Invasive Species Compendium

Detailed coverage of invasive species threatening livelihoods and the environment worldwide

Datasheet

Monilinia fructigena
(brown rot)

Toolbox

Datasheet

Monilinia fructigena (brown rot)

Summary

  • Last modified
  • 27 September 2018
  • Datasheet Type(s)
  • Invasive Species
  • Pest
  • Vector of Plant Pest
  • Preferred Scientific Name
  • Monilinia fructigena
  • Preferred Common Name
  • brown rot
  • Taxonomic Tree
  • Domain: Eukaryota
  •   Kingdom: Fungi
  •     Phylum: Ascomycota
  •       Subphylum: Pezizomycotina
  •         Class: Leotiomycetes
  • Summary of Invasiveness
  • M. fructigena is one of several apothecial ascomycetes causing brown rot and blossom blight of stone fruit and pome fruit trees worldwide. It has a more restricted distribution than the other species, occurring i...

  • There are no pictures available for this datasheet

    If you can supply pictures for this datasheet please contact:

    Compendia
    CAB International
    Wallingford
    Oxfordshire
    OX10 8DE
    UK
    compend@cabi.org
  • Distribution map More information

Don't need the entire report?

Generate a print friendly version containing only the sections you need.

Generate report

Pictures

Top of page
PictureTitleCaptionCopyright
Brown rot of pear caused by M. fructigena in France.  Note wasp (Vespula sp.) emerging from feeding at infected site.
TitleSymptoms
CaptionBrown rot of pear caused by M. fructigena in France. Note wasp (Vespula sp.) emerging from feeding at infected site.
CopyrightM. Fawaz Azmeh/University of Damascus
Brown rot of pear caused by M. fructigena in France.  Note wasp (Vespula sp.) emerging from feeding at infected site.
SymptomsBrown rot of pear caused by M. fructigena in France. Note wasp (Vespula sp.) emerging from feeding at infected site. M. Fawaz Azmeh/University of Damascus
Brown rot of pear, caused by M. fructigena, showing full sporulation. Note distinctive concentric circles of sporulation.
TitleSymptoms
CaptionBrown rot of pear, caused by M. fructigena, showing full sporulation. Note distinctive concentric circles of sporulation.
CopyrightM. Fawaz Azmeh/University of Damascus
Brown rot of pear, caused by M. fructigena, showing full sporulation. Note distinctive concentric circles of sporulation.
SymptomsBrown rot of pear, caused by M. fructigena, showing full sporulation. Note distinctive concentric circles of sporulation.M. Fawaz Azmeh/University of Damascus
Brown rot of pear caused by M. fructigena; Conidiophores and conidia.
TitleConidiophores and conidia
CaptionBrown rot of pear caused by M. fructigena; Conidiophores and conidia.
CopyrightM. Fawaz Azmeh/University of Damascus
Brown rot of pear caused by M. fructigena; Conidiophores and conidia.
Conidiophores and conidiaBrown rot of pear caused by M. fructigena; Conidiophores and conidia.M. Fawaz Azmeh/University of Damascus

Identity

Top of page

Preferred Scientific Name

  • Monilinia fructigena Honey ex Whetzel 1945

Preferred Common Name

  • brown rot

Other Scientific Names

  • Acrosporium fructigenum (Pers.) Pers. 1822
  • Monilia fructigena Pers.: Fr. 1801
  • Oidium fructigenum Kunze & J. C. Schmidt 1817
  • Oidium wallrothii Thüm. 1875
  • Oospora candida Wallr. 1833
  • Oospora fructigena (Pers.: Fr.) Wallr. 1833
  • Sclerotinia fructigena (Pers.: Fr.) J. Schröt. 1893
  • Sclerotinia fructigena Aderh. & Ruhland 1905
  • Torula fructigena Pers. 1796

International Common Names

  • English: blossom blight; blossom blight of fruit trees; blossom wilt; fruit canker; spur blight; spur canker; twig blight; twig canker; wither tip
  • Spanish: momificado; momificado de las frutas; podredumbre de las frutas; pudricion café de la manzana; pudricion café de la pera; pudricion café del chabecano; pudricion café del durazno
  • French: brulure des rameaux du cerisier; brulure sclerotique du cerisier; monilia des arbres fruitiers; moniliose des arbres fruitiers; mycose des arbres fruitiers à noyau; pourriture brune des arbres fruitiers; rot-brun des arbres fruitiers

Local Common Names

  • Germany: Bluetenduerre: Kern- und Steinobst; Braunfaeule: Kern- und Steinobst; Fruchtfaeule: Kern- und Steinobst; Polsterschimmel: Kern- und Steinobst; Zweigduerre: Kern- und Steinobst; Zweigduerre: Obst

EPPO code

  • MONIFG (Monilinia fructigena)

Summary of Invasiveness

Top of page

M. fructigena is one of several apothecial ascomycetes causing brown rot and blossom blight of stone fruit and pome fruit trees worldwide. It has a more restricted distribution than the other species, occurring in Europe and Asia, but not in North America. Reports of its occurrence in South America are likely to be errors in identification. Recent identification of a new species in Japan suggests that it may not be present there, as previously thought, and reports from other parts of eastern Asia may have to be re-examined. It is a quarantine pest for Canada, the USA, Australia and New Zealand. One unusual introduction to the USA was resolved by eradication (Batra, 1979; Ogawa and English, 1991). Introduction could occur through the importation of infected fruit as well as of tree material for propagation and breeding, from which it could spread readily by means of conidia carried by the wind or insects.

Taxonomic Tree

Top of page
  • Domain: Eukaryota
  •     Kingdom: Fungi
  •         Phylum: Ascomycota
  •             Subphylum: Pezizomycotina
  •                 Class: Leotiomycetes
  •                     Subclass: Leotiomycetidae
  •                         Order: Helotiales
  •                             Family: Sclerotiniaceae
  •                                 Genus: Monilinia
  •                                     Species: Monilinia fructigena

Notes on Taxonomy and Nomenclature

Top of page

Persoon first used the specific epithet 'fructigena' in 1796 in assigning the name Torulafructigena to the conidial form of a brown rot fungus that he observed in Europe. However, Harrison (1933) concluded that “it is impossible with certainty to allocate Persoon's description to any of the present day species of Brown Rot Fungi”. In 1801, Persoon further described the conidial fungus under the name Monilia fructigena (Byrde and Willetts, 1977). Kunze and Schmidt later clearly described the same species as Oidium fructigenum, and in 1819, Schmidt included it in a descriptive collection of specimens of German fungi (Byrde and Willetts, 1977). Harrison (1933) studied the material of O. fructigenum and confirmed that it was Monilinia fructigena.

Aderhold and Ruhland (1905) were the first to describe the apothecia of this fungus, and also described the conidial state obtained from ascospore isolates. This description of the asexual form was similar to that for O. fructigenum by Kunze and Schmidt (1817). Sclerotinia fructigena as J. Schröt. ex Aderh. & Ruhland was the name then assigned to the teleomorph, but this is a later homonym of Sclerotinia fructigena (Pers.) J. Schröt. The correct current name is Monilinia fructigena Honey ex Whetzel. Following the establishment of the genus Monilinia by Honey (1928), his placement of the species in this genus (Honey, 1936) was validated by Whetzel (1945). For additional information on the nomenclature of this fungus, see Kohn (1979) and USDA/SMML (2005).

Holst-Jensen et al. (1997) have shown by examination of DNA sequences that the genus Monilinia is polyphyletic, with the two sections, Junctoriae and Disjunctoriae, clearly separate in origin. The section Junctoriae, which includes M. fructigena, also includes the type species Monilinia fructicola, and these species would remain in Monilinia if the sections were recognized as different genera.

Some level of intraspecific variation is observed in M. fructigena. Considerable variation in growth rate in culture has been observed between different Spanish isolates of the species (De Cal and Melgarejo, 1999). However, little intraspecific variation was found in the ITS region of ribosomal DNA in M. fructigena isolates from Denmark and Norway (Holst-Jensen et al., 1997) and France (Ioos and Frey, 2000). After intraspecific variation in the ITS region was observed between European and Japanese isolates (Fulton et al., 1999), morphological differences were described in culture, with the result that the Japanese fungus was proposed as a separate species (Van Leeuwen et al., 2002).

Description

Top of page

Apothecia cupulate, stipitate pale brown, margin entire, 3 mm diameter at maturity. Paraphyses unbranched, septate, 2-3 µm wide, not enlarged at apex.

Asci cylindrical, eight-spored, 160-180(-200) x 9-11 µm. Ascospores obliquely uniseriate or oblique, hyaline, eguttate, smooth, narrow-ellipsoid, ends tapered, but not pointed, 9-11(-13) x 5.0-6.6 µm.

Sporodochia scattered or confluent, buff to pale yellow-brown, 1-2 mm wide, up to 2 mm high. Conidia in branched chains, elongate-ellipsoid, limoniform or ovoid, hyaline, 15-25 x 12-16 µm. Arthric conidia sometimes present, 12-34 x 6-15 µm.

For a more detailed description, see Batra (1979; 1991).

Colony in culture colourless to white, margin entire, aerial mycelium initially sparse, later concentrically zonate. Sporogenous areas buff. Sclerotia present or absent, discoid to elongate, flattened: outer rind dark, three to four cells thick, cell walls thick, pigmented; medulla colourless, hyphae intertwined, 2-11 µm diameter, interhyphal spaces filled with gelatinous material.

For a more detailed description of the anamorph in culture, see Mordue (1979).

Distribution

Top of page

M. fructigena is found throughout western and southern Europe and extends into the Scandinavian countries, eastern Europe, the former Soviet Union, the Middle East, India, and North Africa (CABI/EPPO, 2000; USDA/SMML, 2005). Recent identification of the common brown rot fungus in Japan, previously considered to be M. fructigena, as a separate anamorphic species, Monilia polystroma, may suggest reconsideration of other reports of M. fructigena from eastern Asia (Van Leeuwen et al., 2002). The new species has also been isolated in Hungary, within the known range of M. fructigena (Petróczy and Palkovics, 2009).

UK CAB International (1976) includes a record for presence in Brazil. EMBRAPA have since notified CABI that this record was a misidentification and that M. fructigena is not present in Brazil. Earlier reports of the species from Chile and Uruguay (UK CAB International, 1976) are also due to misidentification of other species of Monilinia (Malvárez et al., 2004; USDA/SMML, 2005).

