scholarly journals Occurrence of Downy Mildew on Sunflower in South Africa

Plant Disease ◽  
1997 ◽  
Vol 81 (1) ◽  
pp. 111-111 ◽  
Author(s):  
A. Viljoen ◽  
P. S. van Wyk ◽  
D. C. Nowell ◽  
T. J. Gulya

Downy mildew, caused by Plasmopara halstedii (Farl.) Berl. & De Toni in Sacc., is an economically important disease of sunflower (Helianthus annuus L.) in Europe and the United States (1). The disease was first noticed in South Africa in a commercial field near Standerton and in a seed production field near Kroonstad during the 1993 to 1994 planting season. During the 1995 to 1996 season, downy mildew was found in experimental hybrids near Heilbron, and in commercial fields near Heil-bron, Marikana, and Potchefstroom. At Heilbron, five hybrids were infected with P. halstedii, whereas three others showed symptoms of downy mildew at Potchefstroom and Marikana. All commercially cultivated hybrids have been developed in South Africa. Disease incidence in all the fields was low, with less than 1% of plants affected by the disease. Diseased plants were dwarfed and displayed veinal chlorosis of leaves typically associated with downy mildew of sunflower. White fungal growth commonly occurred on lower leaf surfaces. Sunflower seedlings inoculated with P. halstedii produced symptoms characteristic of downy mildew. The occurrence of the disease in many geographic areas and on various hybrids in South Africa suggests that the fungus is well established. Recent outbreaks can be attributed to the cool, wet, climatic conditions of the 1993 to 1994 and 1995 to 1996 seasons. The susceptibility of local hybrids suggests that downy mildew is a potentially dangerous disease of sunflower in South Africa. Reference: (1) J. F. Miller and T. J. Gulya. Crop Sci. 27:210, 1987.

Plant Disease ◽  
2004 ◽  
Vol 88 (10) ◽  
pp. 1163-1163 ◽  
Author(s):  
S. Gaetán ◽  
M. Madia

Canola (Brassica napus) is a developing oleaginous crop grown commercially in the Buenos Aires and Santa Fe provinces of Argentina. During the autumn of 2003, typical signs of powdery mildew were observed on canola plants in experimental field plots in Buenos Aires. Average disease incidence was 42% on 3- to 6-month-old canola cultivars developed in the following countries: Argentina (Eclipse, Impulse Master, Mistral, and Nolza); Australia (Oscar and Rainbow); Canada (Sentry); France (Cadillac, Camberra, and Capitol); and Sweden (Maskot, Sponsor, and Wildcat). The range of incidence on these cultivars was 35 to 93%. Other cultivars exhibited an apparent high level of resistance or escaped disease. These included: Charlton (Argentina); 46CO3, Dunkeld, Insignia, Mystic, Monty, Outback, Rivette, and Surpass 400 (Australia), and Caviar (France). Climatic conditions in Buenos Aires, especially rainfall, from March to May 2003 were apparently favorable for powdery mildew development. On susceptible cultivars, fungal growth was observed on leaves, stems, and pods that resulted in premature senescence of the tissues. The mycelium, with multilobed hausthoria, was white to gray, dense or fine, and in patches or covering the entire adaxial leaf surfaces. Appressoria were lobed and conidiophores were straight. Foot cells were cylindrical, straight, measured 35 to 42 × 7 to 10 μm, and were followed by two cells. Conidia were produced singly, cylindrical to ovoid, and measured 36 to 40 × 18 to 20 μm. The conidial length-to-width ratio was 2.0. No fibrosin bodies were observed in the conidia and conidia germinated at the ends. Cleistothecia were not observed. On the basis of mycelial, conidial, and hausthoria characteristics observed on six leaves for each affected cultivar, the fungus was identified as Erysiphe polygoni DC (1). Pathogenicity was confirmed on 5-week-old canola plants of cvs. Eclipse, Impulse, Master, Mistral, and Maskot by gently pressing (1 min) one adaxial infected leaf with abundant sporulation onto one adaxial healthy leaf. The experiment, which included five inoculated plants and three noninoculated control plants for each cultivar, was conducted in a greenhouse at 22 to 24°C and maintained at 75% relative humidity with no supplemental light. Inoculated and control plants were covered with polyethylene bags for 48 h after inoculation. Powdery mildew developed on all inoculated plants of all cultivars after 12 to14 days. The control plants did not develop disease. The experiment was repeated with similar results. E. polygoni has a worldwide distribution (2); however, the results suggest that this fungus may be a threat to the main cultivars being grown in Argentina (Eclipse, Impulse, Master, Mistral, and Nolza), since high levels of disease incidence, as much as 70%, were observed. Under propitious environments, this pathogen could cause severe yield losses in commercially grown canola in Argentina. To our knowledge, this is the first report of canola powdery mildew caused by E. polygoni in Argentina. References: (1) H. J. Boesewinkel. Rev. Mycol. Tome 41:493, 1977. (2) D. F. Farr et al. Fungi on Plants and Plant Products in the United States. The American Phytopathological Society, St.Paul, MN, 1989.


