Disease Models - rapeseed

Rapeseed / Canola disease models

The most important oil seed crop of the cool climate regions is affected by two very destructive diseases and three economic important pest insects. Rape seed growing has gained more and more importance in Northern Europe and in Northern America. Due to the growing market of biofuels it will gain more importance in South America and in parts of Asia too. New varieties have increased the yield potential dramatically. To keep these yields economically worthwhile plant protection strategies will gain more importance. FieldClimate.Com is supporting these strategies with disease and pest models for: Sklerotina sclerotina, Phoma lingam and Pollen Beetle (Meligethes aeneus).

Sclerotinia rot

Sclerotinia rot affects a wide range of plants particularly non-woody species. Sclerotinia rot is caused by S. sclerotiorum. Sclerotinia rot can affect plants at any stage of production including seedlings, mature plants and harvested products. Plants with senescing or dead tissue are particularly susceptible to infection.


The infected area of a plant initially takes on a dark green or brown water-soaked appearance, then may become paler in color. Dense white cottony mycelium usually develops and the plant begins to wilt and eventually dies. Resting or survival structures (sclerotia) are produced externally on affected plant parts and internally in stem pith cavities. The sclerotia are hard, black, irregular in shape, mostly 2-4 mm in size, and difficult to see once incorporated into the soil.

Disease sources and spread

The life-cycle of S. sclerotiorum includes both a soil-borne and an air-borne phase. Sclerotia of S. sclerotiorum can survive in the soil for ten years or more. They germinate to produce small funnel-shaped fruiting bodies (apothecia) that are approximately 1 cm in diameter. Apothecia produce air-borne spores, which can cause infection when they land on a susceptible host plant, either via flowers, or by direct germination on leaves. Occasionally, infection of stem bases can occur when fungal strands (mycelium) develop directly from Sclerotia near the surface. New sclerotia develop in infected plant tissue and when the plant dies they remain on the soil surface or may become incorporated during subsequent soil cultivation.

Conditions for Infection

After a period of cold conditions in winter, sclerotia, overwintering in the top 5 cm of the soil, germinate from spring onwards to produce apothecia, when soil temperatures are 10°C or higher and the soil is moist. Sclerotia do not germinate in dry soil or when the soil temperature is above 25°C. Sclerotia buried below 5 cm in the soil are less likely to germinate. Once apothecia are fully formed, spore release can occur in the light or dark but is temperature dependent, so tends to peak around midday. Apothecia can last about 20 days at 15 to 20°C, but shrivel after less than 10 days at 25°C. For flowering herbs, spores landing on petals and stamens germinate rapidly (germination within 3-6 hours and infection within 24 hours) in optimum conditions of 15-25°C, continuous leaf wetness and high humidity within the crop. Subsequent infection of leaves and stems depends on petals falling and sticking on leaves. The risk of infection is increased if the leaves are wet because this causes more petals to stick. Infected dead or senescing petals provide nutrients for the invasion of the fungus into leaves and stems. For non-flowering herbs, infection is mainly by air-borne spores landing directly on leaves. Spores can survive on leaves for several weeks until conditions favorable for leaf infection occur. Spore germination and infection depend on the presence of nutrients on leaves, either from plant wounds or senescing plant material. As for flowering herbs, the optimum spore germination and infection conditions are 15-25°C with continuous leaf wetness and high humidity. Once plant infection has occurred, rapid disease progress is favoured by warm (15-20°C) and moist conditions in dense crops.

Sclerotinia Infection Model

Carpogenic germination of sclerotia is stimulated by periods of continuous soil moisture. Apothecia are formed on the soil surface from which ascospores are released into the air. Infection of most crop species is principally associated with ascospores but direct infection of healthy, intact plant tissue from germinating ascospores usually does not occur. Instead, infection of leaf and stem tissue of healthy plants results only when germinating ascospores colonize dead or senescing tissues, usually flower parts such as abscised petals, prior to the formation of infection structures and penetration. Myceliogenic germination of sclerotia at the soil surface can also result in colonization of dead organic matter with subsequent infection of adjacent living plants. However, in some crops, for example sunflower myceliogenic germination of sclerotia can directly initiate the infection process of the roots and basal stem resulting in wilt. The stimulus for myceliogenic germination and infection in sunflower is not known but likely depends on nutritional signals in the rhizosphere derived from host plants.