In the USA, M. fructigena was reported from a pear [Pyrus communis] orchard in Maryland (Batra, 1979), but this minor outbreak was eradicated (Batra and Harada, 1986; Ogawa and English, 1991). It has also been erroneously reported from Florida (Florida Department of Agriculture and Consumer Services, USA, correspondence, 2000).

Distribution Table

Top of page

The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.

Continent/Country/RegionDistributionLast ReportedOriginFirst ReportedInvasiveReferenceNotes

Asia

AfghanistanPresentCABI/EPPO, 2000; EPPO, 2014
ArmeniaPresentCABI/EPPO, 2000; EPPO, 2014
AzerbaijanPresentCABI/EPPO, 2000; EPPO, 2014
ChinaRestricted distributionCABI/EPPO, 2000; Guo, 2005; EPPO, 2014
-AnhuiPresentCABI/EPPO, 2000; EPPO, 2014
-BeijingPresentEPPO, 2014
-GansuPresentGuo, 2005; EPPO, 2014
-GuangxiPresentGuo, 2005
-HenanPresentCABI/EPPO, 2000; EPPO, 2014
-HubeiPresentCABI/EPPO, 2000; EPPO, 2014
-HunanPresentCABI/EPPO, 2000; EPPO, 2014
-JiangsuPresentCABI/EPPO, 2000; EPPO, 2014
-LiaoningPresentCABI/EPPO, 2000; EPPO, 2014
-ShaanxiPresentCABI/EPPO, 2000; EPPO, 2014
-ShandongPresentCABI/EPPO, 2000; EPPO, 2014
-ShanxiPresentCABI/EPPO, 2000; EPPO, 2014
-SichuanPresentCABI/EPPO, 2000; EPPO, 2014
-XinjiangPresentNiu et al., 2016
-YunnanPresentCABI/EPPO, 2000; EPPO, 2014
-ZhejiangPresentCABI/EPPO, 2000; EPPO, 2014
Georgia (Republic of)PresentCABI/EPPO, 2000; EPPO, 2014
IndiaRestricted distributionCABI/EPPO, 2000; EPPO, 2014
-Himachal PradeshPresentSharma and Kaul, 1989c; CABI/EPPO, 2000; EPPO, 2014
-Indian PunjabPresentCABI/EPPO, 2000; EPPO, 2014
-Jammu and KashmirPresentCABI/EPPO, 2000; EPPO, 2014
IranPresentCABI/EPPO, 2000; EPPO, 2014
IsraelPresentCABI/EPPO, 2000; EPPO, 2014
JapanPresentCABI/EPPO, 2000; EPPO, 2014probably a different species (Van Leeuwen et al., 2002)
-HonshuPresentCABI/EPPO, 2000; EPPO, 2014
KazakhstanPresentAytkhozhina, 2005
Korea, DPRPresentCABI/EPPO, 2000; EPPO, 2014
Korea, Republic ofPresentCABI/EPPO, 2000; EPPO, 2014
LebanonPresentCABI/EPPO, 2000; EPPO, 2014
NepalPresentCABI/EPPO, 2000; EPPO, 2014
TaiwanPresentCABI/EPPO, 2000; EPPO, 2014
TurkeyPresentCABI/EPPO, 2000; EPPO, 2014
UzbekistanPresentCABI/EPPO, 2000; EPPO, 2014

Africa

EgyptPresentCABI/EPPO, 2000; EPPO, 2014
MoroccoPresentCABI/EPPO, 2000; EPPO, 2014

North America

USAAbsent, formerly presentCABI/EPPO, 2000; EPPO, 2014
-FloridaAbsent, invalid recordCABI/EPPO, 2000; EPPO, 2014
-MarylandEradicatedIntroduced Invasive Batra, 1979; Ogawa and English, 1991; CABI/EPPO, 2000; EPPO, 2014

South America

BrazilAbsent, formerly presentEPPO, 2014
ChileAbsent, formerly presentEPPO, 2014
UruguayAbsent, formerly presentEPPO, 2014

Europe

AustriaWidespreadCABI/EPPO, 2000; EPPO, 2014
BelarusPresentCABI/EPPO, 2000; EPPO, 2014
BelgiumPresentCABI/EPPO, 2000; EPPO, 2014
BulgariaWidespreadCABI/EPPO, 2000; EPPO, 2014
CroatiaPresentCABI/EPPO, 2000; EPPO, 2014
CyprusPresentCABI/EPPO, 2000; EPPO, 2014
Czech RepublicWidespreadEPPO, 2014
Czechoslovakia (former)WidespreadCABI/EPPO, 2000
DenmarkWidespreadCABI/EPPO, 2000; EPPO, 2014
FinlandPresentCABI/EPPO, 2000; EPPO, 2014
FranceRestricted distributionCABI/EPPO, 2000; EPPO, 2014
GermanyWidespreadCABI/EPPO, 2000; EPPO, 2014
GreecePresentCABI/EPPO, 2000; EPPO, 2014
HungaryWidespreadIntroduced Invasive CABI/EPPO, 2000; EPPO, 2014
IrelandPresentCABI/EPPO, 2000; EPPO, 2014
ItalyPresentCABI/EPPO, 2000; EPPO, 2014
-SicilyPresentCABI/EPPO, 2000; EPPO, 2014
LatviaPresentCABI/EPPO, 2000; Volkova et al., 2013; EPPO, 2014
LithuaniaPresentCABI/EPPO, 2000; Valiuskaite, 2002; EPPO, 2014
LuxembourgPresentCABI/EPPO, 2000; EPPO, 2014
MoldovaPresentCABI/EPPO, 2000; EPPO, 2014
NetherlandsPresentCABI/EPPO, 2000; EPPO, 2014
NorwayWidespreadIntroduced Invasive CABI/EPPO, 2000; EPPO, 2014
PolandPresentCABI/EPPO, 2000; EPPO, 2014
RomaniaPresentCABI/EPPO, 2000; EPPO, 2014
Russian FederationRestricted distributionCABI/EPPO, 2000; EPPO, 2014
-Russian Far EastPresentCABI/EPPO, 2000; EPPO, 2014
-Southern RussiaPresentCABI/EPPO, 2000; EPPO, 2014
SerbiaPresentEPPO, 2014
SlovakiaPresentEPPO, 2014
SloveniaPresentCABI/EPPO, 2000; EPPO, 2014
SpainPresentCABI/EPPO, 2000; EPPO, 2014
SwedenWidespreadIntroduced Invasive CABI/EPPO, 2000; EPPO, 2014
SwitzerlandWidespreadCABI/EPPO, 2000; EPPO, 2014
UKWidespreadIntroduced Invasive CABI/EPPO, 2000; EPPO, 2014
-Channel IslandsPresentCABI/EPPO, 2000; EPPO, 2014
-England and WalesWidespreadCABI/EPPO, 2000; EPPO, 2014
UkrainePresentCABI/EPPO, 2000; Dudka et al., 2004; EPPO, 2014
Yugoslavia (Serbia and Montenegro)PresentCABI/EPPO, 2000

Introductions

Top of page
Introduced toIntroduced fromYearReasonIntroduced byEstablished in wild throughReferencesNotes
Natural reproductionContinuous restocking
Maryland <1974 Breeding and propagation (pathway cause) No Batra (1979); Batra and Harada (1986) eradicated

Risk of Introduction

Top of page

Brown rot is a serious disease causing significant losses on fruit crops. M.fructigena is a less serious pathogen than Monilinia laxa or Monilinia fructicola, and controls for brown rot are already in practice in the fruit growing regions. However, most countries quarantine for this pathogen. The most likely means of introduction of M. fructigena would be infected fruit brought in commercially or by individuals from other continents, but trees or scions with twig blight infections, unless quarantined, could carry the fungus more directly to populations of hosts.

Habitat List

Top of page
CategorySub-CategoryHabitatPresenceStatus
Terrestrial
Terrestrial – ManagedCultivated / agricultural land Present, no further details Harmful (pest or invasive)
Managed forests, plantations and orchards Present, no further details Harmful (pest or invasive)
Terrestrial ‑ Natural / Semi-naturalNatural forests Present, no further details Natural

Hosts/Species Affected

Top of page

Under suitable environmental conditions, M. fructigena will infect not only all cultivated drupaceous and pomaceous species, but also many other members of the Rosaceae. The extensive cultivation of fruit trees in temperate regions and their long lifespan ensure that hosts are readily available. The main commercial crops that are hosts to M.fructigena include apple [Malus domestica], pear [Pyrus communis], quince [Cydonia oblonga], plum [Prunus domestica], and sweet cherry [Prunus]. Sour cherry [Prunus] is a less important host than peach [Prunus persica], nectarine [Prunus persica], and apricot [Prunus armeniaca]. There are many records of the brown rot fungi attacking other plants (Byrde and Willetts, 1977; Tzavella-Klonari, 1985; Sharma and Kaul, 1989a; Faivre-Amiot and Geoffrion, 1996). Wild hosts may be sources of inoculum if located near orchards (Zehr, 1982).

Host Plants and Other Plants Affected

Top of page
Plant nameFamilyContext
Actinidia arguta (tara vine)ActinidiaceaeOther
Amelanchier canadensis (thicket serviceberry)RosaceaeOther
Berberis (barberries)BerberidaceaeOther
Capsicum (peppers)SolanaceaeOther
Cornus mas (cornelian cherry)CornaceaeOther
Corylus avellana (hazel)BetulaceaeOther
CotoneasterRosaceaeOther
Crataegus laevigataRosaceaeWild host
Cydonia oblonga (quince)RosaceaeMain
Diospyros kaki (persimmon)EbenaceaeOther
Eriobotrya japonica (loquat)RosaceaeOther
Ficus carica (common fig)MoraceaeOther
Fragaria (strawberry)RosaceaeOther
Fragaria ananassa (strawberry)RosaceaeOther
Malus domestica (apple)RosaceaeMain
Malus sieversiiRosaceaeWild host
Malus sylvestris (crab-apple tree)RosaceaeWild host
Mespilus germanica (medlar)RosaceaeOther
Prunus (stone fruit)RosaceaeMain
Prunus armeniaca (apricot)RosaceaeMain
Prunus avium (sweet cherry)RosaceaeOther
Prunus cerasifera (myrobalan plum)RosaceaeWild host
Prunus cerasus (sour cherry)RosaceaeOther
Prunus domestica (plum)RosaceaeMain
Prunus dulcis (almond)RosaceaeMain
Prunus mandshuricaRosaceaeOther
Prunus persica (peach)RosaceaeMain
Prunus persica var. nucipersica (nectarine)RosaceaeMain
Prunus salicina (Japanese plum)RosaceaeMain
Prunus spinosa (blackthorn)RosaceaeOther
Prunus triloba (Rose tree of China)RosaceaeOther
Psidium guajava (guava)MyrtaceaeOther
Pyrus (pears)RosaceaeMain
Pyrus betulaefoliaRosaceaeWild host
Pyrus communis (European pear)RosaceaeMain
Pyrus pyrifolia (Oriental pear tree)RosaceaeOther
Pyrus ussuriensis (amur pear)RosaceaeOther
Rhododendron (Azalea)EricaceaeOther
Rosa (roses)RosaceaeOther
Rubus (blackberry, raspberry)RosaceaeOther
Rubus occidentalis (black raspberry)RosaceaeOther
Solanum lycopersicum (tomato)SolanaceaeOther
Sorbus (rowan)RosaceaeOther
Sorbus acupariaRosaceaeWild host
Vaccinium (blueberries)EricaceaeOther
Vitis vinifera (grapevine)VitaceaeOther

Growth Stages

Top of page Flowering stage, Fruiting stage, Post-harvest, Vegetative growing stage

Symptoms

Top of page

Blossom blight develops in the spring, particularly in moderately warm, moist weather. Infections occur on stamens, stigmas, petals or sepals, generating brown lesions that spread to other parts of the flower, and through peduncles to other flowers in the cluster and into the twigs. Affected flowers wilt and collapse, and some fall to the ground. Others remain on the tree, and sporulation on the blighted blossoms under moist conditions provides inoculum for further spread (Byrde and Willetts, 1977).

