Latent infection means the fungus has already entered the fruit but stops and waits. It causes no symptom while the fruit is firm and acidic. It is activated on ripening. It was first documented on peach in 1971 and has since been described on apricot, plum and cherry as well [1].

The Greek evidence

The relationship between relative virulence of strains, latent infections and disease development has been studied specifically in Greek peach orchards [19]. In trials in Imathia, latent infections were detected only in nectarines at certain sampling dates and not in the peach cultivars, and a spray of thiophanate-methyl (no longer approved in Greece) at the pit-hardening stage significantly reduced both the percentage of latent infection and preharvest fruit rots [20]. The finding holds as a matter of timing, pit hardening is the moment that counts; the active substance is not.

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12. Susceptibility by crop, by stage and by cultivar

The ranking of crops for blossom blight

Among stone fruit, blossom susceptibility to M. laxa ranks as follows [3]:

Apricot is the most susceptible of all to blossom blight, and only there. The ranking concerns the blossom; no equivalent ranking exists for fruit rot in the literature checked. In practice it means that in apricot, bloom is the decisive moment of the season, whereas in sweet cherry the damage is more significant on the fruit than on the twigs and blossoms [3].

Why green fruit resists

The mechanism is not fully clarified. Three hypotheses explain the relationship [1]: greater mechanical resistance, a different biochemical response of unripe and ripe fruit, and the presence of inhibitory substances in the tissue at this stage. On peach, the latent period lengthens as cuticle and cell-wall thickness increase; on nectarine the opposite occurs, latent infections by M. fructicola increased as cuticle thickness decreased [1]. Chlorogenic acid and neochlorogenic acid, the major phenolics of flesh and peel, are associated with the differences in susceptibility of immature and mature fruit [1].

Cultivars

There is no commercial peach cultivar resistant to brown rot [1]. The cultivar Bolinha is reported as resistant, but has poor fruit quality: small size, high susceptibility to bruising and extensive fruit drop before harvest [1].

What exists is gradations of tolerance, linked to measurable characters:

• In sweet cherry, cultivars with a thinner skin are far more easily penetrated than those with a thicker one [3]. Bigarreau Burlat, János cseresznye and Valerij Cskalov are reported as highly resistant to blossom blight [3].
• In peach, fruit susceptibility increases as ripening advances and depends on the firmness and colour of the flesh, the firmness and thickness of the skin, and pubescence [3].
• In plum, Besztercei, Silvia and Tuleu gras are reported as mildly susceptible, while Čačanska najbolja and President are moderately susceptible [3].
• Under Greek conditions, of 24 cultivars evaluated in Imathia, the nectarine Tasty Free scored as the most susceptible [20].

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13. Wounds, and why they change everything

In infection studies, infection of wounded fruit reached 100% in all four kinds of fruit tested, peach, nectarine, apricot and plum, at both immature and mature stages, and with both Monilinia species used in the study [17]. The wound cancels the fruit's resistance, even the resistance of pit hardening.

The fungus enters in three ways: direct penetration of the skin, through the stomata, and through wounds [2][1]. The third is the easiest, and for M. fructigena almost the only one [3].

The sources of wounds in the orchard:

• Hail. After a hailstorm on ripening fruit, brown rot is almost certain if wetness follows.
• Insects. Particularly codling moth and fruit flies. Insect management is part of brown rot management, not a separate subject. For M. fructigena on pome fruit it is the single most important measure [3].
• Rain cracking in sweet cherry and in certain peach cultivars. Prolonged drought followed by heavy and persistent rain cracks the fruit and opens the way [3].
• Microcracks from fruit-to-fruit contact. Contact surfaces have microcracks, thinner cuticles and a microenvironment that favours infection [1].
• Microlesions from disproportionate irrigation, particularly in the last days before harvest [1].
• Harvest wounds from fingernails, bins and rough handling.

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14. Forecasting models

Why the calendar is not enough

Brown rot is one of the few diseases where forecasting has a demonstrated economic benefit, because risk is concentrated in a few specific wetness windows rather than across the whole season.

The best-documented warning system is Spanish and combines fruit susceptibility, field inoculum, temperature, leaf wetness and rainfall. It was validated across 38 fields and six growing seasons, with disease control equivalent to calendar spraying and treatment reductions above 50% in 96% of trials on early cultivars; on late cultivars, the same level of reduction was achieved in 77% of trials [21].

The Greek application

A blossom blight forecasting model was tested on peach in Imathia: trees sprayed according to the model's predictions showed a statistically lower percentage of blighted shoots than unsprayed trees [20].

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15. Cultural measures that count

The same disease at orchard scale. The brown dried zones stand out against the healthy foliage and show how many limbs the tree has already lost. Every such branch carries a canker that will sporulate with the first wet period of more than twelve hours [13], unless it is removed at pruning.

