Academic literature on the topic 'Field pea blackspot'

Sixty commercial pea crops were surveyed in 1995 to determine the causes of declining yields. Blackspot (Mycosphaerella pinodes and Phoma medicaginis var. pinodella) and downy mildew (Peronospora viciae) were prevalent in most crops and were identified as probable major contributors to the syndrome. Short rotation intervals (<5 years) between pea crops in paddocks were correlated with increased levels of blackspot and lower grain yields. Early sowing dates were correlated with increased levels of blackspot. A detailed survey of blackspot development was conducted in 5 commercial paddocks in 1996. The relative importance of sowing time and rotation varied between regions and seasons. The impact of a range of herbicides and the micronutrients manganese and zinc on blackspot, caused by the M. pinodes component of the blackspot complex, was investigated in a field trial during 1996. The herbicides diuron, metribuzin, and fluazifop significantly increased blackspot crown lesions compared with the nil treatment. There was a significant interaction between blackspot severity, herbicides, and the micronutrients manganese and zinc. Manganese concentration in pea plants was negatively correlated with the severity of blackspot crown lesions and positively correlated with severity of downy mildew.

Black spot is a major disease of field pea (Pisum sativum L.) production across southern Australia. Known causal agents in Australia include one or more of Mycosphaerella pinodes (Berk. & Bloxam) Vestergr., Phoma medicaginis var. pinodella (L.K. Jones), Ascochyta pisi Lib., or P. koolunga (Davidson, Hartley, Priest, Krysinska-Kaczmarek, Herdina, McKay & Scott) (2), but other pathogens may also be associated with black spot symptoms. Black spot generally occurs on most plants and in most pea fields in Western Australia (W.A.), and during earlier winter/spring surveys of blackspot pathogens, some isolates were tentatively allocated to P. medicaginis var. pinodella despite different cultural characteristics on potato dextrose agar (PDA). Recently, single-spore isolations of a single culture each from an infested pea crop at Medina, Moora, and Mt. Barker in W.A. were made onto PDA. A PCR-based assay with TW81 and AB28 primers was used to amplify from the ITS-5.8S rDNA region. Purified DNA products were sequenced for the three isolates and then BLASTn was used to compare sequences with those in GenBank. Our sequences (GenBank Accession Nos. JN37743, JN377439, and JN377438) had 100% nucleotide identity with P. exigua Desm. var. exigua accessions (GI13385450, GI169894028, and GI189163921), an earlier synonym of what is now known as Boeremia exigua var. exigua ([Desm.] Aveskamp, Gruyter & Verkley) (1). Davidson et al. (2) used the same primers to identify P. koolunga, but none of our isolates were P. koolunga. A suspension of 107 conidia ml–1 of each representative isolate was inoculated onto foliage of 15-day-old field pea cv. Dundale plants and maintained at >90% relative humidity for 72 h postinoculation. Control plants inoculated with just water remained symptomless. Brown lesions were evident by 8 to 10 days postinoculation and mostly 1 to 3 mm in diameter. B. exigua var. exigua was readily reisolated from infected leaves. Isolates have been lodged in the W.A. Culture Collection Herbarium maintained at the Department of Agriculture and Food W.A. (Accession Nos. WAC13500, WAC13502, and WAC13501 from Medina, Moora, and Mt. Barker, respectively). Outside Australia, its synonym P. exigua var. exigua is a known pathogen of field pea (4), other legumes including common bean (Phaseolus vulgaris L.) (4) and soybean (Glycine max [L.] Merr.) (3), and is known to produce phytotoxic cytochalasins. In eastern Australia, P. exigua var. exigua has been reported on common bean (1930s and 1950s), phasey bean (Macroptilium lathyroides [L.] Urb.) and siratro (M. atropurpureum (DC.) Urb.) (1950s and 1960s), mung bean (Vigna radiata [L.] Wilczek.) (1960s), ramie (Boehmeria nivea [L.] Gaudich.) (1939), potato (Solanum tuberosum L.) (1980s), and pyrethrum (Tanacetum cinerariifolium [Trevir.] Schultz Bip.) (2004 and 2007) (Australian Plant Pest Database). To our knowledge, this the first report of B. exigua var. exigua on field pea in Australia, and because of its potential to be a significant pathogen on field pea, warrants further evaluation. References: (1) M. M. Aveskamp et al. Stud. Mycol. 65:1, 2010. (2) J. A. Davidson et al. Mycologia 101:120, 2009. (3) L. Irinyi et al. Mycol. Res. 113:249, 2009. (4) J. Marcinkowska. Biul. Inst. Hod. Aklim. Rosl. 190:169, 1994.