Brown rot on ripening or mature fruit typically develops as a rapidly spreading, firm, brown decay. Infection of fruits can take place at any time during fruit development, but the disease is only severe in ripe or ripening fruits. Infections of fruitlets during, or shortly after, flowering may result in quiescent infections on green fruit that become active before or after harvest. The first symptoms on ripe fruits are small, superficial, circular brown spots that quickly begin rotting (Byrde and Willetts, 1977). Conidial pustules usually develop on the infected areas under moist conditions. Within several days the fruits are completely rotten and almost the entire surface is covered with conidial tufts or vegetative mycelium. The cream-white to buff sporulating area may have concentric zones of sporulation produced in response to diurnal cycles. When the relative humidity is low and/or when the fruits are not ripe, no mycelium and very few or no conidial tufts develop (Byrde and Willetts, 1977). Eventually the whole fruit becomes discoloured and water is lost so that a mummified fruit is formed. The fungus often spreads by growth from diseased fruit to healthy ones in the same cluster or as conidia to other tissues (Xu et al., 2001b). Diseased fruits tend to remain attached to the tree as shoot dieback prevents formation of an abscission layer between fruit and peduncle. Mummified fruit hangs on branches of trees until spring or falls to the ground, where it remains throughout the winter months and becomes partly or completely buried beneath the soil or leaf litter (Byrde and Willetts, 1977).

Cankers usually develop from blighted twigs or branches by growth of mycelium into larger limbs of the tree (Byrde and Willets, 1977). An elliptical or spindle-fusoid canker forms with substantial gum production at the advancing margin. At times, the cankered area may girdle the twig and blight the portion distal to it. Leaves of infected twigs turn dark brown and remain attached instead of abscising. Usually cankers are restricted to twigs and do not extend into the previous year's wood. Cankers do not continue to enlarge from one season to the next. If the branch is not girdled, surrounding healthy tissue will produce calluses. When diseased twigs are not removed and environmental conditions are suitable for sporulation, active cankers produce conidia. In pear [Pyrus communis], twig blight occurs mostly through growth of the pathogen into the stem following blossom infection. Other more aggressive canker-causing fungi may colonize cankers and dead shoots.

Symptoms can vary on different crops. On apple [Malus domestica], fruit rot is very common and destructive; sometimes the fungus spreads into branches from the fruit and gives rise to cankers. A symptom referred to as 'black apple' may also develop. The colour of the rot is initially brown, but becomes jet black as the rot progresses (Byrde and Willetts, 1977). The skin of the apple then has a shiny smooth surface unruptured by conidiophores, and shrinkage of the apple tissue is insignificant until late in black apple development. This condition is mostly found in stored fruits. Fruit rot is common in pear and plum [Prunus domestica] as well, but less severe in peach [Prunus persica], nectarine [Prunus persica] and apricot [Prunus armeniaca].

List of Symptoms/Signs

Top of page
SignLife StagesType
Fruit / extensive mould
Fruit / lesions: black or brown
Fruit / mummification
Growing point / dead heart
Growing point / dieback
Inflorescence / blight; necrosis
Leaves / wilting
Leaves / yellowed or dead
Stems / canker on woody stem
Stems / dieback
Stems / gummosis or resinosis
Stems / internal discoloration
Stems / necrosis

Biology and Ecology

Top of page

The conidia of M. fructigena are “dry air” spores (Hirst, 1953) that are not actively discharged, but are set free by air currents and wind. Although short and unspecialized, the conidiophores elevate the spore chains above the infected tissues and thus provide better exposure to air currents. Except when mummified fruit have fallen to the ground, infected fruits and peduncles are in positions on the tree that are suitable for efficient take-off and aerial dispersal of spores (Byrde and Willetts, 1977). The conidia of M. fructigena are disseminated by wind when temperatures are high, when relative humidities are low, and often at high UV light intensities. Rain splashes are important as a means of liberating spores. Apart from providing a method for dislodging conidia, rain droplets supply the moisture for germination and subsequent mycelial development. Shock waves produced ahead of the drops will also lead to the liberation of dry spores (Jarvis, 1962). Aerial dispersal results in the spread of spores over a wide area, whereas water splash dispersal brings about only short-range dissemination, mainly to other parts of the same tree or, in some instances, between adjacent trees. Roberts and Dunegan (1932) considered that transport by air was the most important way that spores of M.fructigena reach their hosts, but transport by water escapes the extreme environmental conditions to which wind-borne inocula are often subjected.

Animals are important vectors of this fungus, either incidentally or because of complex adaptations (Lack, 1989). Almost any insect attracted to rotting flowers or fruit has the potential to pick up and carry spores from sporulating mycelium to healthy, susceptible tissues, but those that create new wounds provide the necessary sites of infection for M. fructigena (Xu and Robinson, 2000; Xu et al., 2001b; 2007). The most important animal vectors are birds, wasps (Vespula spp.), beetles, especially the nitidulid beetles (Carpophilus spp.), flies (Diptera) including Drosophila spp., and Lepidoptera (Byrde and Willetts, 1977).

The brown rot fungi overwinter mainly in or on diseased mummified fruit either attached to the tree or on the ground. Other infected tissues on trees, such as twigs, peduncles and cankers on twigs or branches, can also serve as sources of primary inoculum. In the spring or early summer, when temperatures, day-length and relative humidities are suitable, tufts of conidiophores form sporodochia on the surface of the mummified fruit and infected tissues, and bear chains of conidia. Conidia are transported by wind, water or insects to young fruit. Initial infection is via wounds (Rekhviashvili, 1975; Xu and Robinson, 2000; Xu et al., 2001b; 2007), often scab lesions or sites of insect damage. Subsequent spread by contact between adjacent fruit is a minor cause of infection (Xu and Robinson 2000; Holb and Scherm, 2008). Growth cracks may also be infection courts on apple (Xu and Robinson, 2000; Holb and Scherm, 2008). Free moisture on the plant surface is not essential for the rapid germination and infection by conidia (Xu and Robinson, 2000).

Any infected tissue in which the moisture content is sufficient for sporulation may serve as a source of secondary inoculum. After the initial penetration of fruits, there is active mycelial growth, and the hyphae in the outer tissues of the fruit become closely interwoven to form a stroma. This has an outer rind, a medulla containing both hyphae and host cells, and an inner rind. The tissues in the centre of the fruit rot away leaving a hollow sclerotial sphere of leathery or rubbery consistency usually enclosing the seed or unrotted core of the fruit (Byrde and Willetts, 1977). Fruits may become infected at harvest time and then fruit rots can develop during the postharvest period. The fungus can survive long periods of adverse environmental conditions as mycelium within mummified fruits, twigs, cankers and other infected tissues. When conditions become favourable (usually after a dormant period), spores are produced on infected tissues and the fungus is dispersed to start a new cycle of infection, which coincides with early spring growth of host plants.

There are only a few records of the development of the sexual form of M. fructigena (Ibragimov and Abbasov, 1976; Batra, 1979; Batra and Harada, 1986). Apothecia may be produced in spring on mummified fruit that have overwintered on the ground. Mummified fruits that remain on the tree do not produce apothecia (Byrde and Willetts, 1977). Batra (1991) described apothecia observed from an unusual introduction to North America. The apothecia described in Japan (Batra and Harada, 1986), although not obviously different, may be the sexual state of the Japanese anamorphic species, Monilia polystroma.

The liberation of ascospores normally coincides with the emergence of young shoots and blossoms of plants (Ogawa and English, 1991). When spores alight on susceptible tissues under favourable environmental conditions, they germinate to initiate infections. In addition to the conidium and ascospore, a third type of spore is produced. This spore is known as a microconidium because of its small size. Unlike the conidium (macroconidium) and the ascospore, the microconidia do not function in propagation and dispersal, but rather as spermatia in mating. Microconidia are produced in abundance within small cavities and on the surfaces of mummified fruit (Byrde and Willetts, 1977).

M. fructigena is a pathogen of moist conditions, favoured by rain, fog and other factors that increase humidity, especially at the beginning of the host growth period; brown rot is rare in arid climates. Conidia are generally formed on mummified fruit and blighted twigs at temperatures of >5°C. Germination and germ tube growth are partially inhibited by light, but sporulation is enhanced. Conidia provide the inocula for most primary infections. Xu et al. (2001a) found 97% RH and temperatures of 3-25°C optimum for germination of conidia in the UK.

At harvest, apparently healthy fruit usually can be contaminated with spores, and decay may occur during storage and marketing. In latent infections the early infection of fruit does not produce symptoms of disease, and further differentiation of the fungus cannot take place until the fruit begins to ripen (Byrde and Willets, 1977). Mycelium generally have a greater potential than spores for causing infection in storage because they have greater reserves of food material at their disposal.

