Timing of Occurrence of Claviceps purpurea Ascospores in Northeast Oregon

2010 ◽  
Vol 11 (1) ◽  
pp. 2 ◽  
Author(s):  
Stephen C. Alderman ◽  
Darrin L. Walenta ◽  
Philip B. Hamm

Ergot, caused by Claviceps purpurea, is an important floral disease of grasses, characterized by sclerotium formation within the host flowers. To determine whether annual variation in ergot severity in Kentucky bluegrass is a result of ascospore density and/or timing of ascospore occurrence, Burkard 7-day volumetric spores traps were used to monitor ascospores of C. purpurea in each of two Kentucky bluegrass fields in the Grand Ronde Valley in northeastern Oregon between mid-May and late June, 2008-2010. Ascospores were typically trapped between midnight and 6:00 a.m. In 2008 and 2010, most ascospores were released prior to flowering in Kentucky bluegrass, corresponding to no observed ergot in 2008 and a low level of ergot in 2010. In 2009, ascospore release and pollination coincided, but few airborne ascospores were present, resulting in a low level of ergot. Similar ergot levels were observed in fungicide trials, suggesting that fungicides for ergot control were unnecessary. In years when there are few ascospores during flowering in Kentucky bluegrass, a reduction of up to two fungicide applications may be possible. Accepted for publication 2 November 2010. Published 23 November 2010.

Plant Disease ◽  
2016 ◽  
Vol 100 (10) ◽  
pp. 2080-2086 ◽  
Author(s):  
Sai Sree Uppala ◽  
B. M. Wu ◽  
S. C. Alderman

Claviceps purpurea is an important ovary-infecting pathogen that replaces seed with sclerotia in Kentucky bluegrass grown for seed. Sclerotia overwinter in the soil and germinate in the spring to produce ascospores that infect grass seed ovaries. To better understand environmental conditions affecting ascospore production, the effects of preconditioning cold treatment and subsequent incubation temperature on germination of sclerotia were determined in growth chambers under controlled conditions. Preconditioning cold treatment was essential for germination only in treatments where the incubation temperature was high (at least higher than 20°C). At lower incubation temperatures (10 to 20°C), preconditioning also played a role in improving sclerotial germination. Preconditioning at 4°C (in darkness) for 4 to 8 weeks followed by incubation at 10 and 20°C (cycle of 12 h each of darkness and light), or constant 15°C (cycle of 12 h each of darkness and light), was optimal for ergot germination. When sclerotia were preconditioned for 4 weeks or longer, number of incubation days required for initiation of germination was not affected by temperature in the range from 10 to 25°C (cycle of 12 h each of darkness and light), although the duration of germination (or the progress speed of germination) was still affected by temperature. A simple model was developed based on laboratory results and validated with historic spore trap data collected from various Kentucky bluegrass fields in Oregon (Willamette Valley, central Oregon, and Grande Ronde Valley). The prediction model could predict ascospore onset well and explained 55% of variation in the data.


Plant Disease ◽  
2003 ◽  
Vol 87 (9) ◽  
pp. 1043-1047 ◽  
Author(s):  
Steve C. Alderman ◽  
Reed E. Barker

Ergot, caused by Claviceps purpurea, is an important disease of Kentucky bluegrass grown for seed. Resistance is a preferred means of disease control, although approaches to evaluating ergot resistance in Kentucky bluegrass are not well established. A large scale disease assessment trial was established to compare within-year and year-to-year variability among measures of ergot incidence or severity in Kentucky bluegrass and to determine the most efficient approaches for cultivar evaluation. The susceptibility of 104 Kentucky bluegrass cultivars (78 commercial and 26 experimental) to ergot was assessed, based on percentage of panicles with sclerotia (incidence), sclerotia per panicle (severity), percentage of seeds replaced by sclerotia, or percentage of sclerotia among seed by weight. Cultivar ranking for susceptibility within years was similar for all methods of ergot assessment. Yearly mean incidence of ergot among cultivars ranged from 1.0 to 97.5% for susceptible cv. HV102 to 0.0 to 2.5% for resistant cv. Huntsville, with remaining cultivars distributed between the extremes. Yearly mean values of ergot incidence and severity differed among years. Much of this variability was due to days with rain during the period from flower initiation to maturity (period of susceptibility). Disease incidence was correlated (P ≤ 0.05) with days with rain in 22 of the cultivars. Duration of flowering was correlated (P ≤ 0.05) with ergot incidence in 11 cultivars. Results from this study suggest that variability in host and environment would likely offset any gain in precision of severity data. In large trials in particular, collection of incidence data (percentage of panicles with ergot) would provide the most timely and efficient means for ergot assessment.