Removing mummies and cankers

This is the cheapest and the most neglected measure. Destroying the sources of primary inoculum is the single most important control measure [3]. In Spanish orchards, mummies on the tree were the main source, and their number correlated with postharvest rot [15].

Peach, with the tree still in leaf. The mummified fruit is held on the twig, its surface shrunken and dry with the dried remains of the grey sporodochia, and a second mummy is visible behind it. The dead leaf stuck to it shows that the rot also passed into the peduncle. A mummy like this does not have to fall in order to do damage, it stays centimetres from the blossom buds that will open in spring. This is what is looked for on the tree before winter pruning, and it is found more easily once the leaves have dropped.

• All mummies are removed, from the tree and from the ground, in autumn or early spring [3].
• All fruit remaining after the final picking is removed. This limits infection of peduncles and twigs and prevents mummies forming immediately adjacent to the susceptible blossoms of spring [1].
• Branches with cankers are cut out. Pruning is done on days of low relative humidity.
• The material is taken out of the orchard. On large areas where collection is impractical, the alternative is deep burial of mummies [3], but note that shallow burial of 2 to 3 cm does not prevent apothecium formation [14].
• Rotted fruit is also removed during summer, as soon as the first symptoms appear [3].

Pruning and planting as ventilation tools

What dries quickly does not become infected. The Benaki Institute recommends specifically: wider planting distances, training to a single-leader form, use of rootstocks that impart dwarfing and reduce vigorous growth, and appropriate pruning [2]. To these are added the choice of sloping ground and orienting the rows along the prevailing winds [3].

Excessive fertilisation leads to overcrowding of branches, which limits air circulation and prevents rapid drying [1].

Irrigation and nutrition

• Avoid overhead irrigation near ripening. Water is applied at the root.
• Flood irrigation increases the risk of infection. It keeps the soil and the air inside the canopy wet for hours, and wetness is one of the two conditions the fungus needs. Where there is a choice, drip irrigation is preferable for this reason as well.
• No afternoon irrigation during the susceptible period: the moisture stays all night.
• Consistency in irrigation. Prolonged drought followed by heavy rain cracks the fruit [3].
• Rational nitrogen fertilisation [2]. Excess gives large, soft fruit with thin skin and a dense canopy that holds moisture.
• Sufficiency in calcium and boron [2].

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16. What is approved in Greece

No list of approved products is given here, for a practical reason: approvals change constantly. Active substances are withdrawn, crops are added to or removed from the same authorisation, and pre-harvest intervals change. A table inside an article goes stale with the first revision, and a stale approvals table is worse than none.

What follows in the next sections concerns modes of action and strategy, not specific products. The logic of group alternation holds regardless of which trade name happens to be available in a given season.

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17. Fungicide resistance, with the Greek data

FRAC classifies Monilinia species as a medium risk for resistance development [23]. History, however, shows something less reassuring: the benzimidazoles collapsed within five to six years of their registration [1].

Greece, from three independent studies

The European and international picture

The mechanisms, and an important correction

• Benzimidazoles. Point mutation in the β-tubulin gene. Two levels: H6Y gives low resistance and a cold-sensitive phenotype, E198A high resistance and a heat-sensitive one [31]. In Greece, E198A was detected in all highly resistant strains [24]. In the USA, E198Q and F200Y were also found, never before described in the genus [29].
• Triazoles. The main mechanism is not target mutation but target overexpression: a repetitive genetic element of 65 base pairs, "Mona", inserts into the promoter of the MfCYP51 gene and raises its expression 5 to 11 fold; no amino-acid change was found in the protein itself [32]. In the more northern US states, resistant strains were found without Mona and without increased expression, a second, unknown mechanism therefore exists [29].
• SDHIs. In the Spanish study, no differences were found in the SDHB or SDHC subunits of fluopyram-resistant strains. Instead, amino-acid substitutions were found in oxidative phosphorylation proteins, V-type H⁺-ATPase subunits, COX10, COX15 and components of the ubiquinol cytochrome c reductase, suggesting adaptive modifications of respiratory pathways [26].

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18. Spray strategy by crop

What follows is a framework for thinking, not a recipe. The number of treatments, their timing and the products are determined by the agronomist, on the basis of the crop, the cultivar, the disease pressure in the orchard and the course of the weather.

The six moments, as the Benaki Institute defines them

Preventive sprays are placed [2]: at bud burst when conditions favour the disease; at white or pink bud; at full bloom; additionally, if bloom is prolonged by the weather; after wounds are created on the fruit, for example by hail; and before harvest for protection against postharvest rots.

