Diaporthe phaseolorum var. caulivora (stem canker of soyabean)
Identity
- Preferred Scientific Name
- Diaporthe phaseolorum var. caulivora Athow & Caldwell
- Preferred Common Name
- stem canker of soyabean
- Other Scientific Names
- Diaporthe phaseolorum f.sp. caulivora Kulik
- Phomopsis phaseoli f.sp. caulivora Kulik
- International Common Names
- Englishsoyabean stem cankerstem canker of soybean
- Spanishchancro del cuello de la soja
- Frenchchancre de la tige du soja
- Local Common Names
- Argentinacancrosis del tallo de la soja
- USAnorthern soybean stem cankersoybean stem canker
- EPPO code
- DIAPPC (Diaporthe phaseolorum var. caulivora)
Pictures
Distribution
Host Plants and Other Plants Affected
Host | Host status | References |
---|---|---|
Abutilon theophrasti (velvet leaf) | Wild host | Vrandecic et al. (2005) |
Glycine max (soyabean) | Main | Pioli et al. (2001) Li et al. (2004) Bradley and Li (2006) Lu et al. (2010) Costamilan et al. (2008) Sun et al. (2013) |
Symptoms
StemReddish-brown lesions that produce brown cankers as the season progresses are frequently seen on the lower stem (Backman et al., 1985) or spread to all parts of the stem (Jasnic and Vidic, 1983). These symptoms cause wilting and desiccation of the plants (Vidic and Jasnic, 1988b). Premature death of the upper 5-6 internodes occurs late in the season in some soyabean fields in Ohio, USA. In field studies, isolates induced dieback in tip-inoculated plants and stem canker in plants inoculated at lower internodes (Hobbs et al., 1981). Stem girdling can also occur, resulting in premature plant death. The results of Lalitha et al. (1989) indicate that a toxin may be involved in the development of soyabean stem canker symptoms; the severity of the disease can vary in relation to the occurrence of toxigenic strains of the fungus (Yoder, 1980). Preliminary studies also suggest that differences in toxin levels could explain the pathogenic variation among isolates of var. caulivora and var. meridionalis (Lalitha et al., 1989).LeafLeaves show interveinal chlorosis and necrosis at the early reproductive stages. As the disease progresses, the leaves dry up but remain attached to the plant.RootAscomata were found on soyabean roots at the end of the season in the Serbo-Croatian region, when long, rainy periods occurred (Vidic and Jasnic, 1988c).
List of Symptoms/Signs
Symptom or sign | Life stages | Sign or diagnosis |
---|---|---|
Plants/Leaves/abnormal colours | ||
Plants/Leaves/wilting | ||
Plants/Leaves/yellowed or dead | ||
Plants/Seeds/discolorations | ||
Plants/Seeds/shrivelled | ||
Plants/Stems/canker on woody stem | ||
Plants/Stems/dieback | ||
Plants/Stems/discoloration | ||
Plants/Stems/discoloration of bark | ||
Plants/Stems/internal discoloration | ||
Plants/Whole plant/discoloration | ||
Plants/Whole plant/early senescence | ||
Plants/Whole plant/plant dead; dieback | ||
Plants/Whole plant/wilt |
Prevention and Control
Cultural Control and Sanitary Methods
Crop rotation, deep ploughing and seed disinfection are recommended for control of stem canker in the Caucasus region, Russia (Skripka and Podkina, 1990). The extent to which a soyabean-maize rotation is able to limit the build-up of host-specific pathogens of soyabean and the involvement of plant diseases in the rotation effect was investigated. The incidence and severity of seven diseases and seed yield were recorded at two field locations in Minnesota, USA, in 1987 and 1988. Stem canker, caused by D. phaseolorum var. caulivora, was noted in 1987 at both locations in less than 5% of all plants monitored. It was concluded that, within the conditions of the study, the yield benefit to soyabean from rotation with maize did not appear to be due to the reduced incidence of plant diseases (Whiting and Crookston, 1993).In the Korea Republic, the effect of field sanitation was investigated for controlling Phomopsis seed decay in soyabean. Field sanitation included removing host debris, petioles and cotyledons from the field. It markedly reduced infection of pods and seeds by Phomopsis sp. However, seed infection was 28.7% in the sanitised field. This control strategy was effective in controlling Phomopsis seed decay when infection pressure was low. D. phaseolorum var. sojae, D. phaseolorum var. caulivora and Phomopsis longicolla were mostly identified from soyabean seeds; Colletotrichum truncatum and Cercospora kikuchiana were also isolated. Field sanitation did not significantly increase soyabean yield but a routine application schedule did (Oh JeungHaing, 1998).