Climate

Top of page
ClimateStatusDescriptionRemark
Cf - Warm temperate climate, wet all year Preferred Warm average temp. > 10°C, Cold average temp. > 0°C, wet all year
Cs - Warm temperate climate with dry summer Preferred Warm average temp. > 10°C, Cold average temp. > 0°C, dry summers
Dw - Continental climate with dry winter Tolerated Continental climate with dry winter (Warm average temp. > 10°C, coldest month < 0°C, dry winters)

Notes on Natural Enemies

Top of page

Corke et al. (1975) found a trend towards reduced infection of fruit by M. fructigena on container-grown plum [Prunus domestica] trees experimentally inoculated in the trunk with the fungus, Trichodermaviride. Harada (1998) reported that the mycoparasite Lambertella corni-maris occurs on stroma of M. fructigena on apple fruits [Malus domestica]. Acid production by the host fungus is reported to stimulate production of antibiotic lambertellols by L. corni-maris (Murakami et al., 2007).

Means of Movement and Dispersal

Top of page

Natural Dispersal

Conidia of the Monilia anamorph are dispersed by wind and rain-splash, and, where apothecia are formed, ascospores will be wind-disseminated (Batra, 1991).

Vector Transmission

Various types of insects, including wasps, beetles, flies and butterflies have been identified as vectors of Monilinia species (Byrde and Willetts, 1977). According to Lack (1989), any insect that visits both infected and uninfected fruit could serve as a vector; he specifically observed bees, wasps, fruit flies and syrphid flies on apple [Malus domestica] fruit infected with M. fructigena. Birds may also be vectors (Byrde and Willetts, 1977). Holb and Scherm (2008) and Xu et al. (2001b) report birds as wound agents in fruit orchards affected by M. fructigena.

Accidental Introduction

The Australian phytosanitary authority has intercepted infected fruit (Mackie et al., 2005), as has occurred in the USA (USDA/SMML, 2005). The probable source of M. fructigena found on pear [Pyrus communis] trees at Beltsville, Maryland, USA, was not identified by Batra (1979), but only one variety growing at the experimental orchard at the agricultural station was infected.

Seedborne Aspects

Top of page

The fungus could certainly infect seed or pits in rotted fruit, but fruit trees are not generally propagated by seed, and seedling infection is unlikely. Nevertheless, Richardson (1990) has reported seedborne Monilinia laxa on Corylus (hazelnut), which is also a host for M. fructigena (Mordue, 1979a: Tzavella-Klonari, 1985).

Pathway Causes

Top of page
CauseNotesLong DistanceLocalReferences
Foodinfected fruit Yes Mackie et al., 2005

Pathway Vectors

Top of page

Plant Trade

Top of page
Plant parts liable to carry the pest in trade/transportPest stagesBorne internallyBorne externallyVisibility of pest or symptoms
Flowers/Inflorescences/Cones/Calyx hyphae; spores Yes Yes Pest or symptoms not visible to the naked eye but usually visible under light microscope
Fruits (inc. pods) hyphae; spores Yes Yes Pest or symptoms not visible to the naked eye but usually visible under light microscope
Leaves hyphae; spores Yes Pest or symptoms not visible to the naked eye but usually visible under light microscope
Stems (above ground)/Shoots/Trunks/Branches hyphae; spores Yes Yes Pest or symptoms not visible to the naked eye but usually visible under light microscope
Plant parts not known to carry the pest in trade/transport
Bulbs/Tubers/Corms/Rhizomes
Roots
Seedlings/Micropropagated plants
True seeds (inc. grain)

Impact Summary

Top of page
CategoryImpact
Cultural/amenity Negative
Economic/livelihood Negative

Economic Impact

Top of page

Although M. fructigena causes significant losses both before and after harvest, it is not easy to assess the overall losses it causes in a country or on a worldwide scale (Batra, 1991). Losses are highly visible to the grower, but are rarely worth the implementation of specific control measures in their own right. Early-maturing cultivars are most affected, but the majority of diseased fruits are those that would in any case be rejected for other reasons such as bruising or bird and insect damage (Smith et al., 1992). M. fructigena is less damaging than Monilinia fructicola or Monilinia laxa, although it occasionally causes economically important losses of apple [Malus domestica] and plum [Prunus domestica] fruits in Europe, particularly in hot and humid summers (Smith et al., 1992).

In 1972, Burchill and Edney reported 35.8% fruit infection in an English apple orchard. Ciferri reported 7.3% infection of apples in Italy. Preece reported mean losses of 0.2-1.5% in samples of Cox’s Orange Pippin apples taken from refrigerated stores in England between 1961 and 1965, with a range of 0.1-4.5% for individual orchards. In a survey carried out in a typical English commercial store, Evans stated that brown rot and other rots due to Botrytis cinerea and Penicillium spp. usually accounted for less than 5% loss in storage. See Byrde and Willetts (1977) for further details of these references.

According to Berrie (1993), average commercial losses due to fungal rots in apples have been maintained at <2% under UK conditions by the routine use of postharvest fungicide dips or drenches. In surveys of markets, stores and canning centres in Himachal Pradesh, India, the cumulative incidence of brown rot in harvested apples was 5.0-15.2%; the occurrence of M. fructigena varied from 2.1 to 14.2% (mean 6.72%), being more frequent under low-temperature conditions (Sharma and Kaul, 1989c). In central Europe, pre-harvest losses of apples due to brown rot are usually less than 10%, but losses of up to 46% have been reported (Holb and Scherm, 2007).

Risk and Impact Factors

Top of page Invasiveness
  • Invasive in its native range
  • Proved invasive outside its native range
  • Has a broad native range
  • Abundant in its native range
  • Highly mobile locally
  • Fast growing
  • Has high reproductive potential
  • Reproduces asexually
Impact outcomes
  • Host damage
  • Negatively impacts agriculture
  • Negatively impacts livelihoods
  • Reduced amenity values
Impact mechanisms
  • Pathogenic
Likelihood of entry/control
  • Highly likely to be transported internationally accidentally
  • Difficult to identify/detect as a commodity contaminant
  • Difficult to identify/detect in the field
  • Difficult/costly to control

Diagnosis

Top of page

Identification of Monilinia spp. has generally been based on cultural and morphological characters. The main distinguishing characters between species are: the colour and appearance of the conidial pustules, cultural characteristics of colonies, the host range, and the parts of the plant that are infected (Byrde and Willetts, 1977; Willetts et al., 1977; De Cal and Melgarejo, 1999; Lane, 2002). A commercial ELISA kit is available to identify Monilinia fructicola, but not M. fructigena or Monilinia laxa (Hughes et al., 1998; Gell et al., 2007).

In culture, M. fructigena has entire colony margins, a different conidia colour and longer conidium germ tubes than M. laxa (Penrose et al., 1976; Mordue, 1979a,b). M. fructicola produces more abundant conidia, stromata and microconidia, and has slightly smaller conidia than M.fructigena (Mordue, 1979a,c). M. fructicola is distinguished from M. laxa in having entire colony margins, by the colour of conidia, by the absence of hyphal anastomoses between germinating conidia, and in having longer conidial germ tube extension before branching (Penrose et al., 1976; Mordue, 1979b,c). These characteristics assist in the identification of typical cultures of Monilinia spp., but problems arise with atypical cultures. Differences have been observed among isolates of the same species (Byrde and Willetts, 1977; Harada, 1977; Batra, 1979; Wilcox, 1989; De Cal and Melgarejo, 1999). This variability is especially important when quarantine measures apply to one species, but not to another.

De Cal and Melgarejo (1999) have demonstrated that distance from the conidium to the first germ tube branch and growth rate under a long-wave UV/dark cycle provides a satisfactory method for differentiating species. M. laxa isolates can be easily distinguished from M. fructigena and M. fructicola on distilled water agar (2% agar, Oxoid) by the characteristic short-distance germ tube elongation, less than 60 µm, from the conidium to the first germ tube branch. M. fructigena and M. fructicola both produce germ tubes that grow for at least 220 mm before branching. These two species can then be differentiated from each other in culture under long-wave UV/dark conditions. Maximum growth rate (difference between diameters at days 5 and 3 after inoculation) of M.fructigena was 8 mm, whereas maximum growth rate of M. fructicola was 20 mm. Using different isolates, Van Leeuwen and Van Kesteren (1998) found that the combination of growth on potato dextrose agar (PDA) at 22°C under 12 h light (near-UV): 12 h dark, and length of the germ tube after 18 h incubation is sufficient to differentiate the fungi. Increase in colony diameter from day 3 to day 5 is the highest in M. fructicola, and the germ tubes are the shortest in M. laxa. The synoptic key produced by Lane (2002) relies on seven “critical characters” of colonies in culture for 10 days, including rate of growth under 12 h near-UV: 12 h dark, although growth alone could not be used to separate species due to intraspecific variation. Colony colour on 4% PDA was still useful in distinguishing M. fructigena from the other two species.

Efforts continue to develop a more rapid, simple and objective method of diagnosis that addresses all species. A number of physiological or chemical features separate the three related Monilinia spp: M. fructigena is unable to produce large numbers of conidia in PDA in the dark without the addition of indolyl-3 acetic (Wiltshire, 1920; Kahn, 1966), isoelectric patterns of the extracellular enzymes a-L-arabinofuranosidase and pectinlyase are useful for confirming morphological identifications (Willetts et al., 1977), and a monoclonal antibody-based immunoassay was developed to identify M.fructicola and has been tested with some isolates of Monilinia from an EU collection (Hughes et al., 1998). A 418-bp group-I intron has been located in the small subunit (SSU) rDNA gene of M. fructicola that is absent from the other two species (Fulton and Brown, 1997). Consequently, PCR primers specific to the 3´-region of the intron together with the SSU rDNA primer NS5 enabled amplification of a 444-bp product only from M. fructicola and fruit tissue infected with it. This allows for the rapid and sensitive detection of this invasive species for Europe.

Ioos and Frey (2000) found low interspecific polymorphism in the ITS region of the three Monilinia species, but developed primers permitting identification to species in naturally infected fruit. Also observing a high level of similarity in the ITS region of rDNA among the species, Gell et al. (2007) developed a different PCR protocol using four sets of primers, three of them not related to the ITS region, for identification of the three major Monilinia species in plant material. Côté et al. (2004) reported a multiplex PCR method for distinguishing among four species causing brown rot, including the recently identified Monilia polystroma, in naturally infected fruit. Random Amplified Polymorphic DNA (RAPD) analysis was used to identify a PCR product exhibiting clear differences among the four species, and PCR primers were designed to detect the polymorphisms.

Detection and Inspection

Top of page

Disease symptoms are clearly visible in the field and in storage (see Symptoms).