The susceptible stages by crop, as the literature defines them

In European integrated stone fruit production, the guideline is only two or three chemical treatments with DMI or QoI: one at full bloom and one 7 or 10 days before harvest. No chemical treatment is permitted on stone fruit after harvest [1].

The skeleton of the season

Coverage counts as much as the active substance

Brown rot attacks the fruit from every side, and infects from the contact point between two fruits, that is, from the side the sprayer never reaches. A spray with the wrong water volume, worn nozzles or in wind leaves uncovered areas, and that is where the rot will start. Sprayer calibration is mandatory, and it is cheaper than an extra treatment.

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19. Harvest and postharvest handling

What is gained in the orchard can be lost in a few hours. And since losses here are usually more severe than preharvest ones [2], this section is not an appendix.

Harvest rules

• Never harvest wet fruit.
• Remove rotted fruit from the tree and the ground before harvest, not after. One rotted fruit in the bin infects its neighbours by simple contact.
• Minimise injuries at harvest, in transport, in packing and in storage [2]. Trimmed fingernails, clean bins, no overfilling.
• Clean equipment. Bins and grading lines carry spores from batch to batch.
• Maturity at harvest determines postharvest life. Too advanced a maturity increases susceptibility to decay; too early a maturity reduces flavour and texture [1].

Cooling

Protection from heating after harvest and rapid movement to cooling are among the most important measures, both to avoid excessive flesh softening and to reduce postharvest decay [1]. How many latent infections are finally expressed depends mainly on temperature and time: in trials on nectarines, fewer than eleven days at 4 °C prevented symptom expression, while beyond that threshold expression entered an exponential phase [35].

Maximum storage duration is not exceeded, either in air or in controlled atmosphere, so as to avoid senescence and the chilling injuries that increase susceptibility to brown rot [1].

What is permitted in Europe

The European Union does not permit the use of fungicides after harvest or inside storage facilities [3][1]. In the USA, fludioxonil, fenhexamid, tebuconazole, propiconazole and pyrimethanil have been registered for postharvest dips [3]. This difference is the reason why in Europe postharvest management rests on temperature, hygiene and biological agents, and not on chemistry.

The Benaki Institute summarises packhouse measures: dipping in hot water with or without fungicide, dry heat, moist heat combined with Bacillus sp., water dipping with air drying, hydrocooling, and fumigation with a fungicide exclusively in well-sealed chambers [2].

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20. Organic production

The honest picture is difficult. In organic stone fruit orchards, in a wet season it is not unusual to lose 75% or more of the crop to brown rot, despite the use of copper products. In some regions organic cherry production is almost impossible, because every attempt to control brown rot has failed [1].

What is available:

• Biological agents approved in Greece: Bacillus amyloliquefaciens in four strains, Saccharomyces cerevisiae LAS02, Metschnikowia fructicola. With pre-harvest intervals of 0 to 3 days, they are the only products that fit the last window before harvest [22].
• Epicoccum nigrum, a natural component of the mycoflora of peach twigs and blossoms. Two field applications, at bloom and preharvest, significantly reduced postharvest brown rot in five of seven trials [1]. It acts by producing flavipin, a substance that inhibits respiration and prevents germination of M. laxa conidia [3].
• Aureobasidium pullulans, active against brown rot even at 0 °C on peach [1]. Combined with a hot water dip at 55 °C for 50 seconds, M. laxa infections fell to 17.5%, against 25.8% with the antagonist alone, 30.0% with hot water alone and 74.2% in the untreated control [1].
• Penicillium frequentans, with control above 50% [1].
• Essential oils. In trials on more than 30 plant species, the vapour phase of thyme oil had the strongest inhibitory effect [3]. Carvacrol and thymol control M. fructicola effectively on cherry, apricot and plum, but caused phytotoxic symptoms and off-flavours in cherries and firmer texture and phytotoxicity in apricots [1].
• Chitosan at 1%, with activity comparable to that of synthetic fenhexamid in restricting mycelial growth [1].

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21. Pome fruit and M. fructigena

Brown rot does not stop at stone fruit. M. fructigena is the economically most important species of the genus on apple and pear in Europe [3]. In Greece it is the species recorded on pome fruit [2].

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22. Where the subject continues, crop by crop

Brown rot is not managed in isolation. Each crop has its own framework, cultivars, pruning, nutrition, and the other pests that open the wounds. The related articles on this site:

23. The points that remain

Brown rot is not defeated with "the good product". It is managed with a clean orchard in winter, with correct timing at bloom based on wetness and not on the calendar, with protection of the period when nothing is visible, with serious insect management, with rotation of groups and full rates, and with a cold store that works fast.

24. Sources

Numbers in the text refer to the list below. Where only an abstract was used rather than the full text, this is stated explicitly.