2001 ◽  
Vol 94 (6) ◽  
pp. 1471-1476 ◽  
Author(s):  
M. D. Butler ◽  
S. C. Alderman ◽  
P. C. Hammond ◽  
R. E. Berry

Plant Disease ◽  
2015 ◽  
Vol 99 (10) ◽  
pp. 1410-1415 ◽  
Author(s):  
Stephen C. Alderman ◽  
Darrin L. Walenta ◽  
Philip B. Hamm ◽  
Ruth C. Martin ◽  
Jeremiah Dung ◽  
...  

In Kentucky bluegrass (Poa pratensis), Claviceps purpurea, the causal agent of ergot, typically releases ascospores during the early-morning hours, between about midnight and 10:00 a.m., corresponding to time of flowering, when the unfertilized ovaries are most susceptible to infection. During aeromycology studies of C. purpurea in perennial ryegrass (Lolium perenne) in northeastern Oregon during 2008 to 2010 and 2013, a strain of C. purpurea was found that released ascospores in the afternoon, coinciding with flowering in perennial ryegrass. Under controlled environmental conditions, sclerotia from perennial ryegrass and Kentucky bluegrass released spores in the afternoon and morning, respectively, consistent with timing of spore release under field conditions. Internal transcribed spacer (ITS) sequences of single sclerotial isolates from Kentucky bluegrass and perennial ryegrass were consistent with C. purpurea, although minor variations in ITS sequences among isolates were noted. Differences between Kentucky bluegrass and perennial ryegrass isolates were observed in random amplified polymorphic DNA. Evidence is provided for adaptation of C. purpurea to perennial ryegrass by means of delayed spore release that coincides with afternoon flowering in perennial ryegrass.


2012 ◽  
Vol 38 (No. 1) ◽  
pp. 18-22 ◽  
Author(s):  
B. Cagaš ◽  
R. Macháč

Ergot, caused by the fungus Claviceps purpurea (Fr.) Tul., belongs to the main constraints in seed production of Kentucky bluegrass (Poa pratensis L.). The level of ergot occurrence depends on the weather conditions during the growing period, harvest year, storage conditions of seed, and post-harvest treatment. The degree of resistance of the grown cultivar plays an important role. Based on greenhouse trials with four different ergot populations (Zubří, Czech Republic; Leutewitz and Munich, Germany; Pullman, Washington, USA) during 3 years, we found pathogenicity to be one of the most important factors. There were significant differences in the amount of ergot bodies formed between the Central European populations (Zubří, Leutewitz) and the American one from Washington State. The degree of pathogenicity has a major impact on the occurrence of ergot sclerotia in seed of Poa pratensis. 


2020 ◽  
Vol 110 (11) ◽  
pp. 1773-1780
Author(s):  
Qunkang Cheng ◽  
Kenneth E. Frost ◽  
Jeremiah K. S. Dung