Plant Disease ◽  
2014 ◽  
Vol 98 (5) ◽  
pp. 696-696 ◽  
Author(s):  
J. A. Crouch ◽  
M. P. Ko ◽  
J. M. McKemy

Downy mildew of impatiens (Impatiens walleriana Hook.f.) was first reported from the continental United States in 2004. In 2011 to 2012, severe and widespread outbreaks were documented across the United States mainland, resulting in considerable economic losses. On May 5, 2013, downy mildew disease symptoms were observed from I. walleriana ‘Super Elfin’ at a retail nursery in Mililani, on the Hawai'ian island of Oahu. Throughout May and June 2013, additional sightings of the disease were documented from the islands of Oahu, Kauai, Maui, and Hawai'i from nurseries, home gardens, and botanical park and landscape plantings. Symptoms of infected plants initially showed downward leaf curl, followed by a stippled chlorotic appearance on the adaxial leaf surfaces. Abaxial leaf surfaces were covered with a layer of white mycelia. Affected plants exhibited defoliation, flower drop, and stem rot as the disease progressed. Based on morphological and molecular data, the organism was identified as Plasmopara obducens (J. Schröt.) J. Schröt. Microscopic observation disclosed coenocytic mycelium and hyaline, thin-walled, tree-like (monopodial branches), straight, 94.0 to 300.0 × 3.2 to 10.8 μm sporangiophores. Ovoid, hyaline sporangia measuring 11.0 to 14.6 × 12.2 to 16.2 (average 13.2 × 14.7) μm were borne on sterigma tips of rigid branchlets (8.0 to 15.0 μm) at right angle to the main axis of the sporangiophores (1,3). Molecular identification of the pathogen was conducted by removing hyphae from the surface of three heavily infected leaves using sterile tweezers, then extracting DNA using the QIAGEN Plant DNA kit (QIAGEN, Gaithersburg, MD). The nuclear rDNA internal transcribed spacer was sequenced from each of the three samples bidirectionally from Illustra EXOStar (GE Healthcare, Piscataway, NJ) purified amplicon generated from primers ITS1-O and LR-0R (4). Resultant sequences (GenBank KF366378 to 80) shared 99 to 100% nucleotide identity with P. obducens accession DQ665666 (4). A voucher specimen (BPI892676) was deposited in the U.S. National Fungus Collections, Beltsville, MD. Pathogenicity tests were performed by spraying 6-week-old impatiens plants (I. walleriana var. Super Elfin) grown singly in 4-inch pots with a suspension of 1 × 104 P. obducens sporangia/ml until runoff using a handheld atomizer. Control plants were sprayed with distilled water. The plants were kept in high humidity by covering with black plastic bags for 48 h at 20°C, and then maintained in the greenhouse (night/day temperature of 20/24°C). The first symptoms (downward curling and chlorotic stippling of leaves) and sporulation of the pathogen on under-leaf surfaces of the inoculated plants appeared at 10 days and 21 days after inoculation, respectively. Control plants remained healthy. Morphological features and measurements matched those of the original inoculum, thus fulfilling Koch's postulates. To our knowledge, this is the first report of downy mildew on I. walleriana in Hawai'i (2). The disease appears to be widespread throughout the islands and is likely to cause considerable losses in Hawai'ian landscapes and production settings. References: (1) O. Constantinescu. Mycologia 83:473, 1991. (2) D. F. Farr and A. Y. Rossman. Systematic Mycology and Microbiology Laboratory, ARS, USDA. Retrieved from http://nt.ars-grin.gov/fungaldatabases/ July 16, 2013. (3) P. A. Saccardo. Syllogue Fungorum 7:242, 1888. (4) M. Thines. Fungal Genet Biol 44:199, 2007.