• [1] Martini, C. and Mari, M. (2014). Monilinia fructicola, Monilinia laxa (Monilinia Rot, Brown Rot). In: Postharvest Decay, chapter 7, pages 233-265. Elsevier. Source for the history from Persoon (1796) and the invasion of Europe by M. fructicola, taxonomy and morphology, germ tube and anastomosis, the 48 to 72 hours to visible rot, the history of the benzimidazoles, 55 °C for 60 seconds and 60 °C for 20 seconds, curing with hot moist air at 50 °C for 2 hours at 95 to 99% relative humidity, the biocontrol agents and essential oils, the postharvest chain, thinning before and after pit hardening, calcium in New Zealand and losses in organic production. Full text.
• [2] Tsirogiannis, D. (2021). Brown rot of stone fruit, a most serious disease: early diagnosis and management. Georgia - Ktinotrofia 03/2021:49-51, AgroTypos (in Greek). Mycology Laboratory, Benaki Phytopathological Institute. Source for Greece's fifth place in world stone fruit production, the species recorded in Greece by crop group, the four million spores per fruit, the 36 hours to the first fruiting structures, the next conidial generation at seven days, the diagnostic problems and confusions, the six moments for preventive spraying and the packhouse measures. Full text. Two claims of this source are not used: the "38 species of the genus", which the taxonomic literature does not support, as source [41] explains, and the "losses of 1.7 billion euros per year", which is a citation-chain error, as section 1 explains.
• [3] Hrustić, J., Mihajlović, M., Grahovac, M., Delibašić, G., Bulajić, A., Krstić, B. and Tanović, B. (2012). Genus Monilinia on Pome and Stone Fruit Species. Pesticidi i fitomedicina 27(4):283-297. Source for the profiles of the three species, the blossom susceptibility ranking (apricot > sweet cherry > peach > sour cherry > plum), the speed of rotting by fruit, the chronology of M. fructicola detection in Europe, the distance to the first branching point of the germ tube, under 60 µm in M. laxa and over 220 µm in the other two, the multiplex PCR of Côté and co-workers, the cultivars, the number of treatments per crop, M. fructigena on pome fruit and black rot, and the European Union prohibition of postharvest fungicides. Full text.
• [4] De Miccolis Angelini, R. M., Landi, L., Raguseo, C., Pollastro, S., Faretra, F. and Romanazzi, G. (2022). Tracking of diversity and evolution in the brown rot fungi Monilinia fructicola, Monilinia fructigena, and Monilinia laxa. Frontiers in Microbiology 13:854852. Source for M. fructicola having largely replaced M. fructigena in Europe, for the comparative genomics of the three species, and for the genome signatures that indicate frequent sexual reproduction in M. fructicola. Full text, open access. Note: the paper does not contain Greek data and does not give species composition percentages by country. It is also cited as the example of how the 1.7 million euro estimate of source [1] was reproduced as 1.7 billion.
• [5] EPPO Standard PM 7/18 (3), Diagnostic protocol for Monilinia fructicola, approved 2020. EPPO Bulletin 50(1):5-18. Stable file: pm7-018-3-en.pdf. Source for the table separating the four species (colony colour, growth in 24 hours, sporulation, concentric rings of spores, colony margin), for conidial dimensions and germ tube length on water agar at 18 hours and 25 °C, and for the molecular identification protocols. Conidial dimensions and germ tube length are given in the text of the protocol, not inside the table. Full text.
• [6] EPPO Global Database, Monilinia fructicola (MONIFC), Datasheet. Source for the A1 listing from 1984 and A2 from 2004, for the presence of the species in mainland Greece, for the finding that with 15 hours of wetness more than 80% of cherries are infected while with only 3 hours infection remains very low, and for the most susceptible fruit phase two to three weeks before harvest.
• [7] EPPO Global Database, Categorization for European Union (EU), the listing of every organism regulated by Regulation (EU) 2019/2072. Source for the fact that Monilinia fructicola is not included among Union quarantine pests nor among regulated non-quarantine pests. Checked September 2026.
• [8] Casals, C., Viñas, I., Torres, R., Griera, C. and Usall, J. (2010). Effect of temperature and water activity on in vitro germination of Monilinia spp. Journal of Applied Microbiology 108(1):47-54. Source for conidial germination at every temperature tested from 0 to 30 °C, for complete inhibition at 38 °C, and for the finding that at a water activity of 0.87 no species germinated at any temperature. The range studied was 0 to 38 °C and the temperatures tested were 0, 5, 15, 25, 30 and 38 °C; 35 °C was not tested and the paper gives no optimum range. It reports over 80% germination at 25 °C and a water activity of 0.99 within two hours for M. fructicola and M. fructigena and within four for M. laxa. Abstract used.
