Leptosphaeria maculans (stem canker)
Identity
- Preferred Scientific Name
- Leptosphaeria maculans (Desm.) Ces. & de Not.
- Preferred Common Name
- stem canker
- Other Scientific Names
- Phoma brassicae Thüm.
- Phoma lingam (Tode) Desm.
- Phoma oleracea Sacc.
- Phome napobrassicae Rostr.
- Phyllosticta brassicae (Curr.) Westend.
- Phyllosticta napi Sacc.
- Plenodomus lingam (Tode) Höhn.
- Pleospora maculans (Desm.) Tul.
- Sphaeria lingam Tode
- Sphaeria maculans Desm.
- International Common Names
- Englishblack leg of cabbageblackleg of cabbagecrucifers black legcrucifers cankercrucifers dry rotPhoma leaf spot
- Spanishpie negro de las cruciferaspodredumbre seca de las cruciferas
- Frenchchancre des crucifereschancre du chouchancre du colzajambe noire des cruciferesjambe noire du chounecrose du collet des cruciferesphoma des cruciferespied noir du chou
- Local Common Names
- GermanyFussfaeule: KohlHalsnekrose: RapsStengelfaeule: RapsTrockenfaeule: KohlUmfallkrankheit: KohlWurzelhalsfaeule: Raps
- EPPO code
- LEPTMA (Leptosphaeria maculans)
Pictures
Distribution
Host Plants and Other Plants Affected
Symptoms
Leaf Spots These may be confusingly variable depending on host resistance and age. Initially L. maculans causes small light brown spots which may be surrounded by chlorotic tissue. As the spots enlarge and age they become round to irregular shaped lesions, dirty white or pale grey in colour and they may contain tiny dark specks which are pycnidia (see Morphology) within which the asexual spores (conidia) develop. Alternatively the centre of the spot may break or drop out completely (also see Brun et al. (1997)).Stem Lesions Stem lesions, which often develop from infected leaves via the petiole, are often oval, long, irregular in shape and grey or cream in colour, and can appear as long black transverse streaks in the cortex.Pod LesionsPod lesions, which develop from rain-splashed pycnidiospores and wind-borne ascospores, are round to irregular in shape, with pycnidia, and the pod is often constricted.Stem Cankers Stem cankers develop from stem lesions at the root collar or crown of the plant. The brown lesions become darker and crack open. When severe, the stem is weakened considerably and this may result in disruption of water transport, lodging and death of the plant.Root InfectionRoot infection occurs either by spreading from the crown region into the roots or directly from soil through wounds (Sosnowski et al., 2001a). Tap roots have blackened areas and may be constricted, and lateral roots appear blackened with little or no new root growth.
List of Symptoms/Signs
Symptom or sign | Life stages | Sign or diagnosis |
---|---|---|
Plants/Leaves/abnormal colours | ||
Plants/Leaves/necrotic areas | ||
Plants/Stems/canker on woody stem | ||
Plants/Whole plant/early senescence | ||
Plants/Whole plant/plant dead; dieback | ||
Plants/Whole plant/uprooted or toppled |
Prevention and Control
Host Plant Resistance
Resistant cultivars are important in the integrated management of this pathogen. However, due to the variability in the virulence of L. maculans, cultivars which are resistant in one part of the world may be susceptible in other areas. Until 1997 the cultivar Jet Neuf was widely used as a resistance source in Europe (Ferreira et al., 1995), but its efficiency is diminishing in some locations. In Canada, the cultivar Quantum is considered to have the best resistance (Ansan-Melayah et al., 1995). A great deal of research is underway to find new sources of resistance (from brassicas or other plants) which can be engineered or conventionally bred (using double haploids) into rape. To cope with the variability of L. maculans, breeding for resistance must be given a high priority since cultural and chemical control measures are generally insufficient (Somda et al., 1996). In Australia, the cultivar Hyola 60 has proven to be extremely resistant to L. maculans (Sosnowski et al. 2001b). This resistance originated from a wild accession of B. rapa var. sylvestris which was collected in Sicily and then crossed with B. oleracea var. albogabra to produce a hybrid (Crouch et al. 1994).The physical strength of a cultivar is also important as this increases the tolerance to infection, i.e. infection occurs but does not reduce the yield greatly. Thicker, tougher stems with a high lignin and calcium content are thought to have greater tolerance.