Black spot disease on field pea (Pisum sativum) in Australia is generally caused by one or more of the four fungi: Mycosphaerella pinodes (anamorph Ascochyta pinodes), Phoma medicaginis var. pinodella (synonym Phoma pinodella), Ascochyta pisi, and Phoma koolunga (1,2,4). However, in 2010 from a field pea blackspot disease screening nursery at Medina, Western Australia, approximately 25% of isolates were a Phoma sp. that was morphologically different to Phoma spp. previously reported on field pea in Western Australia, while the remaining 75% of isolates were either M. pinodes or P. medicaginis var. pinodella. Single-spore isolations of 23 isolates of this Phoma sp. were made onto potato dextrose agar. A PCR-based assay with the TW81 and AB28 primers was used to amplify from the 3′ end of 16S rDNA, across ITS1, 5.8S rDNA, and ITS2 to the 5′ end of the 28S rDNA. The DNA products were sequenced and BLAST analyses were used to compare sequences with those in GenBank. In each case, the sequence had ≥99% nucleotide identity with the corresponding sequence in GenBank for P. herbarum. Isolates also showed morphological similarities to P. herbarum as described in other reports (e.g., 3). The relevant information for a representative isolate has been lodged in GenBank (Accession No. JN247437). The same primers were used by Davidson et al. (2) to identify P. koolunga, but none of our 23 isolates were P. koolunga. A conidial suspension of 107 conidia ml–1 from a single-spore culture was spray inoculated onto foliage of 10-day-old Pisum sativum cv. Dundale plants maintained under >90% relative humidity conditions for 72 h postinoculation. Symptoms evident by 11 days postinoculation consisted of pale brown lesions that were mostly 1.5 to 2 mm long and 1 to 1.5 mm wide. Approximately 50% of lesions showed a distinct chlorotic halo extending 1 to 2 mm outside the boundary of the lesion. P. herbarum was readily reisolated from infected foliage. A culture of this representative isolate has been lodged in the Western Australian Culture Collection Herbarium maintained at the Department of Agriculture and Food Western Australia (Accession No. WAC13499). Outside of Australia, P. herbarum, while generally considered a soilborne opportunistic pathogen, has been reported on a wide range of species, including field pea (3). Molecular analysis of historical isolates collected from field pea in Western Australia, mostly in the late 1980s, did not show any incidence of P. herbarum, despite this fungus being reported on alfalfa (Medicago sativa) and soybean (Glycine max) in Western Australia in 1985 (Australian Plant Pest Database). In Western Australia, this fungus has also been recorded on a Protea sp. in 1991 and on Arabian pea (Bituminaria bituminosa) in 2010 (Australian Plant Pest Database). To our knowledge, this is the first report of P. herbarum as a pathogen on field pea in Australia. These previous reports of P. herbarum on other hosts in Western Australia and the wide host range of P. herbarum together suggest the potential for this fungus to be a pathogen on a wider range of genera/species than field pea. References: (1) T. W. Bretag and M. Ramsey. Page 24 in: Compendium of Pea Diseases and Pests. 2nd ed. The American Phytopathologic Society, St Paul, MN, 2001. (2) J. A. Davidson et al. Mycologica 101:120, 2009. (3) G. L. Kinsey. Phoma herbarum. No 1501. IMI Descriptions of Fungi and Bacteria, 2002. (4) T. L. Peever et al. Mycologia 99:59, 2007.