• [9] Tamm, L. and Flückiger, W. (1993). Influence of temperature and moisture on growth, spore production, and conidial germination of Monilinia laxa. Phytopathology 83:1321-1326. Source for mycelial growth at 2.5 to 30 °C with a calculated optimum of 24.8 °C, and for conidial germination in the absence of free moisture at relative humidities of 97 to 100%. Abstract used.
• [10] Tamm, L., Minder, C. E. and Flückiger, W. (1995). Phenological analysis of brown rot blossom blight of sweet cherry caused by Monilinia laxa. Phytopathology 85:401-408. Source for the incubation-period table by temperature and necrosis stage, for the abortion of infections when petals or calyx abscise, for the recommendation to assess at the one-third-pedicel stage, and for the maximum growth temperature of 31 °C. Full text.
• [11] Biggs, A. R. and Northover, J. (1988). Influence of temperature and wetness duration on infection of peach and sweet cherry fruits by Monilinia fructicola. Phytopathology 78:1352-1356. Source for the optimum fruit-infection conditions: 20 to 22.5 °C with 15 hours of wetness for cherry giving over 80% infection, and 22.5 to 25 °C with 12 hours for peach giving over 70% infection at all temperatures except 27.5 and 30 °C. Abstract used. The wetness range tested on cherry was 6 to 18 hours, but the over-80% figure corresponds to 15 hours.
• [12] Biggs, A. R. and Northover, J. (1988). Early and late-season susceptibility of peach fruits to Monilinia fructicola. Plant Disease 72:1070-1074. Source for the three phases of fruit susceptibility: susceptible for two to three weeks in June, resistant at pit hardening, susceptible again about two weeks before full ripeness. Abstract used.
• [13] Watson, W. A., Zehr, E. I. and Grimes, L. W. (2002). Influence of temperature and wetting period on inoculum production by Monilinia fructicola in peach twig cankers. Plant Disease 86(6):666-668. Source for the canker sporulation table by temperature and wetting hours, for the requirement of at least 12 hours and the absence of sporulation at 3, 6 and 9 hours, for the 31% of 480 cankers that sporulated, for twig cankers as the principal overwintering site, for the 5 hours of wetting on sour cherry blossoms when inoculum is high, which the paper reports secondhand, and for the impossibility of quantifying inoculum. Full text. For blossom blight the paper gives two figures, and both are used here: the authors’ field observation in South Carolina that it seldom becomes widespread unless the wet period reaches 24 hours, and their calculation of 17 to 30 hours of wetting or high humidity at bloom, unless viable conidia are already present from an earlier wet period. Of the 480 cankers assayed in 1991, 149 sporulated, that is 31%, and no sporulation was observed at 3, 6 or 9 hours.
• [14] Holtz, B. A., Michailides, T. J. and Hong, C. X. (1998). Development of apothecia from stone fruit infected and stromatized by Monilinia fructicola in California. Plant Disease 82:1375-1380. Source for the requirements of apothecium formation: only from fully stromatized mummies, more than eight weeks at 2 °C with relative humidity above 97%, no production below 90%, burial depth immaterial, and presence only in plots with undisturbed floor vegetation. Abstract used.
• [15] Villarino, M., Melgarejo, P., Usall, J., Segarra, J. and De Cal, A. (2010). Primary inoculum sources of Monilinia spp. in Spanish peach orchards and their relative importance in brown rot. Plant Disease 94(8):1048-1054. Source for mummies on the tree being the main source of primary inoculum, for more than 90% of isolates from mummies being M. laxa, for the correlations with postharvest rot and latent infection, and for the complete absence of apothecia over three growing seasons. Abstract used.
• [16] Luo, Y., Ma, Z. and Michailides, T. J. (2001). Analysis of factors affecting latent infection and sporulation of Monilinia fructicola on prune fruit. Plant Disease 85(9):999-1003. Source for the latent infection equation, for the negative sign of temperature within the 15 to 30 °C range, for sporulation of thinned fruit over 7 to 9 days at a fruit water content of 67.2%, and for 100% of fruits sporulating on the first day. Full text. The five moisture levels tested were 67.2, 53.8, 40.3, 26.9 and 13.4% and refer to water content inside the fruit, not the relative humidity of the air. The Biggs and Northover figures are now given by source [11], in their correct form (15 hours for cherry).
• [17] Kreidl, S., Edwards, J. and Villalta, O. N. (2015). Assessment of pathogenicity and infection requirements of Monilinia species causing brown rot of stone fruit in Australian orchards. Australasian Plant Pathology 44(4):419-430. Source for 100% infection of wounded fruit in all four kinds of fruit tested (peach, nectarine, apricot, plum), at immature and mature stages, for the 3 hours of wetness at 24 °C sufficient on peach blossom for M. fructicola, and for the greater susceptibility of ripe over young fruit with a minimum at pit hardening. Two Monilinia species were tested, not four; M. laxa gave lower infection levels and did not infect plum.