Plant Disease ◽  
1998 ◽  
Vol 82 (5) ◽  
pp. 591-591 ◽  
Author(s):  
S. T. Koike ◽  
P. A. Nolan ◽  
S. A. Tjosvold ◽  
K. L. Robb

In California, hybrid statice (Misty series; Limonium bellidifolium × Limonium latifolium) is grown as a commercial cutflower crop in fields and greenhouses. In 1997, downy mildew was observed on statice plantings in both southern (San Diego County) and central (Monterey and Santa Cruz counties) parts of coastal California. Initial symptoms consisted of light green, irregularly shaped leaf spots that, after a few days, became chlorotic. As disease progressed, chlorotic spots coalesced and turned necrotic, at times resulting in extensive death of leaf tissues. Under favorable conditions, the purple to gray sporulation of the pathogen could be seen on abaxial surfaces of leaves. Conidiophores had main trunks with dichotomous branches and measured 194 to 335 μm in length (mean = 229 μm) from the base to the first branches and 7 to 8 μm across at the widest part. Branch ends were slender with curved tips that measured 5 to 8 μm long. Conidia were ovoid to globose with very short pedicels, and measured 14 to 19 μm × 14 to 17 μm. Conidial surfaces appeared slightly roughened when viewed with a scanning electron microscope. Clearing leaf sections with 10% NaOH (1) revealed the presence of yellow-brown, globose oospores that measured 31 to 47 μm. The pathogen was identified as Peronospora statices (1). Pathogenicity was demonstrated by pressing leaves with abundant sporulation against healthy leaves of test plants (Misty White) and then placing inoculated plants in a humidity chamber. After 10 to 12 days, symptoms similar to those originally observed developed on inoculated plants; after 14 to 16 days, purple fungal growth morphologically similar to the original isolates grew on leaves. Uninoculated control plants did not develop symptoms or signs of downy mildew. This is the first report of downy mildew caused by P. statices on statice in California and the rest of the United States. The disease has also been confirmed on Blue Fantasia (L. bellidifolium × L. perezii). This disease has been reported previously in Italy, The Netherlands, and the United Kingdom (1). Reference: (1) G. S. Hall et al. Eur. J. Plant Pathol. 103:471, 1997.


Plant Disease ◽  
2004 ◽  
Vol 88 (8) ◽  
pp. 909-909 ◽  
Author(s):  
S. N. Wegulo ◽  
S. T. Koike ◽  
M. Vilchez ◽  
P. Santos

During February 2004, diseased double impatiens (Impatiens walleriana) plants were received from a commercial grower in southern California. The upper surfaces of symptomatic leaves were pale yellow with no distinct lesions. Diseased leaves later wilted, and severely affected leaves abscised from the stem. At the nursery, only double impatiens plants in the Fiesta series were infected, and some cultivars were more heavily infected than others. Disease incidence in cv. Sparkler Hot pink was nearly 100%. The interior of infected leaves was colonized by coenocytic mycelium. A conspicuous white growth was observed only on the underside of leaves. Sporangiophores were hyaline, thin walled, emergent from stomata, and had slightly swollen bases. Sporangiophore branching was distinctly monopodial. Smaller sporangiophore branches were arranged at right angles to the supporting branches, and tips of branches measured 8 to 14 μm long. Sporangia were ovoid and hyaline with a single pore on the distal ends. Distal ends of sporangia were predominantly flat but occasionally had a slight papilla. Short pedicels were present on the attached ends. Sporangia measured 19.4 to 22.2 (-25.0) μm × 13.9 to 16.7 (-19.4) μm. Oospores were not observed in leaf tissue. On the basis of symptoms and morphology of the organism, the pathogen was identified as Plasmopara obducens J. Schröt. Pathogenicity tests were done on double type cvs. Fiesta, Tioga Red, and Tioga Cherry Red and on single type cvs. Cajun Watermelon and Accent Lilac. Plants were spray inoculated with sporangiospore suspensions (1 × 104 sporangiospores per milliliter), incubated for 24 h in a dew chamber (18 to 20°C), and then maintained in a greenhouse (22 to 24°C). Symptoms and signs of downy mildew developed after 12 days only on inoculated cv. Fiesta plants, and the pathogen morphology matched that of the originally observed pathogen. Nontreated control plants did not develop downy mildew. To our knowledge, this is the first report of downy mildew on impatiens in California. P. obducens is one of two causal agents of downy mildew of impatiens (2,4). The other pathogen, Bremiella sphaerosperma, has dichotomous sporangiophore branching and causes lesions with well-defined margins (2,4). In the United States, the disease has been recorded in the eastern and northeastern states and in Indiana, Minnesota, Mississippi, Montana, and Wisconsin (3). In Canada, the disease has been recorded in Manitoba and Quebec (1). References: (1) I. L. Conners. An Annotated Index of Plant Diseases in Canada and Fungi Recorded on Plants in Alaska, Canada, and Greenland. Research Branch, Canada Department of Agriculture, Publication 1251, 1967. (2) O. Constantinescu. Mycologia 83:473, 1991. (3) D. F. Farr et al. Fungi on Plants and Plant Products in the United States. The American Phytopathological Society, 1989. (4) G. W. Wilson. Bull. Torrey Bot. Club 34:387, 1907.