Cultural Control
To prevent serious attacks of stem canker in infected areas it is essential to control early infection of rape plants by airborne ascospores. Good crop rotation to reduce exposure to inoculum and to improve plant vigour through improved nutrition requires at least 3 seasons before replanting with rape (Petrie, 1986).Additionally, deeply ploughing rape stubble followed by a minimal tillage the following year and sowing of a non-brassica crop minimises spore release from infected residue. Gladders and Musa (1980) reported that severe leaf spot infection of seedlings near unploughed oilseed rape stubble resulted in complete crop loss and that ploughing infected rape stubble was effective in reducing the amount of debris on the soil surface and apparently reduced the spread of infection to newly sown crops. Field selection, planting date and weed control are also important factors to reduce inoculum (Hall, 1992). It has also been suggested that a separation of 5 to 8 km from infested stubble is necessary to avoid severe stem canker in rape (Bokor et al., 1975).
Biological Control
Research is currently assessing the potential of several organisms such as Bacillus bacterium (Yang et al., 1997) and species of bird's nest fungus, Cyathus striatus and C. olla (Tewari et al., 1997), as biocontrol agents (see Natural Enemies).
Chemical Control
Chemical control is most efficient when directed at critical points in the disease cycle (Hall, 1992). The most sensitive period for infection of oilseed rape plants by L. maculans is from emergence to the 8th leaf stage in terms of subsequent canker development and related yield loss. For winter oilseed rape crops, epidemics occur when there is particularly wet weather just before and during crop establishment (autumn in western Europe). Until 1995 in the UK, few crops were sprayed in the autumn against stem canker (Gladders et al., 1997). Experiments applying fungicides at different times in the season have suggested that at least 2 sprays (autumn and spring) are necessary to obtain adequate control of severe stem canker epidemics. In the autumn, sprays may be needed against the leaf spot phase of stem canker to prevent the spread of the pathogen from the leaves into the stems (Hammond and Lewis, 1986). Early warning schemes are currently under development at IACR-Rothamsted, UK.Fungicides currently in use include: difenaconazole and carbendazim (in the UK, Sun et al. 2001), difenaconazole plus carbendazim (France and Spain), flutriafol (Australia; Khangura and Barbetti, 2002), prochloraz (Canada), propiconazole (Canada; Kharbanda et al., 1999).
Impact
Introduction
L. maculans occurs throughout the world and causes leaf spotting and stem rot of vegetable brassicas, swede and raddish and stem canker or blackleg of oilseed rape (canola) (Brassica napus var. oleifera or B. rapa). Stem infections can reduce seed yield if the infection becomes severe enough to cause early senescence or lodging. In the distant past, the disease has caused marketable yield losses on vegetable crops by infecting leaves and stems (Henderson, 1918), and more recently on seed crops of vegetable brassicas (Humpherson-Jones, 1983). The vast majority of yield losses caused by this disease have been recorded on the most economically important and most widely grown host, oilseed rape. Currently in Europe, North America and Australia, total devastation of the crop can occur due to seedling death, although this is rare. In harvested crops, yield losses are usually 0-10% but can often reach 30-50% in individual fields (Gladders and Musa, 1979; Gugel and Petrie, 1992; Hall et al., 1993; Barbetti and Khangura, 1999; Zhou et al., 1999).There is confusion over the importance of the B group (L. biglobosa) in crop protection. In Canada, the B group generally is not considered to be a serious pathogen. The structure of populations of L. maculans in different regions, the climate, cultivar resistance and cultural practices influence the economic impact of the disease.The following table shows the type of oilseed rape grown in different regions and the typical yields, which vary considerably - an important consideration in deciding whether the impact of L. maculans is significant and whether it is economic to apply fungicides.Type of oilseed rape and typical yields in different regions (1999/2000 data) Type of oilseed rape Typical yieldCanada West: spring B. napus and 1.5 t/ha some B. rapa Ontario: B. napus of both 2.2 t/ha winter and spring type Europe West: winter B. napus 4 t/ha Central: 60% winter, 40% 1.5 t/ha spring B. napus Australia >95% B. napus (spring type Western Australia 1.1 t/ha grown over winter period South east 1.6 t/ha <5% B. juncea