• [18] Thomidis, T., Michailides, T. and Exadaktylou, E. (2009). Contribution of pathogens to peach fruit rot in northern Greece and their sensitivity to iprodione, carbendazim, thiophanate-methyl and tebuconazole fungicides. Journal of Phytopathology 157:194-200. Pomology Institute, Naoussa. Source for M. laxa accounting for about 70% and 78% of rotted peaches in Imathia and Pella in 2005 and 2006, for the 5% attributable to Phomopsis amygdali, for the full list of the other pathogens, for the resistance rates of 14% and 11% to thiophanate-methyl and 15% and 12% to carbendazim, for complete sensitivity to tebuconazole and iprodione, and for the field finding that fruit sprayed with benzimidazoles had significantly more rot than fruit sprayed with tebuconazole or iprodione. Full text.
• [19] Thomidis, T. (2017). Influence of relative virulence and latent infections on the development of Monilinia to Greek peach orchards. Crop Protection 94:159-165. Source for the relationship between relative virulence of strains, latent infections and disease development in Greek peach orchards. Abstract used.
• [20] Thomidis, T. and Michailides, T. J. (2010). Development and implementation of cost-effective strategies to manage brown rot of peach trees in Imathia, Greece. European Journal of Plant Pathology 126(4):575-582. Source for the evaluation of 24 cultivars in Imathia with the nectarine Tasty Free as the most susceptible, for the reduction of latent infections and preharvest rots by a spray at pit hardening, and for the finding that trees sprayed according to a forecasting model had statistically fewer blighted shoots than unsprayed trees, not than calendar-sprayed trees. Abstract used.
• [21] Casals, C., Segarra, J., Torres, R., Teixidó, N., De Cal, A. and Usall, J. (2023). Validation of a warning system to control brown rot in peach and nectarine. Agronomy 13(1):254. Source for the validation across 38 fields and six growing seasons, for treatment reductions above 50% in 96% of trials on early cultivars and 77% on late ones, and for postharvest infection of 9.3% on late against 3.1% on early cultivars.
• [22] Greek Ministry of Rural Development and Food, Plant Protection Products Database. Data retrieved 14 September 2026. Source for the 156 products approved against brown rot on peach, sweet cherry, apricot, plum, sour cherry and almond, for the 26 distinct active-substance combinations, for the distribution by crop, for the pre-harvest intervals, and for the 54, 57, 16 and 8 products on apple, pear, quince and medlar respectively. These approvals are valid in Greece only.
• [23] Fungicide Resistance Action Committee (FRAC): FRAC Code List 2026, Pathogen Risk List 2019, and the minutes and recommendations of the SDHI working group (2021 and 2022). Source for the mode-of-action group codes (Code List), for the classification of Monilinia species as medium risk (Pathogen Risk List 2019, table 2), for the limit of three SDHI products per year and two consecutive applications in mixture on stone fruit, and for the 2020 monitoring results. Three clarifications are needed. The three-SDHI limit applies over all diseases of the crop and not to brown rot specifically, for which FRAC gives no separate recommendation; the two-consecutive limit applies only in mixture, while solo use requires strict alternation; and the 2020 monitoring did not show full sensitivity in all eight countries, but reduced sensitivity in single M. fructigena isolates from one location each in Hungary and Poland.
• [24] Malandrakis, A. A., Markoglou, A. N. and Ziogas, B. N. (2012). PCR-RFLP detection of the E198A mutation conferring resistance to benzimidazoles in field isolates of Monilinia laxa from Greece. Crop Protection 39:11-17. Source for 37% of Greek M. laxa isolates belonging to the highly resistant phenotype, for resistance factors above 500, for the E198A mutation in all highly resistant strains, and for the absence of a fitness cost. Abstract used.
• [25] Testempasis, S. G., Tsintila, V. and Karaoglanidis, G. (2021). Assessment of sensitivity to boscalid, fluopyram and tebuconazole in Monilinia fructicola isolates obtained from peach orchards in Greece. 2nd International Electronic Conference on Plant Sciences. Laboratory of Plant Pathology, Aristotle University of Thessaloniki. Source for the 230 Greek M. fructicola isolates, for the 46.1% resistant to at least one active, for the rates of 29.6% to tebuconazole, 8.7% to boscalid and 7.8% to fluopyram, and for this being the first report of SDHI and DMI resistance in Greece.