Host-Plant Resistance
Hildebrand (1952) reported pathogenic specialization among D. phaseolorum var. caulivora isolates on seedlings of different soyabean cultivars from Ontario.In northern USA, soyabean stem canker has essentially been under control since highly susceptible cultivars were withdrawn in the late 1950s (Athow, 1987). A limited amount of screening for resistance has been done since then, but resistance is not generally considered to be at a high level (Tisselli et al., 1980). Two isolates of D. phaseolorum var. caulivora, one from Ohio and other from Indiana (northern USA) were non-pathogenic to the soyabean line J77-339, whereas isolates from Tennessee and Mississippi (southern USA) were severely pathogenic to this line (Keeling, 1985; 1988a). Moreover, the cultivars Blackhawk, Harosoy, L4404, Nathan, Tracy-M and Williams were all susceptible to one isolate from Iowa, and resistant to two isolates from Mississippi; whereas J77-339, Clark and Pike were susceptible to all three isolates. It was proposed that the Iowa isolate be designated race 1 and the Mississippi isolate race 2 (Higley and Tachibana, 1987). Similar results were reported for the behaviour of Blackhawk, Hawkeye, and Tracy-M, cited as susceptible to northern isolates of D. phaseolorum var. caulivora, but were highly resistant to the southern isolates (Backman et al., 1985; Keeling 1985, 1988a, b).Monoascosporic isolates from Maryland, north-eastern USA, exhibited dimorphism associated with their degree of pathogenicity to soyabean seedlings. Isolates that were fast growing on APDA were largely non-pathogenic to seedlings of the soyabean cultivars Blackhawk and Zane, whereas slow-growing isolates were largely pathogenic. In contrast, Alabama and Florida (south-eastern USA) isolates did not exhibit a sharply defined separation into two groups on the basis of their culture morphology. A clear association of pathogenicity with colony diameter, as seen in the Maryland isolates, was not evident in the Alabama isolates. Inoculation of Blackhawk seedlings with Alabama isolates failed to produce cankers, whereas inoculation of seedlings of the same cultivar with the Maryland isolates produced many cankers (Kulik, 1989).Seedlings of soyabean varieties Mandarin, Harosoy, Tracy-M and the line J 77-339 were inoculated with five isolates collected in different areas of Vojvodina, Serbia. Cultivar Tracy-M was highly susceptible whereas the line J 77-339 was relatively resistant to these isolates. It was concluded that the Vojvodina isolates were similar to the northern race, which is dominant in north-central USA, and different from the race dominant in southern USA (Vidic, 1991). The virulence of D. phaseolorum var. caulivora isolates was evaluated by inoculating soyabean cultivars Granger, Mandarin and Elgin BC, and the line NS-L-2023 with two D. phaseolorum var. caulivora isolates from former Yugoslavia, S4-Erdevik and S1-Novi Sad. The cultivars Granger and Mandarin were highly susceptible to S4-Erdevik and highly resistant to S1-Novi Sad. The cultivar Elgin BC showed a similar degree of susceptibility to both isolates, while the line NS-L-2023 showed more intensive disease symptoms with S4-Erdevik than with S1-Novi Sad, although the percentage of wilted seedlings was similar with both isolates at the end of the test period. It was concluded that the genotypes tested are suitable for the differentiation of physiological races of D. phaseolorum var. caulivora (Vidic et al., 1994).In Bulgaria, experimental mutagenesis was used as an alternative method for obtaining soyabean resistant to stem canker and charcoal rot (Macrophomina phaseolina). M2 plants obtained by gamma irradiation of cv. Elezir showed the lowest percentage of diseased plants for both diseases. The M2 variants derived from cv. Gemma had the lowest percentage of plants infected by charcoal rot. Lines resistant to both diseases were selected from both cultivars in the M3 (Aleksieva et al., 1999).Pathogenicity trials were conducted under greenhouse cnditions in Argentina. Plant-genotype/pathogen-isolate interactions were measured as percentage of dead plants (%DP) using soyabean genotypes carrying major resistance genes. The soyabean genotypes (and resistance genes, Rdc) tested were: Tracy-M (Rdc1 and Rdc2), Isoline T-1 (homozygous for Rdc1), Isoline T-2 (homozygous for Rdc2), Crockett (homozygous for Rdc3), Dowling (homozygous for Rdc4), Hutchenson (homozygous for Rdc4) and RA 702 (highly susceptible to var. meridionalis). Interactions among soyabean genotypes carrying different resistance genes and D. phaseolorum var. caulivora isolates were different from those observed with isolates of D. phaseolorum var. meridionalis. Cultivar Tracy-M was compatible with all isolates of D. phaseolorum var. caulivora assayed. The level of susceptibility to var. caulivora was very similar, on average, in Tracy-M and RA 702. The fact that Rdc1 and Rdc2 genes together (as in Tracy-M) conferred an almost immune reaction to all isolates of D. phaseolorum var. meridionalis assayed (mean = 0.9% DP) but were ineffective in conferring resistance to any of D. phaseolorum var. caulivora isolates evaluated (mean = 57.3% DP) suggests that the virulence/avirulence genes in both varieties of D. phaseolorum are different. However, when interacting with single resistance genes, two isolates of D. phaseolorum var. caulivora isolates, one from Santa Fe, Argentina, and the other from the USA, were compatible with each single resistance gene (i.e. Rdc1, Rdc2, Rdc3 or Rdc4). An isolate of D. phaseolorum var. caulivora obtained from infected soyabean seeds showed compatible interactions with the Rdc1 gene (33% DP) and Rdc4 gene in Dowling background only (52.4% DP) (Pioli et al., 2003).