The infection process
Infection of healthy tissue depends on the formation of an appressorium, which may be simple or complex in structure depending on the host surface. In most cases, penetration is directly through the cuticle and not through stomata. Appressoria develop from terminal dichotomous branching of hyphae growing on the host surface and consist of a pad of broad, multi-septate, short hyphae that are orientated perpendicular to the host surface to which they are attached by mucilage. Complex appressoria are often referred to as infection cushions. Although earlier workers considered penetration of the cuticle to be a purely mechanical process there is strong evidence from ultra-structural studies that enzymatic digestion of the cuticle also plays a role in the penetration process. Little is known about S. sclerotiorum cutinases, however, the genome encodes at least four cutinase-like enzymes (Hegedus unpublished). A large vesicle, formed at the appressorium tip prior to penetration, appears to be released into the host cuticle during penetration. After penetration of the cuticle, a subcuticular vesicle forms from which large hyphae fan out growing over and dissolving the subcuticular wall of the epidermis.

Infection by enzymatic degratation of the epidemic cells: Oxalic acid works in concern with cell wall degrading enzymes, such as polygalacturonase (PG), to bring about the destruction of host tissue by creating an environment conducive for PG attack on pectin in the middle lamella. This in turn releases low molecular weight derivatives that induce the expression of additional PG genes. Indeed, overall PG activity is induced by pectin or pectin-derived monosaccharides, such as galacturonic acid, and is repressed by the presence of glucose. Examination of the expression patterns of individual Sspg genes has revealed that the interplay among PGs and with the host during the various stages of infection is finely co-ordinated. (Dwayne D. Hegedus *, S. Roger Rimmer: Sclerotinia sclerotiorum: When ‘‘to be or not to be’’ a pathogen? FEMS Microbiology Letters 251 (2005) 177–184)

Looking for Climate Conditions for Infection of S. sclerotiorum has to take consideration of the apothecia formation, the sporulation, the direct infection by apothecia (even if it does not take place very frequent) and the infection from established mycelia by encymatic degradation of the epidemic cells .

Apothecia formation and sporulation takes place if a rain of more than 8 mm is followed by a period of high relative humidity lasting longer than 20 hours at optimum temperature of 21°C to 26°C.

Direct Infection by Apothecia can be expected after a leaf wetness period followed by 16 hours of relative humidity higher than 90% under optimum 21°C to 26°C (“appressoria infection”). Wheras saprophytic growth followed by encymatic degratation of the epidermic cells (“hydrolytic infection”) can be expected under a slightly lower relative humditiy of 80% lasting for a period of 24 hours under optimum conditions of 21°C to 26°C.


  • Lumsden, R.D. (1976) Pectolytic enzymes of Sclerotinia sclerotiorum and their localization on infected bean. Can. J. Bot. 54,2630–2641.
  • Tariq, V.N. and Jeffries, P. (1984) Appressorium formation by Sclerotinia sclerotiorum: scanning electron microscopy. Trans. Brit. Mycol. Soc. 82, 645–651.
  • Boyle, C. (1921) Studies in the physiology of parasitism. VI. Infection by Sclerotinia libertiana. Ann. Bot. 35, 337–347.
  • Abawi, G.S., Polach, F.J. and Molin, W.T. (1975) Infection of bean by ascospores of Whetzelinia sclerotiorum. Phytopathology 65, 673–678.
  • Tariq, V.N. and Jeffries, P. (1986) Ultrastructure of penetration of Phaseolus spp. by Sclerotinia sclerotiorum. Can. J. Bot. 64, 2909– 2915.
  • Marciano, P., Di Lenna, P. and Magro, P. (1983) Oxalic acid, cell wall degrading enzymes and pH in pathogenesis and their significance in the virulence of two Sclerotinia sclerotiorum isolates on sunflower. Physiol. Plant Pathol. 22, 339–345.
  • Fraissinet-Tachet, L. and Fevre, M. (1996) Regulation by galacturonic acid of ppectinolytic enzyme production by Sclerotinia sclerotiorum. Curr. Microbiol. 33, 49–53.