• [26] Veloso, J., Villarino, M., Guerra, L., Vazquez, F., Cabrera, J. E., Torres, R., Gómez, M., Larena, I., Melgarejo, P., De Cal, A. and Guijarro, B. (2026). Fungicide resistance profile of Monilinia fructicola and Monilinia laxa isolates from commercial peach and nectarine orchards in the Ebro Valley, Spain. Plant Pathology 75:e70213. Source for the species composition of 53% M. laxa and 47% M. fructicola in Spain, for 75% and 67% sensitivity of the two species, for the first moderate resistance to fluopyram and pyraclostrobin, for the absence of resistance to fenpyrazamine and fludioxonil, for the recommended field rate being twenty-fold the concentration at which reduced sensitivity was measured, for the absence of differences in the SDHB and SDHC subunits and the substitutions in oxidative phosphorylation proteins. Full text, open access. The Serbian data are not a finding of this paper, which concerns the Ebro Valley, and are now attributed to source [40].
• [27] Dardani, G., Guarnaccia, V., Nari, L., Testempasis, S. I., Karaoglanidis, G. S. and Gullino, M. L. (2023). Identification of pathogens causing brown rot of stone fruit in Cuneo province (Italy) and assessment of sensitivity to azoxystrobin, cyprodinil, fenhexamid, fludioxonil, and tebuconazole. Phytopathologia Mediterranea 62(3):455-465. Source for the 50 Italian isolates, for the nine M. laxa and two M. fructicola with a resistance factor above 10, for the highest factor of 48.96 for azoxystrobin, and for the absence of resistance findings for fenhexamid and fludioxonil.
• [28] Ivić, D., Fazinić, T., Novak, A., Šajbić, L., Stepanović, M., Gotlin Čuljak, T. and Miličević, T. (2021). Resistance of Monilinia fructicola to thiophanate-methyl in Croatia. European Journal of Plant Pathology 159:211-217. Source for 44% of Croatian M. fructicola strains being resistant or highly resistant to thiophanate-methyl, and for detection of the β-tubulin mutation in 15 of 16 strains. Abstract used. Two clarifications are needed. The 44% is calculated on the 34 M. fructicola isolates and not on the 66 total (nine resistant, 26%, and six highly resistant, 18%), and the group of 16 strains is "highly resistant, resistant and less sensitive", not resistant only.
• [29] Chen, F., Liu, X. and Schnabel, G. (2013). Field strains of Monilinia fructicola resistant to both MBC and DMI fungicides isolated from stone fruit orchards in the eastern United States. Plant Disease 97:1063-1068. Source for the significant brown rot despite preharvest sprays in Pennsylvania, Maryland and South Carolina in 2012, for the 22 of 140 isolates with dual resistance, for the E198Q and F200Y mutations not previously described in the genus, for Mona being detected only in South Carolina within the sample of this study, while later work found it in Georgia and Alabama as well, for the second unknown mechanism of triazole resistance, and for label rates being unable to control dual-resistant strains on detached fruit. Full text.
• [30] Yoshimura, M. A., Luo, Y., Ma, Z. and Michailides, T. J. (2004). Sensitivity of Monilinia fructicola from stone fruit to thiophanate-methyl, iprodione, and tebuconazole. Plant Disease 88(4):373-378. Source for the fall in thiophanate-methyl resistance from 75% (39 of 52 isolates from 1992 to 1998) to 22% (22 of 100 isolates in the 2002 collection) in California, and for the absence of strains resistant to iprodione or tebuconazole. Abstract used.
• [31] Ma, Z., Yoshimura, M. A. and Michailides, T. J. (2003). Identification and characterization of benzimidazole resistance in Monilinia fructicola from stone fruit orchards in California. Applied and Environmental Microbiology 69(12):7145-7152. Source for the two β-tubulin mutations, H6Y for low and E198A for high resistance, for the cold- and heat-sensitive phenotypes, and for the finding that benzimidazoles cannot control blossom blight caused by highly resistant strains. Full text.
• [32] Luo, C.-X. and Schnabel, G. (2008). The cytochrome P450 lanosterol 14α-demethylase gene is a demethylation inhibitor fungicide resistance determinant in Monilinia fructicola field isolates from Georgia. Applied and Environmental Microbiology 74(2):359-366. Source for the 65-base-pair genetic element "Mona" at position −117 of the MfCYP51 promoter, for the 5- to 11-fold increase in expression, and for the absence of any amino-acid change in the protein. Full text.
• [33] Hily, J.-M., Singer, S. D., Villani, S. M. and Cox, K. D. (2011). Characterization of the cytochrome b (cyt b) gene from Monilinia species causing brown rot of stone and pome fruit and its significance in the development of QoI resistance. Pest Management Science 67(4):385-396. Source for the group-I-like intron directly after codon 143 in M. fructicola and M. laxa but not in M. fructigena, for the conclusion that the G143A mutation is not likely to arise in the first two species, and for the higher risk in M. fructigena. Full text.