To distinguish M. fructigena from the other two brown rot fungi, the fruit with lesions should be incubated to obtain sporulation or/and the fungus isolated on suitable media to observe cultural characteristics. Molecular tests may be done on mycelium from pure culture or on infected fruit (see Diagnosis).

Similarities to Other Species/Conditions

Top of page

The brown rot fungi on species of Rosaceae are all virulent pathogens with similar life cycles and biology, producing the same types of symptoms on blossoms, leaves and fruits (Byrne and Willetts, 1977). Therefore, it is difficult to differentiate M. fructigena from the other two widespread brown rot fungi, Monilinia fructicola and Monilinia laxa, by its morphological characteristics (Batra, 1979) or by symptoms on hosts. Major distinctions from M. laxa include the presence of entire colony margins, buff conidium colour, and long conidium germ tubes (Mordue, 1979a,b). Features distinguishing the species from M. fructicola in culture include generally fewer conidia, stromata and microconidia in M. fructigena, and slightly larger conidia with a different colour in mass (Mordue, 1979a,c). M. fructigena grows more slowly than M. fructicola on potato dextrose agar (PDA) medium under long-wave UV light (De Cal and Melgarejo, 1999). Light is essential for sporulation in M. fructigena, but not in the other two species (Sharma and Kaul, 1989b). Byrde and Willetts (1977) provide a table of contrasted characters of the brown rot fungi, and Lane (2002) has produced a synoptic key to these three species in culture, based on examination of representative isolates.

In Japan, the brown rot fungus previously considered to be M. fructigena has been identified as a separate anamorphic species, Monilia polystroma, differing in cultural characters (Van Leeuwen et al., 2002) as well as the sequence of the ITS region of rDNA (Fulton et al., 1999). The Japanese isolates produced more stromata on cherry agar, had a significantly higher mean growth rate on PDA, and produced generally smaller conidia on both cherry agar and inoculated pear fruit [Pyrus communis].

Prevention and Control

Top of page

Prevention
 
SPS Measures
 
M. fructigena has been intercepted by phytosanitary authorities in Australia (Mackie et al., 2005), New Zealand (Byrde and Willetts, 1977) and North America (USDA/SMML, 2005). The species is a Regulated Pest for both Canada (CFIA, 2009) and the USA (USDA/APHIS, 2009), and a “notifiable” pest in New Zealand (Biosecurity New Zealand, 2006). The government of Australia has developed a protocol for its diagnosis to assist in preventing entry into that country (DAFF, 2008).
 
A key for identification of the major Monilinia species causing brown rot was published by EPPO (Lane, 2002) and molecular methods for rapid diagnosis in infected fruit have been developed (Ioos and Frey, 2000; Côté et al., 2004; Gell et al., 2007).
 
Control
 
Introduction

Losses due to M. fructigena are rarely worth specific control measures in their own right. Apart from avoidance of very susceptible cultivars in disease-prone districts, few control measures are specifically aimed at this fungus. By reducing the amount of inoculum produced, fungicides used for the routine control of foliar diseases provide an element of incidental control that, in practice, is often sufficient. Prospects for resistance breeding are limited, at least in apple [Malus domestica], because most resistant cultivars are of the cider type with fruit unsuitable for dessert use. However, much research has been done in Europe in breeding for resistance, particularly in eastern Europe.
 
Chemical Control

Protective fungicidal treatments provide the best control for fruit rot. The proper use of fungicides with some systemic activity protects fruit, reduces the amount of sporulation formed on the infected tissue, and reduces sources of overwintering inoculum. There is an extensive range of fungicides available for brown rot control, including the dicarboximides (iprodione and vinclozolin), benzimidazoles (benomyl and thiophanate-methyl), triforine, chlorothalonil, ergosterol biosynthesis inhibitors (myclobutanil, fenbuconazole, and propiconazole), and anilinopyrimidines (Zhang et al., 1991; Vucinic, 1994; Reynaud, 1997; Rueegg et al., 1997; Cotroneo et al., 1998). Other fungicides used are copper compounds, sulphur, and captan (Byrde and Willetts, 1977). The new fungicides, pyraclostrobin and boscalid, are effective against M. fructigena and Monilinia laxa (Spiegel and Stammler, 2006). The selection of a fungicide or mixture of compounds is often influenced by the need to control other diseases that may occur more or less simultaneously with brown rot, such as scab, powdery mildew, rust, russet scab, or grey mould. Insect control may be an important consideration because M. fructigena must infect primarily through wounds (Xu and Robinson, 2000; Holb and Scherm, 2008).
 
Fungicide resistance in M. laxa and Monilinia fructicola has become evident following multiple applications of dicarboximides and benzimidazoles in several parts of the world (Gilpatrick, 1982; Ogawa et al., 1984). However, evidence of resistance to these fungicides in M. fructigena has not been reported in the field. To prevent selection of fungicide-resistant strains, it may be better to combine fungicides having different modes of action (Ogawa et al., 1975; Zehr, 1982).
 
Cultural Control and Sanitary Methods
 
The intelligent location of orchards can reduce the likelihood of severe outbreaks of disease. Limited benefit may also follow from measures designed to alter the environment in established orchards in the host's favour, e.g. pruning for increased air circulation (Byrde and Willetts, 1977). Cultural practices such as the removal of mummified fruit and pruning of infected twigs, with subsequent burning or deep-burying, and the removal of wild host plants near orchards, reduce the inoculum level, but these procedures alone are not sufficient to control the disease (Zehr, 1982). Nevertheless, Holb and Scherm (2007) found that fallen or thinned immature fruit infected with M. fructigena on the ground provided a significant source of inoculum in Hungarian apple orchards. Labour-intensive removal of such fruit could be economically feasible for organic management operations where chemicals used for disease control chemicals were less effective. Wormald (1954) emphasized that hygiene is equally necessary during and after seasons of light infection. Good hygiene can also reduce the population of insects that serve as spore vectors.
 
Manuring can have some influence on disease incidence and applications of potassium have brought about a reduction in disease incidence on apricots [Prunus armeniaca] (Vasudeva, 1930; Byrde and Willetts, 1977). High doses of nitrogen fertilizer are positively correlated with infection by M. fructigena (Daane et al., 1996).
 
Injuries to the plant may result from weather conditions. Hail can readily damage fruit, and it is useful to apply a protectant fungicide without delay when such injury occurs (Byrde and Willetts, 1977). Care during picking and handling is essential, and fruit should be picked with its stalk intact (Wormald, 1954). Particular care is needed in packing and storage of fruit because the fungus can grow from one fruit to others in contact with it. Damaged fruit should not be stored (Wormald, 1954). Mechanical harvesting of peaches [Prunus persica] can also cause injuries that may lead to severe rotting.
 
Control of Vectors
 
Control of insects that serve as vectors and/or provide wounds for infection, is essential for effective control of M. fructigena. Fungicides do not control infection if applied after mechanical injuries have become inoculated. Bird feeding may be reduced in orchards remote from houses by the use of explosive scares; wasp nests can be sought out and destroyed. Direct control of other vectors that are often attracted to rotten and damaged fruit seems difficult to achieve (Byrde and Willetts, 1977). However, Holb and Scherm (2007) attributed lower level of brown rot in orchards under integrated management in part to control of wound-creating insects through the use of insecticides that are not part of organic management. Forecasting for insect control, particularly of codling moth (Cydia pomonella), in organic management is needed to prevent injuries that are major infection courts for M. fructigena (Holb and Scherm, 2008).
 
Postharvest Control
 
Once the fruit is picked, alteration of the environment to the selective disadvantage of the pathogen is easily achieved. When fruit is chilled to below about 5°C in transit and storage, the growth of the fungus is very slow. Hydro-cooling, or hydrair-cooling, is now extensively used on peaches to prevent rot after harvest in the southeastern USA, but it is generally necessary to add fungicide to the chilled water (McClure, 1958; Wells and Bennet, 1975; 1976), or to have already treated the fruit in a non-emulsifiable wax formulation of a fungicide (Bennet and Wells, 1976). Gamma irradiation of apples reduces rot caused by M. fructigena (Janitor and Paulech, 1978; Tiryaki et al., 1994; Marcadi et al., 1998). A combination of hot water and fungicides also controls M. fructigena rot of apples (Sharma and Kaul, 1990).
 
Non-fungicidal postharvest treatments under investigation involve the use of materials that induce resistance, such as calcium treatments or surface coatings (Bancroft, 1995). The search for natural anti-microbial substances of metabolic origin is also promising. Of these compounds, the hydrolytic reaction products from glucosinolates are good candidates due to both their anti-microbial action and their tolerance by the plants; the isothiocyanates are generally active for in vitro and in vivo control of M. laxa (Mari et al., 1993; 1996), but have not been tested against M. fructigena. They are found in a number of edible plants, particularly the Brassicaceae.
 
Host-Plant Resistance
 
Many factors have been implicated in host resistance to M. fructigena, but the genetic basis of resistance is poorly understood. Breeding for M. fructigena resistance is a major objective in Europe (Barsukova and Tuz, 1985; Grigortsevich, 1985; Nitransky, 1986; Barsukova and Gryuner, 1986; Grigorov, 1987; Bozhkova, 1995; Cantoni et al., 1996; Paunovic et al., 1996). In practice, many cultivars of fruit trees have been proved resistant (Rekhviashvili, 1973; Vasilev, 1975; Byrde and Willetts, 1977; Iliev and Shchrkova, 1979; Angelov, 1980; Iliev et al., 1986; Nitransky, 1986; Sharma and Kaul, 1988; Cimanowski and Pietrzak, 1991). Difficulty occurs with incorporation of factors from resistant varieties due to customer preferences with respect to apple and pear [Pyrus communis] fruit (Byrne and Willetts (1977).
 