Practical Use of the Sclerotinia Model

The White Leg Infection Model shows the periods when the formation of apothecia are expected. If these periods are coinsitent with the flowering period of rape seed or canola we have to expect S. sclerotiorum infections during a moist period. The spores formed in the apothecia might be available for one to several days. The opportunity of infections is indicated by the calculation of the infection progress for direct or indirect infections by appressoria or encymatic cell wall degratation. If the infection progress line reaches 100% an infection has to be assumed. These infections should be covered preventative or a fungicid with a curative action against S. sclerotiorum has to be used.

Black leg disease

Disease Cycle

The disease has four main stages on winter oilseed rape:

  1. The most important sources of infection for newly-emerged plants are air-borne spores produced on oilseed rape stubble after harvest. Fruiting bodies that produce air-borne spores need about 20 days with rain to mature, eg spores were released early after the wet August in 2005 and in 2006, but late in 2003 when that month was dry.
  2. Air-borne spores, released mainly on rainy days, infect leaves to produce the leaf spot stage. Symptoms appear after 5-7 days at 15-20°C but take over 30 days to develop at 3°C.
  3. No symptoms are visible while the fungus grows from the leaf spot, down the petiole, to the stem. The growth rate down the petiole may be up to 5mm/day at 15-20°C but slows to 1mm/day at 3-5°C. Fungicides give no control once the stem has been infected.
  4. The fungus spreads within the stem, leading to visible stem canker symptoms about six months after leaf infection. Early leaf spotting leads to early stem cankers, which are most likely to reduce yield potential.

Weather: August and September rainfall is the key factor determining the onset of leaf spotting. Above average rainfall, particularly in August, indicates early risk.


Leptosphaeria maculans or Phoma lingam survives the intercrop period as mycelium and pseudothecia in crop residues. In Canada, leaf tissue does not persist long enough to allow pseudothecia to develop, but pseudothecia do form on basal stem tissue. Upon maturity, the pseudothecia produce ascospores.

Ascospores of the fungus are released after rainfall when temperatures are between 8-12ºC/46-54ºF. These spores can be wind-dispersed for hundreds of meters (yards). Pycnidia can and do overwinter readily in stubble, but because pycnidiospores are not airborne to any significant extent, they are of minor importance in initiating the first cycle of disease.

Ascospores germinate in the presence of free water from 4-28ºC (40-82ºF). Penetration is through stomates. The pathogen also may be seedborne. Seeds may be infected and/or infested by the pathogen. Infected seeds can give rise to infected seedlings, but levels of seed contamination are always very low. Primary infections usually occur on the cotyledons or basal rosette leaves of the plant. Wet weather favors these primary infections.

The fungus invades the intercellular spaces between the palisade and epidermal layers of the leaf. This symptomless biotrophic phase is followed by invasion of the mesophyll with the resultant death of cells and the appearance of gray-green lesions. The hyphae continue to ramify through the leaf tissue until they reach a leaf vein. The fungus then colonizes the cortex and/or xylem parenchyma of the petiole. At the junction of the petiole and the stem, the fungus invades the stem cortex where it causes a canker. It is at this point that stem resistance is expressed and determines the ability of the disease to proceed to the damaging stem canker phase. Stem cankers form when the plants bolt (produce an upright stem from the rosette on which the flowers form). Stem cankers develop most quickly at 20-24ºC/68-75ºF and are most severe under stress conditions such as mechanical, insect, or herbicide injury.

Pycnidiospores (conidia) are released from the pycnidia under moist conditions in a mucilage, a watery, sticky solution. These spores are responsible for secondary cycles of the disease, but ascospores are the more important source of inoculum because they are more infective and are airborne.

The pynidiospores are dispersed to new infection sites by rain splash. Pycnidiospores germinate more slowly than ascospores and require more than 16 hr of continuous wetness at the optimal temperature range of 20-25ºC/68-77ºF. The minimum latent period (the time from infection to the production of new inoculum) following infection by pycnidiospores is 13 days. Although secondary infections by pycnidiospores do occur, most losses are due to primary infections of leaves by ascospores that lead to basal stem cankers and eventual lodging of the plants.