Koedoe ◽  
1991 ◽  
Vol 34 (1) ◽  
Author(s):  
G.H. Groenewald

Five types of burrow casts from the Lystrosaurus- Procolophon Assemblage-zone (Palingkloof Member and Katberg Formation, Triassic, Karoo sequence. South Africa) are associated with casts of desiccation cracks and red mudstone. Vertebrate remains of Lystrosaurus sp. and Procolophon sp. indicate that these animals probably made the burrows during the Triassic. It is possible that burrowing was an adaptive advantage during periods of severe and unfavourable climatic conditions. Similar burrow casts were found in the Dicynodon-Theriognathus Assemblage-zone, suggesting a burrowing habit for fauna represented in this zone. In structure, the burrow casts resemble those of Scoyenia, Thalassinoides, Histioderma, Gyrolithes and Planolites reported from Germany, France, Asia, Ireland, Spain and the United States of America.


2002 ◽  
Vol 92 (7) ◽  
pp. 794-802 ◽  
Author(s):  
T. L. Peever ◽  
A. Ibañez ◽  
K. Akimitsu ◽  
L. W. Timmer

Sixty-five isolates of Alternaria alternata were sampled from brown spot lesions on tangerines and mandarins (Citrus reticulata) and tangerine × grapefruit (C. reticulata × C. paradisi) hybrids in the United States, Colombia, Australia, Turkey, South Africa, and Israel to investigate the worldwide phylogeography of the fungus. Genetic variation was scored at 15 putative random amplified polymorphic DNA (RAPD) loci and 465 bp of an endo-polygalacturonase (endo-PG) gene was sequenced for each isolate. Cluster analysis of RAPD genotypes revealed significant differentiation between United State and Colombia isolates and Turkey, South Africa, Israel, and Australia isolates. Sequencing of endo-PG revealed 21 variable sites when the outgroup A. gaisen (AK-toxin-producing pathogen of Japanese pear) was included and 13 variable sites among the sampled isolates. Nucleotide substitutions at 10 of 13 variable sites represented silent mutations when endo-PG was translated in frame. Eight distinct endo-PG haplotypes were found among the sampled isolates and estimation of a phylogeny with endo-PG sequence data revealed three clades, each with strong bootstrap support. The most basal clade (clade 1) was inferred based on its similarity to the outgroup A. gaisen and consisted exclusively of pathogenic isolates from the United States and Colombia. Clade 2 consisted of pathogenic and nonpathogenic isolates from the United States, Australia, South Africa, and Israel and clade 3 contained pathogenic and nonpathogenic isolates from Australia, South Africa, Israel, and Turkey. Quantitative estimates of virulence (disease incidence) were obtained for isolates from the United States, Colombia, South Africa, Israel, and Turkey by spray inoculating detached citrus leaves and counting the number of lesions 24 h after inoculation. Large differences in virulence were detected among isolates within each location and isolates from the United States were significantly more virulent than isolates from other locations. Several isolates from Colombia, South Africa, Israel, and Turkey had low virulence and 8% of all isolates were nonpathogenic. All but one of the nonpathogenic isolates were found in clade 2 of the endo-PG phylogeny, which also included the most highly virulent isolates sampled.