Crop Losses In Oilseed Brassicas
North AmericaOilseed rape or canola is grown extensively in the western Canadian provinces of Alberta, Saskatchewan and Manitoba, and also in Ontario, plus a few states of the USA. The disease was not important until the mid-1970s when the damaging A group began to spread in Saskatchewan, western Canada, causing estimated losses of 20% in one field by 1977 (Petrie, 1978). However, the disease was not considered to be widespread in that province until 1982 when the estimated average yield loss was 6% (reaching 56% in individual fields) (Gugel and Petrie, 1992). Gugel and Petrie (1992) reported yield losses in Saskatchewan of 7.2% in 1984 and 5.2% in 1985 (over 30% in some individual fields). The disease continued to spread west into Alberta by 1983 and east into Manitoba by 1984. By 1988, 62% of fields in southwest Manitoba were infected with an average plant incidence of 30% leading to a 10% yield loss (Platford and van den Berg, 1989) while the province-wide yield loss was 5% (Gugel and Petrie, 1992). By 1991, the yield loss for Alberta was 1% with substantial losses in some areas (Evans et al., 1991).In Ontario, Peters and Hall (1987) found the A group in 1986 and 1987 in 92% and 100% of fields, respectively. The mean disease incidence increased from 32 to 69% with estimated yield losses 5% and 7.5% respectively. Hall et al. (1993) found that winter oilseed rape was more heavily infected than spring crops. They found infection in 60-100% of fields of winter oilseed rape, and 27-31% of fields of spring rape. Mean annual seed yield losses were 1.1-7.5% (maximum estimated loss per field was 29.2%) for winter rape, and 0.3-1.6% (maximum estimated loss per field was 8.8%) for spring rape. Canker severity (X) at harvest was related to seed yield loss (Y%) in winter rape by the equation;Log10(Y+1) = a + bX. Rempel and Hall (1995) found yield responses, caused by fungicide application at the late rosette stage, of 17-33%; however, some of this increase may be due to growth regulatory effects of the chemicals.EuropeThe disease is important on oilseed rape in England, France and Germany. Schramm and Hoffmann (1992) used different fungicide applications in Germany to show yield losses of 8-20% compared with single autumn fungicide treated crops (mainly attributable to stem canker) and losses of 12-17% compared with double (autumn and spring) applications. Even a single spring application showed up to a 13% loss on untreated plots although this was not all attributable to stem canker. In France, severe epidemics occurred in the 1960s but more recently, resistant cultivars and chemical control have helped to manage the disease. In England, yield losses of up to 50% occurred in individual crops in severe years during the late 1970s (Gladders and Musa, 1979). Humpherson-Jones (1983) reported that over 70% of crops (cv. Primor) were infected in 1977 and 1978 with a mean incidence of 21.3% infected plants and severe cankers were found in 22 out of 34 crops (maximum incidence of severe cankers was 36%, 20% had lodged). Less disease occurred in 1979 and 1980 possibly due to the use of new resistant cultivars. Humpherson-Jones (1983) noted that these resistant cultivars Jet Neuf and Rafal had less severe cankers but still produced abundant pseudothecia on the stubble residue. In the early 1990s losses of 10-20% occurred on susceptible and moderately susceptible varieties (Gladders, 1995). More recently, West (IACR - Rothamsted, Harpenden, UK, personal communication) found a yield loss, attributed to stem canker, of 25% in 1998 (compared with a mean yield of two fungicide treated cultivars). However, no reduction occurred in yield in 1999 when the disease incidence on leaves had been greater than 1998 but the epidemic was relatively late to start. Zhou et al. (1999) showed that the earlier stem canker symptoms appeared, the greater the yield loss. In older plants, beyond flowering stage, new cankers seldom develop while existing cankers become more severe. They found that yield loss (L%) could be modelled with areas under disease progression