Model for First Possible Infection in Fall

The development of a phoma stem canker epidemic is seperatet into three stages.

  1. In the first stage, the date when phoma leaf spot epidemics start in autumn was predicted from the summer weather data. Since phoma stem canker is a monocyclic disease (one cycle per growing season), the date in autumn when leaf spotting starts to develop is a crucial factor affecting the severity of phoma stem canker epidemics on stems the following summer (West et al. 2001). The date when phoma leaf spotting starts in autumn is estimated from the temperature and rainfall during the intercrop period between the harvest of the previous crop and the establishment of the new crop. Where approximately 4 mm of rain will make the occurence of Black Leg Disease one day earlier and the impact of temperature is higher at the begin of the period in mid summer than in autumn.
    If the ascospore infection is possible do to the autumn climate, we have to look for the climate needs of ascospore infection.
  2. In this second stage we can look for mature ascospores. To mature the ascospores it needs depending on temperature more than 288 hours of air temeprature in between 5 and 25°C and relative humidity higher than 85%. Now it needs 4 mm or rain or more to distribute the ascospores. A leaf wetness period has to start an ascopore infection and if can be completed within 8 hours under optimum temperature.
    In later autum and in spring conidia can be formed on mature lesions of Black Leg Disease.
  3. In the third stage we have to expect conidia infections, which are started by a leaf wetness period and which are completed by periods of relative humidity higher than 85% for longer than 8 hours at optimum temperature.

Practical Use of the Black Leg Models

The Black Leg Model starts with the assessment if a Black Leg infection is possible in late summer and early autumn. This part of the model can be used as an negativ prognosis. It has been tested for the UK climate to estimate the first occurence of P. lingam infections. This model is valid for cool and humid climate. It should be used with some caution in continental climate like Hungaria or Austria. The models for Ascospore maturation, ascospore realse and ascospore infection are showing possible ascospore infections during autumn. This models are basing on the biology of the pathogen and will most propably show more ascospore infecitons than you might find in the field. This is because on base of the climate data we do not know anything about the inoculum density and the precrops of the rape fields. Anyhow if one or several ascospore infecitons are fitting to the susceptible plant stages after emergence P. lingam infections will take place and secundary infections from conidia have to be expected during warm and moist periods in fall or spring.
Conidia infections are indicated do to the leaf wetness periods needed for a conidia infection.

Pollen beetle

Rape seed is affected by three main pests. On all three species it is needed to control the adulds. The flight of this three species is very much triggered by the temperatures.

Pollen beetles Meligethes spp. occur in high abundance at temperatures above 10°C. They overwinter in litter of forests and start to immigrate to rape fields in spring. Most damage is done, when adult beetles feed on buds. Females lay their eggs into buds, but once the flower occurs no damage is done by larval feeding on pollen. There are a lot of reports, which describe the resistance of the pollen beetle against special insecticides.

Color: Metallic green, blue, violet, bronze or black.
Size: 1,5 – 2,7 mm
Habitat: Fields, Pastures, Gardens
Cycle: Females are laying eggs into the buds of the rape seed plant. Therefore they have to bit trough petal and sepal leafs. Eggs are deposited on anther and stigma. The hatched larvae feed at the already opened flower (no damage) and the last larval stage leaves the flower and goes to the soil, where it pupate for about one week. First generation of beetles are hatching during summer. They still feed on different flowers (mostly attrackted from yellow) and at the end of summer they start to fly to refuges to hibernate. Pollen beetle has one generation per year.
Feeding: Pollen of many varieties with preferation for cruciferes.
Flight Period: Pollen beetle start flying if the soil temperature is higher than 9°C and the air temperature about 15°C and low relative humidity. Flight of Pollen beetle lasts about four weeks (in Austria between begin to mid of April til mid of May). In FieldClimate.com we just determine the occurrence of the flight by “Yes” or “NO”- so if the immigration to the field was already determined by soil and air temperatures it will stay at “YES” for the saison and the farmer has to check the occurrence on the field at that time.

Recommended equipment

Check which sensor set is needed for monitoring this crop’s potential diseases.