• [34] Zúñiga, E., Aparicio-Durán, L., Torres, R., Miarnau, X., Casals, C. and Torguet, L. (2026). Efficacy of fungicide products against the blossom blight disease of almond caused by Monilinia laxa in the Ebro Valley. Crop Protection 208:107697. Source for the finding that of ten products field-tested against almond blossom blight, seven significantly reduced incidence, and for the inconsistent effectiveness of the biologicals across seasons, with the recommendation that they be regarded as complementary rather than primary tools. Abstract used.
• [35] Garcia-Benitez, C., Casals, C., Usall, J., Sánchez-Ramos, I., Melgarejo, P. and De Cal, A. (2020). Impact of postharvest handling on preharvest latent infections caused by Monilinia spp. in nectarines. Journal of Fungi 6(4):266. Source for the effect of postharvest handling on the proportion of latent infections that are ultimately expressed, and for fewer than eleven days at 4 °C preventing symptom expression. Full text, open access. The paper measures cold storage temperature and duration, not cooling speed.
• [36] UC IPM Pest Management Guidelines, Cherry, Bacterial Canker. University of California Agriculture and Natural Resources. Source for: the statement that in bacterial canker "the inner bark is brown, fermented, and sour smelling", and for the fact that this feature marks the sour sap phase, in which no typical canker forms on the surface. Full text.
• [37] Commission Implementing Regulation (EU) 2020/1498 of 15 October 2020 concerning the non-renewal of approval of the active substance thiophanate-methyl. Source for: the non-renewal of the approval, the withdrawal of product authorisations by 19 April 2021 (article 3), and the expiry of any grace period by 19 October 2021 (article 4). Full text.
• [38] Papavasileiou, A., Testempasis, S., Michailides, T. J. and Karaoglanidis, G. S. (2015). Frequency of brown rot fungi on blossoms and fruit in stone fruit orchards in Greece. Plant Pathology 64(2):416-424. Laboratory of Plant Pathology, Aristotle University of Thessaloniki. Source, as the peer-reviewed publication of the Greek survey, for there being two species on Greek stone fruit, M. laxa and M. fructicola, and for the absence of M. fructigena. The full text was not read, because the publisher does not make it freely available; the exact percentages are given by source [39], the doctoral thesis of the first author on the same data.
• [39] Papavasileiou, A. (2017). Brown rot of stone fruit: molecular and biological characterisation of the causal agents. Doctoral thesis, Faculty of Agriculture, Laboratory of Plant Pathology, Aristotle University of Thessaloniki, 231 pages (in Greek). Greek National Archive of Doctoral Dissertations 10442/41307. Source for the 1,433 isolates from the main stone fruit producing regions of Greece, for the figures of M. laxa 59% and M. fructicola 41%, for the absence of M. fructigena, and for M. fructicola being more frequent on fruit while M. laxa occurred at similar frequency on blossoms and fruit. Abstract used. A thesis does not stand alone behind a quantitative claim, which is why it is accompanied by source [38].
• [40] Hrustić, J., Mihajlović, M., Grahovac, M., Delibašić, G. and Tanović, B. (2018). Fungicide sensitivity, growth rate, aggressiveness and frost hardiness of Monilinia fructicola and Monilinia laxa isolates. European Journal of Plant Pathology 151(2):389-400. Institute of Pesticides and Environmental Medicine, Belgrade. Source for M. fructicola isolates being significantly less sensitive than M. laxa to iprodione, tebuconazole, chlorothalonil, azoxystrobin, fluopyram and boscalid, for M. laxa showing little variation in sensitivity while M. fructicola showed a wide range, and for the higher growth rate and greater aggressiveness of M. fructicola. Abstract used.
• [41] Marin-Felix, Y. et al. (2017). Genera of phytopathogenic fungi: GOPHY 1. Studies in Mycology 86:99-216, and the accompanying database entry for the genus Monilinia Honey. Source for the genus comprising about 25 accepted species, from M. amelanchieris to M. yunnanensis. Full text, open access. The figure of "38 species" that circulates most probably derives from counting names in Index Fungorum, which includes synonyms and invalid names.
• [42] Miessner, S. and Stammler, G. (2010). Monilinia laxa, M. fructigena and M. fructicola: risk estimation of resistance to QoI fungicides and identification of species with cytochrome b gene sequences. Journal of Plant Diseases and Protection 117(4):162-167. Source for the priority of the finding: the absence of the intron in M. fructigena and the conclusion that the G143A mutation is relatively unlikely in M. laxa and M. fructicola were published here first, a year before source [33]. Abstract used.
• [43] Obi, V. I., Barriuso, J. J. and Gogorcena, Y. (2018). Peach Brown Rot: Still in Search of an Ideal Management Option. Agriculture 8(8):125. Source for M. laxa not being known to produce apothecia, in contrast with M. fructicola. Full text, open access.