Ergot, caused by Claviceps purpurea, is a primary disease concern in irrigated cool-season grass seed production systems of Oregon. In order to better understand the genetic diversity, population structure, and the epidemiology of C. purpurea in grasses grown for seed, 226 isolates were obtained using a hierarchical sampling strategy from two fields each of Kentucky bluegrass (n = 102) and perennial ryegrass (n = 124) and characterized using 12 microsatellite markers. A total of 194 unique multilocus genotypes (MLGs) were identified in this study. There were moderate levels of genotypic diversity (H = 3.43 to 4.23) and gene diversity (Hexp = 0.45 to 0.57) within fields. After clone correction, analysis of molecular variance revealed that 66% of the genetic variation occurred between the two C. purpurea isolates collected from the same seed head of individual plants, indicating that many of the seed heads bearing multiple sclerotia were infected by ascospores rather than conidia. However, the majority of the clonal isolates obtained in this study were collected from the same seed head (i.e., the two isolates were identical MLGs), indicating a role of conidia (honeydew) in secondary infections within seed heads. Genetic differentiation was observed between populations from different hosts (22%) but was confounded by geography. The standardized index of association ranged from 0.007 to 0.122 among the four populations, suggesting potential outcrossing and differences in the relative contribution of ascospores and conidia to ergot among the fields. The results from this study provide insights into the epidemiology of ergot in cool-season grass seed crops of Oregon.


Plant Disease ◽  
1997 ◽  
Vol 81 (7) ◽  
pp. 830-830 ◽  
Author(s):  
G. P. Munkvold ◽  
T. Carson ◽  
D. Thoreson

An outbreak of ergot, caused by Claviceps purpurea, occurred in barley (Hordeum vulgare) grown in northeastern Iowa and southwestern Wisconsin in 1996. In a nine-county area of intensive dairy production in Iowa, approximately 40% of the barley hectarage (approximately 1,200 ha) was affected by the disease. Several cultivars were affected, including Robust, Excel, and Chilton, and no differences in ergot contamination levels were observed among cultivars. Barley samples examined by the Iowa State University Seed Science Center averaged 0.2% ergot by weight, with a maximum of 0.53%. Prolonged cool, wet weather during heading and greater barley planting than usual contributed to the high incidence of infection, but other influential factors have not been identified. Symptoms were not noticed in barley in the field and much of the infested grain was fed to cattle (primarily dairy cows), resulting in a considerable incidence of ergotism. An estimated 1,000 animals displayed symptoms of ergotism, manifested as loss of milk production and hyperthermia. Approximately 10 to 15 animals died or were destroyed. Ergot also was prevalent in forage grasses, including brome (Bromus spp.), Kentucky bluegrass (Poa pratensis), orchardgrass (Dactylis glomerata), quackgrass (Agropyron repens), and timothy (Phleum pratense). Minor symptoms of ergotism were associated with consumption of infested hay and pasture grasses. Negligible incidences of ergot occur annually in small grains and forage grasses in Iowa; ergotism of this extent has not been observed for several decades. Crop rotation and early harvest of grass hay have been recommended for 1997 to prevent a recurrence of the disease.


2006 ◽  
Vol 76 (1) ◽  
pp. 28-33 ◽  
Author(s):  
Yukari Egashira ◽  
Shin Nagaki ◽  
Hiroo Sanada

We investigated the change of tryptophan-niacin metabolism in rats with puromycin aminonucleoside PAN-induced nephrosis, the mechanisms responsible for their change of urinary excretion of nicotinamide and its metabolites, and the role of the kidney in tryptophan-niacin conversion. PAN-treated rats were intraperitoneally injected once with a 1.0% (w/v) solution of PAN at a dose of 100 mg/kg body weight. The collection of 24-hour urine was conducted 8 days after PAN injection. Daily urinary excretion of nicotinamide and its metabolites, liver and blood NAD, and key enzyme activities of tryptophan-niacin metabolism were determined. In PAN-treated rats, the sum of urinary excretion of nicotinamide and its metabolites was significantly lower compared with controls. The kidneyα-amino-β-carboxymuconate-ε-semialdehyde decarboxylase (ACMSD) activity in the PAN-treated group was significantly decreased by 50%, compared with the control group. Although kidney ACMSD activity was reduced, the conversion of tryptophan to niacin tended to be lower in the PAN-treated rats. A decrease in urinary excretion of niacin and the conversion of tryptophan to niacin in nephrotic rats may contribute to a low level of blood tryptophan. The role of kidney ACMSD activity may be minimal concerning tryptophan-niacin conversion under this experimental condition.


1983 ◽  
Vol 28 (1) ◽  
pp. 79-79
Author(s):  
Claire B. Ernhart

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