Biological Control
 
Few attempts have been made in the biological control of M. fructigena; some of them are described by Byrde and Willetts (1977), including experiments with Trichoderma viride, which has not been prepared for commercial application. Some experimental applications of the bacteria Bacillus subtilis and Pseudomonas cepacia in strawberries [Fragaria ananassa] and sweet cherries [Prunus] have been made (Marquenie et al., 1999). Falconi and Mendgen (1994) showed that isolates of Aureobasidium pullulans, Epicoccum purpurascens [Epicoccum nigrum], Sordaria fimicola, and Trichoderma polysporum, applied individually or in mixtures to wounded apples, gave good protection from M. fructigena. Some experiments have been undertaken in commercial orchards involving control of twig blight and fruit rot of peaches and plums [Prunus domestica] due to M. laxa by the application of fungal antagonists such as E. nigrum, Penicillium frequentans [Penicillium glabrum], or Penicillium purpurogenum (De Cal et al., 1988; 1990; Madrigal et al., 1994; Larena and Melgarejo, 1996; Pascual et al., 1996; 1998; Melgarejo et al., 1998) or the control of fruit rot of peaches induced by M. fructicola using Bacillus subtilis (Pusey and Wilson, 1984; Pusey et al., 1988). These antagonists may also be effective against M. fructigena. Formulations of P. frequentans were found more effective than a fungicide in reducing conidial numbers of Monilinia spp. (primarily M. laxa) on peaches in the orchard in Spain (Guijarro et al., 2007). Four applications of E. nigrum conidia in the season significantly reduced post-harvest brown rot in most of a set of trials controlled in Italy, France and Spain (Larena et al., 2006), but the greatest effect for stone fruit was found at the time of pit hardening and in the month before harvest (De Cal and Melgarejo, 2009).
 
IPM
 
Integration of the various means of control of brown rot in order to reduce costs and damage to the environment due to the application of fungicides and insecticides can be achieved, but requires considerable study of the variables of the host crop, environmental factors and interactions between the fungus, its vectors, and biological control agents. As Zehr (1982) notes, the need to control other fungal pathogens of the particular host in a certain location must also be considered in a chemical application programme for brown rot.
 
Older cultural and sanitary control methods were (and still can be) directed at removing sources of inoculum; chemical controls are directed at protecting the host from infection by inoculum regardless of its source. Therefore investigation of factors affecting the production and distribution of conidia is necessary for determination of effective and timely chemical use. Holb and Scherm (2007) found that rotting of dropped and thinned fruit provided a source of inoculum between early spring and the appearance of ripening apple fruit later in season. According to Holb (2008), disease incidence in apple orchards was significantly related to cumulative conidium numbers in air, which increased through the season, particularly after the first appearance of infected fruit. A diurnal periodicity was observed for conidium numbers, with peaks in the afternoon, corresponding to periods of higher temperatures and lower relative humidity. In the UK, Xu et al. (2001a) determined that conditions of temperature and relative humidity are not limiting for sporulation or spore germination.
 
Bannon et al. (2009) also observed a diurnal pattern of spore concentrations of M. fructigena in the air, with an increase occurring with higher temperature that can be related to the development of the fungus. Wind effects on inoculum density in the air appeared to be related to the local physical and topological conditions in the orchard.

Gaps in Knowledge/Research Needs

Top of page

The identity of the Monilinia species reported as M. fructigena in eastern Asia, and possibly also western Asia, should be clarified using molecular methods.

References

Top of page

Aderhold R; Ruhland W, 1905. Arbeiten aus der Biologischen Abteilung fnr Land-u. Forstwirtchaft, Berlin, 4:427-444.

Angelov A, 1980. The effectiveness of breeding in fruit growing in Bulgaria. Ovoshcharstvo, 59(7):12-16

Aytkhozhina N, 2005. First report of Monilia fructigena on small fruits in Kazakhstan. Phytopathology, 95:960.

Bancroft RD, 1995. The use of a surface coating to ameliorate the rate of spread of post-harvest fungal diseases of top fruit. International Biodeterioration & Biodegradation, 36(3/4):385-405; 37 ref.

Bannon F; Gort G; Leeuwen Gvan; Holb I; Jeger M, 2009. Diurnal patterns in dispersal of Monilinia fructigena conidia in an apple orchard in relation to weather factors. Agricultural and Forest Meteorology, 149(3/4):518-525. http://www.sciencedirect.com/science/journal/01681923

Barsukova ON; Gryuner AM, 1986. Disease resistance of Malus orientalis and local Caucasian varieties. Sbornik Nauchnykh Trudov po Prikladnoi Botanike, Genetike i Selektsii, 101:89-94.

Barsukova ON; Tuz AS, 1985. Immunological characteristics of wild pear species. Mikologiya i Fitopatologiya, 19(2):142-148

Batra LR, 1979. First authenticated North American record of Monilinia fructigena, with notes on related species. Mycotaxon, 8(2):476-484

Batra LR, 1991. World species of Monilinia (Fungi): their ecology, biosystematics and control. Mycologia Memoir, No. 16, 246 pp.

Batra LR; Harada Y, 1986. A field record of apothecia of Monilinia fructigena in Japan and its significance. Mycologia, 78(6):913-917

Bennett AH; Wells JM, 1976. Hydraircooling: a new precooling method with special application for waxed peaches. Journal of the American Society for Horticultural Science, 101:428-431.

Berrie AM, 1993. Progress towards integrated control of post harvest rots of cox apples in the United Kingdom. Acta Horticulturae, No. 347:107-114; 9 ref.

Biosecurity New Zealand, 2006. Schedule of notifiable organisms 2006. Schedule of notifiable organisms 2006., New Zealand: Ministry of Agriculture and Forestry, Government of New Zealand, unpaginated. http://www.biosecurity.govt.nz/files/pests/schedule-notifiable-organisms.pdf

Bozhkova V, 1995. Susceptibility of myrobalan plum varieties and forms to brown rot. Rasteniev"dni Nauki, 32(5):253-254; 3 ref.

Byrde RJW; Willetts HJ, 1977. The Brown Rot Fungi of Fruit. Their Biology and Control. Oxford, UK: Pergamon Press, 171 pp.

CABI/EPPO, 2000. Monilinia fructigena. [Distribution map]. Distribution Maps of Plant Diseases, April (Edition 6). Wallingford, UK: CAB International, Map 22.

CABI/EPPO, 2000. Monilinia fructigena. Distribution Maps of Plant Diseases, Map No. 22. Wallingford, UK: CAB International.

Cal A de; Sagasta EM; Melgarejo P, 1988. Antifungal substances produced by Penicillium frequentans and their relationship to the biocontrol of Monilinia laxa. Phytopathology, 78(7):888-893

Cal A de; Sagasta EM; Melgarejo P, 1990. Biological control of peach twig blight (Monilinia laxa) with Penicillium frequentans. Plant Pathology, 39(4):612-618

Cal Ade; Larena I; Liñán M; Torres R; Lamarca N; Usall J; Domenichini P; Bellini A; Eribe XOde; Melgarejo P, 2009. Population dynamics of Epicoccum nigrum, a biocontrol agent against brown rot in stone fruit. Journal of Applied Microbiology, 106(2):592-605. http://www.blackwell-synergy.com/loi/jam

Cantoni L; Bassi D; Tacconi M, 1996. Brown rot in stone fruits: aspects of biology and techniques of selection for resistance. Rivista di Frutticoltura e di Ortofloricoltura, 58(5):59-65; 58 ref.

CFIA, 2009. Pests regulated by Canada. Pests regulated by Canada. Ottawa, Ontario: Government of Canada, unpaginated. http://www.inspection.gc.ca/english/plaveg/protect/listpespare.shtml

Cimanowski J; Pietrzak B, 1991. Preliminary observations on the occurrence and control of brown rot (Monilinia fructigena Aderh. Ruhl. Honey) on apples. Prace Instytutu Sadownictwa i Kwiaciarstwa w Skierniewicach. Seria A, Prace Doswiadczalne z Zakresu Sadownictwa, No. 30:79-87

CMI, 1990. Distribution Maps of Plant Diseases, No. 27. Wallingford, UK: CAB International.

Corke ATK; Hunter T; Collins SA, 1975. Silver leaf in plums. In: Report of Long Ashton Research Station for 1974. Long Ashton, UK: Long Ashton Research Station, 131-132.

Côté MJ; Tardif MC; Meldrum AJ, 2004. Identification of Monilinia fructigena, M. fructicola, M. laxa, and Monilia polystroma on inoculated and naturally infected fruit using multiplex PCR. Plant Disease, 88(11):1219-1225. http://www.apsnet.org

Cotroneo A; Galliano A; Vittone F; Capello PF, 1998. Control trials against Monilinia laxa on peach in Piedmont. Informatore Agrario Supplemento, 54(16):16-18.

Daane KM; Dlott JW; Yokota GY; Johnson RS; Crisosto CH; Morgan DP; Michailides TJ; Ramirez HT, 1996. Influence of nitrogen fertilization on the susceptibility of nectarines to pathogens and pests. Rivista di Frutticoltura e di Ortofloricoltura, 58(3):41-45; [^italic~Translated and adapted from California Agriculture^roman~ 49(4), (1995).].

DAFF, 2008. Diagnostic protocol for Monilinia fructigena (apple brown rot). Diagnostic protocol for Monilinia fructigena (apple brown rot). Canberra, Australia: Department of Agriculture, Forestry and Fisheries, Australian Government. http://www.daff.gov.au/__data/assets/pdf_file/0016/1061332/diag-protocol-apple-brown.pdf

De Cal A; Melgarejo P, 1999. Effects of long-wave UV light on Monilinia growth and identification of species. Plant Disease, 83:62-65.

Dudka IO; Heluta VP; Tykhonenko YY; Anrianova TV; Hayova VP; Prydiuk MP; Dzhagan VV; Isikov VP, 2004. Fungi of the Crimean Peninsula. Kiev, Ukraine: National Academy of Sciences of Ukraine, 452 pp.

EPPO, 2014. PQR database. Paris, France: European and Mediterranean Plant Protection Organization. http://www.eppo.int/DATABASES/pqr/pqr.htm

Faivre-Amiot A; Geoffrion R, 1996. Monilioses des arbres et arbustes d'ornement. Phytoma, 481:42-44.

Falconi CJ; Mendgen K, 1994. Epiphytic fungi on apple leaves and their value for control of the postharvest pathogens Botrytis cinerea, Monilinia fructigena and Penicillium expansum. Zeitschrift fur Pflanzenkrankheiten und Pflanzenschutz, 101(1):38-47

Fulton CE; Brown AE, 1997. Use of SSU rDNA group-I intron to distinguish Monilinia fructicola from M. laxa and M. fructigena. FEMS Microbiology Letters, 157(2):307-312; 16 ref.

Fulton CE; Leeuwen GCMvan; Brown AE, 1999. Genetic variation among and within Monilinia species causing brown rot of stone and pome fruits. European Journal of Plant Pathology, 105(5):495-500; 16 ref.

Gell I; Cubero J; Melgarejo P, 2007. Two different PCR approaches for universal diagnosis of brown rot and identification of Monilinia spp. in stone fruit trees. Journal of Applied Microbiology, 103(6):2629-2637. http://www.blackwell-synergy.com/loi/jam

Gilpatrick JD, 1982. Case study 2: Venturia of pome fruits and Monilinia of stone fruits. In: Dekker J, Georgopoulos SG, eds. Fungicide resistance in Crop Protection. Wageningen, Netherlands: Centre for Agricultural Publishing and Documentation, 195-206.