curves of either incidence (% plants infected, X) or severity (mean stem score, 0-4 scale, S) in the equations;L = -0.76 + 0.0075 X, L = 0.26 + 0.53S.More recently, Sun et al. (2000) have constructed models to study the relationship between phoma leaf spot and development of stem canker and Zhou et al (2000) used correlation regression analysis to study the effects of stem canker on yield of winter oilseed rape in southern England.AustraliaIn Western Australia in the early 1970s, severe stem canker epidemics caused the oilseed rape industry to collapse (Bokor et al., 1975). In the 1980s, cultivars with increased host resistance reduced the impact of the disease (Salisbury et al., 1995). Subsequently, the crop increased in Australia from 175,000 ha in 1993 to 1.8 million ha in 1999 (Burton et al., 1999). Barbetti and Khangura (1999) devised a system, based on the risk of yield loss due to blackleg infection, which considers different disease pressure scenarios and shows maximum potential yield losses for each scenario (disease pressures are based on the age of nearby residue, such that mild = 4, moderate = 3, severe = 2, and very severe = 1 year-old residue). This gives growers the opportunity to make informed choices as to which level of cultivar host resistance to use and the level of laborious stubble management necessary. In addition, Barbetti et al. (2000) expanded the prediction. They consider different disease pressures to be produced from factors such as proximity and age of inoculum (stubble residue) and rainfall. They predict maximum yield losses on moderately susceptible cultivars such as Karoo (Western Australian adult canker resistance score = 4, using a scale where 1 = susceptible and 9 = resistant) of 15, 35, 65 and 100% in mild, moderate, severe and very severe disease pressures, respectively. This compares with resistant cultivars such as Dunkeld (Western Australian adult canker resistance score = 7) which has predicted losses of 0, 10, 40 and 80%, respectively. Khangura and Barbetti (2001) showed that between 1996 and 1999, the mean incidence of crown cankers across Western Australia ranged between 55 and 85%, and this high disease incidence was attributed to the accumulation of large amounts of infested canola residues. AsiaAlthough present in China, L. maculans is not currently considered to be a problem on oilseed rape. Isolates collected from central China in 1999 were exclusively B group (West et al., 2000) and labour intensive cultural practices, such as hand planting young plants and removal of stubble at harvest, help to avoid the disease. Little is known about the impact of the disease on vegetable brassicas in China.In India, B. juncea and B. rapa are the main oil-seed brassicas grown and little disease caused by L. maculans has been reported. Although L. maculans is pathogenic to B. juncea (Indian mustard), the severity of stem infections is low (Purwantara et al., 1998).
Other Crops
B. nigra has been found to have high levels of resistance to L. maculans in experiments in Germany (Zhu et al., 1993).In the UK, L. maculans was a problem in the north on broccoli, swede and turnip before the 1950s when hot water seed treatment (currently a fungicide treatment is used) reduced the incidence of the pathogen (Moore, 1948; Humpherson-Jones, 1983). In a subsequent study reported by Humpherson-Jones (1983), L. maculans was not found on horticultural brassica seed crops in 1976, but was abundant on these and oilseed rape in the late 1970s, apparently in relation to the severe epidemic on oilseed rape in 1977. The mean incidences of stem canker in the seed crops of B. oleracea sampled were 5.1% in 1977 and 32.2% in 1980, however, most infections were of low severity and did not cause premature ripening. The exceptions were some seed crops of kale which had approximately 30% of plants severely cankered in 1977 and 1978. Since these crops were grown from fungicide-treated seed, it is thought that the infections were initiated by ascospores from nearby oilseed rape residue. In the same study, turnip and swede crops were found to have stem canker (dry rot) between 1977 and 1980 (mean of 43% plants infected, 9% severely, 4% lodged). In one turnip crop 42% of plants were infected in 1978 (20% had lodged).
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Published online: 9 October 2023
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