Ascochyta blight (blackspot) is a significant disease of field pea (Pisum sativum) with worldwide distribution, causing grain production losses of 15 % per annum in Australia. Phoma koolunga is a relatively new pathogen of this complex disease in Australian field pea crops. This thesis reports information about aspects of the epidemiology of this fungus in Australian conditions.The survival of P. koolunga on field pea stubble and as pseudosclerotia buried in field soil was examined. The frequency of recovery of this fungus declined over time and it was not recovered from stubble buried in soil or placed on the soil surface in pots outdoors at months 11 and 15, respectively, and later. Pseudosclerotia were produced in Petri dishes containing potato dextrose agar (PDA) amended with fluorocytocin or with sand. The maximum longevity of pseudosclerotia buried in soil in pots outdoors was less than 18 months. Infectivity of inoculum of the fungus decreased over time, as the mean number of lesions on plants inoculated with stubble buried or left on the soil surface for up to 6 and 5 months, respectively, and pseudosclerotia retrieved at 14 months and later from field soil did not differ from the water control in a pot bioassay. P. koolunga was isolated from field pea seed samples harvested from South Australia and Victoria. Disease was transmitted to 98 % of seedlings that emerged from artificially inoculated seeds (AIS) in growth room conditions. Seedling emergence rate from AIS at 8° C soil temperature was lower than at 12, 16 and 20° C and also disease severity on seedlings was greater at the lower temperature. Efficacy of fungicides as seed dressings was examined on AIS. P-Pickel T® and Jockey Stayer® were the most effective fungicides among six tested for reducing disease incidence and severity due to P. koolunga on seedlings that emerged from AIS sown in soil and on germination paper, respectively. The reaction of 12 field pea genotypes to one moderately virulent isolate of P. koolunga was evaluated by spraying a pycnidiospore suspension on plants in controlled conditions and assessing disease severity at 2-5 day intervals for 21 days. Sturt, Morgan and Parafield showed more severe disease on leaves than the other genotypes at 21 days post-inoculation (dpi), and Kaspa, PBA Twilight, PBA Oura, PBA Wharton and WAPEA2211 were less susceptible. When three isolates of P. koolunga which varied in virulence were sprayed on four genotypes of short, semi-leafless type peas, Morgan and WAPEA2211 showed more disease than Kaspa at 21 dpi. Aggressiveness of isolates of P. koolunga on these four genotypes differed based on % leaf area diseased up to 14 dpi, but this difference had disappeared by 21 dpi. Some isolates of P. koolunga from seeds showed atypical morphology and reproductive behaviour. These cultures had rhizoid form mycelia on growth media such as PDA. Also, some atypical cultures of P. koolunga sectored from typical colonies on PDA. These sectors and cultures were confirmed as P. koolunga by DNA test using P. koolunga-specific primers. Mycelium from these sectors produced small lesions on leaves and stems of field pea seedling resembling ascochyta blight symptoms in controlled conditions. Pycnidium-like structures of these atypical cultures did not contain pycnidiospores, but had many round and hyaline fatty guttulae of different sizes, usually smaller than normal spores of P. koolunga which never germinated. Crossing 19 isolates of P. koolunga in vitro failed to initiate formation of pseudothecia of P. koolunga on pea stem pieces or on several growth media. This fungus might need specific environmental conditions for production of pseudothecia which still are unknown. The results of this study provide information about survival of P. koolunga, transmission to seedlings via infected seed, control of the fungus in seed and also reaction of field pea genotypes to this pathogen in South Australian conditions. These findings improve the understanding of epidemiology of this disease and consequently can help to improve management of this pathogen in the field.
Thesis (Ph.D.) (Research by Publication) -- University of Adelaide, School of Agriculture, Food and Wine, 2015.