Grigorov IN, 1987. Results of breeding new peach cultivars in Bulgaria. Symposium papers on Fruit Growing; 60 years of horticultural research in Czechoslovakia, 185-187.

Grigortsevich LN, 1985. Disease resistance of apple varieties in intensive type plantations. Zaschita Rastenii, Minsk, 10:36-40.

Guijarro B; Melgarejo P; Torres R; Lamarca N; Usall J; Cal Ade, 2007. Effects of different biological formulations of Penicillium frequentans on brown rot of peaches. Biological Control, 42(1):86-96. http://www.sciencedirect.com/science/journal/10499644

Guo YL, 2005. Anamorphic fungi. In: Fungi of Northwestern China [ed. by Zhuang, W. Y.]. Ithaca, New York, USA: Mycotaxon Ltd., 125-232.

Harada Y, 1977. Studies on the Japanese species of Monilinia (Sclerotiniaceae). Bulletin of the Faculty of Agriculture, Hirosaki University, No. 27:30-109

Harada Y, 1998. Taxonomic studies of plant parasitic fungi on fruit trees and forest trees in Japan. Nippon-Kingakukai Kaiho, 39:89-96.

Harrison TH, 1933. Brown rot of fruits and associated diseases of deciduous fruit trees. I. Journal and Proceedings of the Royal Society of New South Wales, 67:131-177.

Hirst JM, 1953. Changes in atmospheric spore contents: diurnal periodicity and the effects of weather. Transactions of the British Mycological Society 36: 375-393.

Holb IJ, 2008. Monitoring conidial density of Monilinia fructigena in the air in relation to brown rot development in integrated and organic apple orchards. European Journal of Plant Pathology, 120(4):397-408. http://springerlink.metapress.com/link.asp?id=100265

Holb IJ; Scherm H, 2007. Temporal dynamics of brown rot in different apple management systems and importance of dropped fruit for disease development. Phytopathology, 97(9):1104-1111. http://www.apsnet.org/phyto/

Holb IJ; Scherm H, 2008. Quantitative relationships between different injury factors and development of brown rot caused by Monilinia fructigena in integrated and organic apple orchards. Phytopathology, 98(1):79-86. http://www.apsnet.org/phyto/

Holst-Jensen A; Kohn LM; Jakobsen KS; Schumacher T, 1997. Molecular phylogeny and evolution of Monilinia (Sclerotiniaceae) based on coding and noncoding rDNA sequences. American Journal of Botany, 84(5):686-701; 64 ref.

Honey EE, 1928. The monilioid species of Sclerotinia. Mycologia, 20:127-157.

Honey EE, 1936. North American species of Monilinia. I. Occurrence, grouping, and life-histories. American Journal of Botany, 23(2):100-106 pp.

Hughes KJD; Banksi JN; Rizvii RH; McNaughton J; Lane CR; Stevenson L; Cook RTA, 1998. Development of a simple ELISA for identification of Monilinia fructicola. International Congress of Plant Pathology. Edinburgh, UK: BSPP, 1998.

Ibragimov GR; Abbasov TF, 1976. The occurrence of the ascus state of Monilia fructigena (Schroet.) Honey and M. cydonip (Schell.) Honey in Azerbaijan. Mikologiya i Fitopatologiya, 10(3):219-222

Iliev P; Shchrkova I, 1979. Promising introduced varieties of plum. Ovoshcharstvo, 58(8):25-28

Iliev P; Shchrkova I; Sturkova I, 1986. Cacansla Lepotica, a new early plum variety. Rastenievdni Nauki, 23:90-94.

Ioos R; Frey P, 2000. Genomic variation within Monilinia laxa, M. fructigena and M. fructicola, and application to species identification by PCR. European Journal of Plant Pathology, 106(4):373-378.

Janitor A; Paulech C, 1978. Some remarks on the study of the effect of gamma irradiation on pathogenic fungi. Pathophysiology of plants. II. Collection of papers read at the 2nd seminar on the pathophysiology of plants. Acata Botanica Slovaka B, 2:251-261.

Jarvis WR, 1962. The dispersal of spores of Botrytis cinerea Fr. in a raspberry plantation. Transactions of the British Mycological Society, 45:549-559.

Jenkins PT; Reinganum C, 1968. In: Australian Brown Rot Research Committee, ed. Report of the research work on brown rot of stone fruits. Melbourne, Australia: Government Printer, 48.

Kahn M, 1966. Substitution of light by indolyl-3 acetic acid in the sporulation of Sclerotinia fructigena. Nature (London), 212:640.

Kohn LM, 1979. A monographic revision of the genus Sclerotinia. Mycotaxon, 9(2):365-444

Lack KJ, 1989. The spread of apple brown rot (Monilinia fructigena) by insects. Annals of Applied Biology, 115(2):221-227

Lane CR, 2002. A synoptic key for differentiation of Monilinia fructicola, M. fructigena and M. laxa, based on examination of cultural characters. Bulletin OEPP, 32(3):489-493.

Larena I; Melgarejo P, 1996. Biological control of Monilinia laxa and Fusarium oxysporum f.sp. lycopersici by a lytic enzyme-producing Penicillium purpurogenum. Biological Control, 6(3):361-367; 32 ref.

Larena I; Torres R; Cal ADe; Liñàn M; Melgarejo P; Domenichini P; Bellini A; Mandrin JF; Lichou J; Ochoa de Eribe X; Usall J, 2006. Biological control of postharvest brown rot (Monilinia spp.) of peaches by field applications of Epicoccum nigrum. Biological Control, 32:305-310.

Leeuwen GCMvan; Baayen RP; Holb IJ; Jeger MJ, 2002. Distinction of the Asiatic brown rot fungus Monilia polystroma sp. nov. from M. fructigena. Mycological Research, 106(4):444-451; 24 ref.

Leeuwen GCMvan; Kesteren HAvan, 1998. Delineation of the three brown rot fungi of fruit crops (Monilinia spp.) on the basis of quantitative characteristics. Canadian Journal of Botany, 76(12):2042-2050; 26 ref.

Mackie A; Eyres N; Kumar S, 2005. Brown rot Monilinia fructigena. Brown rot Monilinia fructigena., Australia: Government of Western Australia, unpaginated. [Department of Agriculture and Food Factsheet.] http://www.agric.wa.gov.au/objtwr/imported_assets/content/pw/ph/dis/fn/fs2006_brownrot_amackie.pdf

Madrigal C; Pascual S; Melgarejo P, 1994. Biological control of peach twig blight (Monilinia laxa) with Epicoccum nigrum. Plant Pathology, 43(3):554-561

Malvárez G; Rodríguez A; Aguilar C; Silveira AC; Silvera E; Burgueño J; Mondino P, 2004. Monilinia fructicola, the only Monilinia species currently causing brown rot of peach (Prunus persica) in Uruguay. (Monilinia fructicola, única especie presente ocasionando la podredumbre morena del duraznero (Prunus persica) en Uruguay.) Fitopatología, 39(3):126-132.

Marcaki P; Petropoulou E; Mavroyannakis M, 1998. Investigation of the radiation effects on brown rot disease of Golden delicious apples, inoculated with the fungus Monilinia fructigena. Mycopathologia, 142(1):33-36; 16 ref.

Mari M; Iori R; Leoni O; Marchi A, 1993. In vitro activity of glucosinolate-derived isothiocyanates against postharvest fruit pathogens. Annals of Applied Biology, 123(1):155-164

Mari M; Iori R; Leoni O; Marchi A, 1996. Bioassays of glucosinolate-derived isothiocyanates against postharvest pear pathogens. Plant Pathology, 45(4):753-760; 33 ref.

Marquenie D; Schenk A; Nicolai B, 1999. VCBT investigates non-chemical methods to increase the storage life of strawberries and sweet cherries. Fruitteelt-nieuws, 12(3):18-19.

McClure TT, 1958. Brown and Rhizopus rots of peaches as affected by hydrocooling, fungicides, and temperature. Phytopathology, 48:322-324.

Melgarejo P; De Cal A; Pascual; S; Larena; I, 1998. Biological control of post-harvest diseases of stone fruits: prospects and problems. In: Bertolini P, Sijmons ME, Guerzoni ME, Serra F, eds. Non Conventional Methods for the Control of Postharvest Disease and Microbiological Spoilage. Belgium: Directorate General Science, Research and Development, 65-70.

Mordue JEM, 1979. Sclerotinia fructicola, S. fructigena, S. laxa. CMI Descriptions of Pathogenic Fungi and Bacteria, Nos 616, 617, 619. Wallingford, UK: CAB International.

Mordue JEM, 1979. Sclerotinia fructicola. [Descriptions of Fungi and Bacteria]. IMI Descriptions of Fungi and Bacteria, No. 62. Wallingford, UK: CAB International, Sheet 616.

Mordue JEM, 1979. Sclerotinia fructicola. In: CMI Descriptions of pathogenic fungi and bacteria, No. 616. Wallingford, UK: CAB International.

Mordue JEM, 1979. Sclerotinia fructigena. [Descriptions of Fungi and Bacteria]. IMI Descriptions of Fungi and Bacteria, No. 62. Wallingford, UK: CAB International, Sheet 617.

Mordue JEM, 1979. Sclerotinia fructigena. In: CMI Descriptions of pathogenic fungi and bacteria, No. 617. Wallingford, UK: CAB International.

Mordue JEM, 1979. Sclerotinia laxa. [Descriptions of Fungi and Bacteria]. IMI Descriptions of Fungi and Bacteria, No. 62. Wallingford, UK: CAB International, Sheet 619.

Mordue JEM, 1979. Sclerotinia laxa. In: CMI Descriptions of Pathogenic Fungi and Bacteria, No. 619. Wallingford, UK: CAB International.

Murakami T; Takada N; Harada Y; Okuno T; Hashimoto M, 2007. Stimulation of the biosynthesis of the antibiotics lambertellols by the mycoparasitic fungus Lambertella corni-maris under the acidic conditions produced by its host fungus in vitro. Bioscience, Biotechnology and Biochemistry, 71(5):1230-1235. http://www.jstage.jst.go.jp/browse/bbb/-char/en

Nitransky S, 1986. Field tolerance of apricot cultivars to unfavourable factors in 1983. Vedecke Prace Vyskumneho Ustavu Ovocnych a Okrasnych Drevin v Bojniciach 6: 51-61.