Plant Disease ◽  
2007 ◽  
Vol 91 (11) ◽  
pp. 1392-1396 ◽  
Author(s):  
B. M. Irish ◽  
J. C. Correll ◽  
S. T. Koike ◽  
T. E. Morelock

Spinach downy mildew, caused by Peronospora farinosa f. sp. spinaciae, is the most economically important disease of spinach worldwide. During the past few years, spinach cultivars resistant to the seven previously described races of P. farinosa f. sp. spinaciae were observed to be severely affected by downy mildew in both the United States and the European Union. Four new isolates of P. farinosa f. sp. spinaciae were collected from California and The Netherlands and characterized based on disease reactions on two modified sets of spinach differentials. The results led to the description of three new races of the downy mildew pathogen, designated races 8, 9, and 10. Four differential cultivars with resistance to races 1 to 7 were used to distinguish the three new races. Dolphin was susceptible to races 8 and 10 but resistant to race 9; Lion was susceptible to race 10 but resistant to races 8 and 9; Lazio was resistant to races 1 to 7 as well as races 8, 9, and 10; and Tarpy was susceptible to all three new races. The three new races also were used to evaluate the disease reactions on 43 contemporary commercial spinach cultivars in greenhouse trials. A survey of 58 isolates of P. farinosa f. sp. spinaciae collected in California and Arizona between 2004 and 2006 revealed that race 10 predominated in the areas sampled.


Plant Disease ◽  
2005 ◽  
Vol 89 (5) ◽  
pp. 530-530 ◽  
Author(s):  
S. Gaetán ◽  
M. Madia

Canola (Brassica napus) was introduced as an alternative crop for wheat in Argentina. During 2003, typical symptoms of stem rot disease were observed on canola plants in two commercial fields located at Bragado, in northern Buenos Aires Province in Argentina. Average disease incidence across four canola cultivars was 21% (range = 13 to 29%). Symptoms included chlorosis and wilting of foliage and necrosis of basal stems. The disease appeared singly or in patches consisting of 4- to 5-month-old plants. The first visible symptom noticed was chlorosis and wilting of the foliage beginning from the basal leaves. Infection of the main stem at ground level typically was followed by a grayish white discoloration that progressed above the soil line to the apex. In advanced stages of the disease, stems and branches became bleached and eventually died. Black and irregularly shaped sclerotia (average size 5.5 × 2.8 mm) inside necrotic stem tissue were the typical signs of the pathogen. From September to October 2003, four samples consisting of six affected plants per sample were arbitrarily collected from two commercial fields located at Bragado. Sclerotia were taken from diseased stems, dipped in 70% ethanol, surface sterilized with 1% sodium hypochlorite for 1 min, and rinsed in sterile water. Each sclerotium was blotted dry on sterile Whatman's filter paper and placed on potato dextrose agar. Plates were incubated in the dark at 25°C for 2 to 3 days, followed by incubation under 12-h NUV light/12-h dark for 6 to 8 days. Six resulting colonies were identified as Sclerotinia sclerotiorum (Lib.) de Bary on the basis of taxonomic characteristics of the plant pathogenic species of Sclerotinia (3). Koch's postulates for three fungal isolates from infected plants were carried out on 6-week-old canola plants (cvs. Eclipse, Impulse, Master, and Mistral) by placing a colonized agar disk into wounds made in the basal stem region with a sterile scalpel. Pathogenicity tests, which included five inoculated and three control plants potted in a sterilized soil mix (soil/sand, 3:1), were conducted in a greenhouse at 23 to 26°C and 75% relative humidity with no supplemental light. Characteristic symptoms identical to the original observations developed within 12 days after inoculation on 100% of the inoculated plants for three isolates. Symptoms included wilted foliage, collapsed plants, and plant death. White mycelium and sclerotia developed on infected tissues, and the pathogen was successfully reisolated from symptomatic plants in all instances. Control plants, which were treated similarly except that the agar disk did not contain fungal growth, remained healthy. The experiment was repeated, and the results were identical to the first inoculations. Canola stem rot disease incited by S. sclerotiorum was first reported in Argentina during 1995 at experimental field plots in Buenos Aires. S. sclerotiorum, which has been reported to cause disease in canola in Canada (2) and the United States (1,4), currently represents a serious problem to the main canola cultivars grown in Argentina. To our knowledge, this is the first report of the occurrence of S. sclerotiorum causing a high incidence of stem rot in commercial crops of canola in Argentina. References: (1) D. F. Farr et al. Fungi on Plants and Plant Products in the United States. The American Phytopathological Society, St. Paul, MN, 1989. (2) L. B. Jamaux et al. Plant Pathol. 44:22, 1995. (3) L. M. Kohn. Phytopathology 69:881, 1979. (4) D. V. Phillips et al. Phytopathology 92:785, 2002.