Chemical Control
The results obtained by Athow and Caldwell (1954) showed that natural infection by stem canker occurred through the leaves of soyabean plants and that removal of the first six trifoliate leaves prevented the development of the disease. Consequently, spray trials have indicated that, for adequate control of stem canker, fungicides should be applied between the two- and eight-leaf stages. These results indicate that the release of ascospores and plant infection typically occurs early in the crop season (Backman et al., 1985). However, during the 1984 season, perithecia matured later and infection occurred after the 10-leaf stage, but only susceptible cultivars showed symptoms. These observations indicate the need for further research on a prediction system for spore release in order to time spray applications accurately (Backman et al., 1985). In the former Yugoslavia, two sprays of benomyl and mancozeb (Vidic et al., 1986) or benomyl plus vinclozolin (Vrataric et al., 1991a) gave effective control of stem canker and increased the yield, expressed as seed number, 1000-seed weight and seed oil content. Spraying with fungicides was recommended by Skripka and Podkina (1990) for control of stem canker in the Caucasus region of Russia.The fields sanitized by benomyl around the soyabean plants also decreased seed infection with Phomopsis sp. Total seed infection including that with miscellaneous pathogens, was 75-79% with no applications, compared with 34-42% in the routine application schedule (Oh JeungHaing, 1998).
Impact
Stem canker caused major crop losses in the north-central region of the USA in the 1950s, with up to 80% of plants infected and yield reductions of 50% in individual fields. The epidemic was attributed to the widespread use of two highly susceptible cultivars, Hawkeye and Blackhawk (Athow, 1987). The disease declined in importance with reduced plantings of these cultivars (Kulik, 1983), and has remained as a minor problem in the region. In 1987-88, less than 5% of plants were infected in experimental field plots in Minnesota (Whiting and Crookston, 1993).A second epidemic of stem canker developed in the southern states of the USA in the early 1980s, was shown to be caused by a different pathogen and the disease was name southern stem canker (McGee and Biddle, 1987; Morgan Jones, 1989). Southern stem canker has been a major problem in Brazil since 1989 (Yorinori, 1990). A significant epidemic of stem canker broke out in Europe in the 1980s (Vidic and Jasnic, 1988a). Yield was reduced by 50-62% when stem canker infection by the fungus occurred early, with premature wilting and desiccation of the plants. Yield was reduced by 9-20% in plants that were less infected, with spots on the stalk. Yield reductions were dependent on the cultivar; late maturing cultivars were more susceptible than early maturing ones. A highly significant negative correlation was found between yield and severity of infection (R = -6.697), and between 1000-grain weight and degree of infection (R = -0.565) (Vidic and Jasnic, 1988a). In a study of European isolates of D. phaseolorum var. caulivora, seedlings of soyabean varieties Mandarin, Harosoy and Tracy-M and the line J 77-339 were inoculated with five isolates collected in different areas of Vojvodina, Serbia. The reaction of Tracy-M soyabean indicated that the isolates were similar to the northern race, but different from the southern race. A study of Italian isolates of D. phaseolorum var. caulivora reached the same conclusion (DC McGee, Iowa State University, USA, personal communication, 1996).During the 2001-2002 growing season, isolates of D. phaseolorum var. caulivora were obtained from stems of soyabean, exhibiting symptoms of soyabean stem canker, grown in Marcos Juarez, Cordoba; Salto, Buenos Aires; and Diego de Alvear, Santa Fe. Disease incidence in the fields was 10-60, 5-15 and 10-20%, respectively. The isolates were classified as D. phaseolorum var. caulivora on the basis of morphological analysis and pathogenicity tests on cultivars Tracy M, Crockett, Hutchenson and RA 702 (Pioli et al., 2002).
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Published online: 16 November 2021
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