Niu ChengWang; Wang JingRu; Zhu XiaoQiong; Chen XiaoYu; Guo LiYun, 2016. Brown rot pathogens on stone and pome fruit trees in Xinjiang wild forest. Mycosystema, 35(12):1514-1525. http://journals.im.ac.cn/jwxten/ch/index.aspx

Ogawa JM; English H; eds, 1991. Brown rot of stone fruit. Diseases of Temperate Zone Tree Fruit and Nut Crops. California, USA: University of California, Division of Agriculture and Natural Resources, 142.

Ogawa JM; Manji BT; Bostock RM; Canez VM; Bose EA, 1984. Detection and characterization of benomyl-resistant Monilinia laxa on apricots. Plant Disease, 68(1):29-31

Ogawa JM; Manji BT; Schreader WR, 1975. Monilinia life cycle on sweet cherries and its control by overhead sprinkler fungicide applications. Plant Disease Reporter, 59(11):876-880

Pascual S; Magan N; Melgarejo P, 1996. Improved biological control of peach twig blight by physiological manipulation of Epicoccum nigrum. Brighton Crop Protection Conference: Pests & Diseases - 1996. Volume 1. Proceedings of an International Conference, Brighton, UK, 18-21 November, 1996., 411-412; 2 ref.

Pascual S; Magan N; Melgarejo P, 1998. Production of Epicoccum nigrum 282 for biocontrol of brown rot (Monilinia laxa). In: Bertolini P, Sijmons ME, Guerzoni ME, Serra F, eds. Non Conventional Methods for the Control of Postharvest Disease and Microbiological Spoilage. Belgium: Directorate General Science, Research and Development, 115-120.

Paunovic SA; Paunovic AS, 1996. Investigation of peach germplasm (Prunus persica ssp. vulgaris = vineyard peach) in situ in Yugoslavia. Acta Horticulturae, No. 374:201-207; 4 ref.

Penrose LJ; Tarran J; Wong A-L, 1976. First record of Sclerotinia laxa Aderh. & Ruhl. in New South Wales: differentiation from S. fructicola (Wint.) Rehm. by cultural characteristics and electrophoresis. Australian Journal of Agricultural Research, 27(4):547-556

Petróczy M; Palkovics L, 2009. First report of Monilia polystroma on apple in Hungary. European Journal of Plant Pathology, 125(2):343-347. http://springerlink.metapress.com/link.asp?id=100265

Pusey PL; Hotchkiss MW; Dulmage HT; Baumgardner RA; Zehr EI; Reilly CC; Wilson CL, 1988. Pilot tests for commercial production and application of Bacillus subtilis (B-3) for postharvest control of peach brown rot. Plant Disease, 72(7):622-626; 13 ref.

Pusey PL; Wilson CL, 1984. Postharvest biological control of stone fruit brown rot by Bacillus subtilis.. Plant Disease, 68(9):753-756; [2 col. fig., 4 tab.]; 21 ref.

Rekhviashvili L, 1975. The pathogenicity, specialization and the ways of infection of Monilia fructigena Pers. Trudy Nauchno-Issledovatel'skogo Instituta Zashchity Rastenii Gruz. SSR, 27:162-165

Rekhviashvili LM, 1973. Varietal resistance and some resistance indices of fruit trees to Monilia fructigena in Georgia. Trudy NII Zashchity Rastenii GruzSSR, 25:143-147

Reynaud L, 1997. Cherry orchard. Control of Monilia. Arboriculture Fruitiere, 506:23-25.

Richardson MJ, 1990. An annotated list of seed-borne diseases. Zurich, Switzerland: The International Seed-Testing Association.

Roberts JW; Dunegan JC, 1932. Peach brown rot. United States. Department of Agriculture Technical Bulletin. No. 328, 1-59.

Rueegg J; Lauber HP; Siegtried W; Viret O; Hilber U, 1997. Experiences with anilinopyrimidines in Switzerland. Pesticide Outlook, 8:28-33.

Sharma RL; Kaul JL, 1988. Susceptibility of apples to brown rot in relation to qualitative characters. Indian Phytopathology, 41(3):410-415

Sharma RL; Kaul JL, 1989. Host range of brown rot fungi (Monilinia spp. ) in India. Plant Disease Research, 4(2):177-178

Sharma RL; Kaul JL, 1989. Incidence of brown rot (Monilinia spp.) of apple in Himachal Pradesh. Indian Journal of Mycology and Plant Pathology, 19(2):208-211

Sharma RL; Kaul JL, 1989. Influence of light on growth and sporulation of Monilinia spp. Indian Journal of Mycology and Plant Pathology, 19(2):236-238

Sharma RL; Kaul JL, 1990. Efficacy of hot water and carbendazim treatments in controlling brown rot of apple. Indian Journal of Mycology and Plant Pathology, 20(1):47-48

Smith IM; Dunez J; Lelliott RA; Phillips DH; Archer SA(Editors), 1992. Handbook of plant diseases. Madrid, Spain; Ediciones Mundi-Prensa, 671 pp.

Spiegel J; Stammler G, 2006. Baseline sensitivity of Monilinia laxa and M. fructigena to pyraclostrobin and boscalid. Journal of Plant Diseases and Protection, 113(5):199-206. http://www.ulmer.de

Tiryaki O; Aydin G; Gnrer M, 1994. Post-harvest disease control of apple, quince, onion and peach, with radiation treatment. Journal of Turkish Phytopathology, 23(3):143-152; 14 ref.

Tzavella-Klonari K, 1985. Attack of hazel-nut fruits by the fungus Monilia fructigena. Annales de l'Institut Phytopathologique Benaki, 14(2):171-173

UK CAB International, 1976. Sclerotinia fructigena. [Distribution map]. Distribution Maps of Plant Diseases, October (Edition 4). Wallingford, UK: CAB International, Map 22.

USDA/APHIS, 2009. Regulated plant pest list. Regulated plant pest list. Washington, D.C., USA: US Department of Agriculture, Animal and Plant Heath Inspection Service, unpaginated. http://www.aphis.usda.gov/import_export/plants/plant_imports/downloads/RegulatedPestList.pdf

USDA/SMML, 2005. Nomenclature fact sheets. Monilinia fructigena and related brown fruit rots. Nomenclature fact sheets. Monilinia fructigena and related brown fruit rots. Beltsville, Maryland, USA: Systematic Mycology and Microbiology Laboratory, Agricultural Research Service, USDA, unpaginated. http://nt.ars-grin.gov/sbmlweb/fungi/nomensheets.cfm

Valiuskaite A, 2002. Micromycetes infecting stone fruit trees. Biologija, No.1:18-21.

Vasilev V, 1975. The sour cherry cultivar Meteor. Ovoshcharstvo, 54:37-38.

Vasudeva Mme RS, 1930. Studies in the physiology of parasitism. XI. An analysis of the factors underlying specialization of parasitism, with special reference to the fungi Botrytis allii, Munn, and Monilia fructigena, pers. Annals of Botany, 44(174):469-493 pp.

Volkova J; Vilka L; Stanke L; Rancane R; Bazenova A, 2013. Molecular characterization of Monilinia laxa and M. fructigena causing brown rot of sweet cherry in Zemgale Region of Latvia. Acta Biologica Universitatis Daugavpiliensis, 13(1):165-172.

Vucinic Z, 1994. Brown rot of fruit trees. Zastita Bilja, 45(1):5-17

Wade GC, 1956. Investigations on brown rot of Apricots caused by Sclerotinia fructicola (Wint.) Rehm. I. The occurrence of latent infection in fruit. Australian Journal of Agricultural Economics, 7(6):504-515 pp.

Wells JM; Bennett AH, 1975. Postharvest decay, weight loss, and fungicide residues on peaches hydro- or hydraircooled before or after waxing. Plant Disease Reporter, 59(11):931-935

Wells JM; Bennett AH, 1976. Hydrocooling and hydraircooling with fungicides for reduction of postharvest decay of peaches. Phytopathology, 66(6):801-805

Whetzel HH, 1945. A synopsis of the genera and species of the Sclerotiniaceae, a family of stromatic inoperculate discomycetes. Mycologia, 37:648-714.

Wilcox WF, 1989. Influence of environment and inoculum density on the incidence of brown rot blossom blight of sour cherry. Phytopathology, 79(5):530-534

Willetts HJ; Byrde RJW; Fielding AH; Wong A-L, 1977. The taxonomy of the brown rot fungi (Monilinia spp.) related to their extracellular cell wall-degrading enzymes. Journal of General Microbiology, 103(1):77-83

Witshire S, 1920. The production of conidia in pure cultures by the brown rot fungus of apple. Report Agricultural Horticultural Research Station Bristol, 1919:34-36.

Wormald H, 1954. The brown rot diseases of fruit trees. Technical Bulletin of the Ministry of Agriculture No.3. London, UK: HMSO.

Xu XM; Bertone C; Berrie A, 2007. Effects of wounding, fruit age and wetness duration on the development of cherry brown rot in the UK. Plant Pathology, 56(1):114-119. http://www.blackwell-synergy.com/loi/ppa

Xu XM; Guerin L; Robinson JD, 2001. Effects of temperature and relative humidity on conidial germination and viability, colonization and sporulation of Monilinia fructigena. Plant Pathology, 50(5):561-568.

Xu XM; Robinson JD, 2000. Epidemiology of brown rot (Monilinia fructigena) on apple: infection of fruits by conidia. Plant Pathology, 49(2):201-206.

Xu XM; Robinson JD; Berrie AM; Harris DC, 2001. Spatio-temporal dynamics of brown rot (Monilinia fructigena) on apple and pear. Plant Pathology, 50(5):569-578.

Zehr EI, 1982. Control of brown rot in peach orchards. Plant Disease, 66(12):1101-1105

Zhang Y; Bodmer M; Ruegg J, 1991. Variation in sensitivity to sterol biosynthesis inhibitors (SBI) of different isolates of Monilinia species. Zeitschrift fur Pflanzenkrankheiten und Pflanzenschutz, 98(3):317-322

Links to Websites

Top of page
WebsiteURLComment
Department of Agriculture and Food, Government of Western Australiawww.agric.wa.gov.au

Contributors

Top of page

10/09/09 Updated by:

Systematic Mycology & Microbiology Laboratory, USDA-ARS, 10300 Baltimore Ave., Beltsville, MD 20705, USA

Distribution Maps

Top of page
You can pan and zoom the map
Save map