Plant Disease ◽  
2002 ◽  
Vol 86 (5) ◽  
pp. 562-562 ◽  
Author(s):  
R. Buonaurio ◽  
G. Natalini ◽  
L. Covarelli ◽  
C. Cappelli

Between 1997 and 2000, black dot of potato (Solanum tuberosum L.), caused by the polyphagous soilborne fungus Colletotrichum coccodes (Wallr.) Hughes, was observed each summer in fields located in Umbria (central Italy). Disease incidence ranged from 50 to 100%, and early potato cultivars were generally more susceptible than late-maturing ones. Disease symptoms were first observed during August as a yellowing and wilting of foliage in the tops of plants, followed by rotting of the roots and stems, which led to the premature death of 50 to 70% of plants. Setose1 sclerotia (300 to 500 mm in diameter) and acervuli of the fungus were found on roots and stems of infected plants. Acervuli produced hyaline, aseptate, cylindrical conidia (16 to 22 × 2.5 to 4.5 μm) formed on unicellular cylindrical phialidic conidiophores. The fungus was isolated from diseased stems and roots on potato dextrose agar (PDA) at pH 6.5. Pathogenicity of the fungus was confirmed by fulfilling Koch's postulates using 3- to 4-week-old potato plants of a local cultivar. A superficial 5-mm vertical cut was made with a scalpel into the base of potato stems (2 cm beneath the soil surface), and 5-mm-diameter plugs of PDA alone (control plants) or PDA plus fungal growth were placed over the cuts. The wounds were sealed with wet cotton swabs that were held in place with Parafilm. Symptoms that resembled those in the field were observed on inoculated plants 6 to 8 weeks postinoculation. Symptoms did not appear on the control plants. The same fungus was reisolated from the diseased plants. Based on morphological characteristics of sclerotia, acervuli, and conidia, as well as pathogenicity tests, the fungus was identified as C. coccodes. To our knowledge, this is the first report of C. coccodes as the causal agent of black dot of potato in central Italy. We did not observe foliar outbreaks of the disease, which were reported from the United States (2). In both 1921 (1) and 1951 (3), the fungus was reported to cause severe outbreaks of the disease in northern Italy. Since then, its presence in Italy has been rarely recorded in potato (4). The occurrence of extremely dry and hot weather conditions during the summers of 1997 to 2000, which are favorable for disease development, made the disease particularly severe. We cannot exclude the possibility that the disease may have been present in central Italy before our observations, as it can be misdiagnosed and its symptoms can be masked by the symptoms of other diseases. The significance of black dot in central Italy needs to be reappraised in terms of both yield loss and tuber quality. References: (1) C. Arnaudi. Atti Ist. Bot. Univ. Pavia. Ser. 3, 1:71, 1924. (2) A. W. Barkdoll and J. R. Davis. Plant Dis. 76:131, 1992. (3) G. Goidanich. Inf. Fitopatol. 1:5, 1951. (4) S. Vitale et al. J. Plant Pathol. 80:265, 1998.


2017 ◽  
Vol 38 (SI 2 - 6th Conf EFPP 2002) ◽  
pp. 590-592
Author(s):  
T. Duvnjak ◽  
M. Vrataric ◽  
A. Sudaric ◽  
J. Cosic

The main objective of this study was to determinate the occurrence and intensity of attack by the more important fungal diseases on soybean in Eastern Croatia. Four-year investigation (1998–2001) was undertaken on 10 domestic soybean cultivars with different level of disease resistance. The investigation was set in two planting date (optimal and delayed) on experimental fields of the Agricultural Institute Osijek. Following more important diseases were established: Downy mildew, Pod and stem blight and Stem canker. Significant differences in disease incidence were caused by genetic diversity of tested materials as well as different climatic conditions among growing seasons. According to planting date, significantly higher incidence of Downy mildew and Pod and stem blight was in optimal planting date.


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