scholarly journals First Report of Resistance to Mefenoxam in Phytophthora cactorum in the United States and Elsewhere

Plant Disease ◽  
2004 ◽  
Vol 88 (5) ◽  
pp. 576-576 ◽  
Author(s):  
S. N. Jeffers ◽  
G. Schnabel ◽  
J. P. Smith

Phytophthora cactorum causes crown rot of strawberry (Fragaria × ananassa) (2), a disease that has been particularly severe during the last 5 years in the southeastern United States. In the fall of 2001, strawberry plants (cv. Camarosa) in a field in Lexington County, South Carolina exhibited typical crown rot symptoms (2) 1 to 2 weeks after transplanting, even though plants had been drenched with mefenoxam (Ridomil Gold; Syngenta Crop Protection, Greensboro, NC) immediately after transplanting. Initially, we observed leaves that had marginal necrosis, were smaller than normal, and were discolored. Soon after, diseased plants appeared stunted and unthrifty compared with other plants in the field, and some of these plants eventually wilted and died. Severely affected plants had necrotic roots and decayed crowns. Ten symptomatic plants were collected for isolation. In the laboratory, root and crown tissues were rinsed in running tap water and blotted dry, small pieces of necrotic tissue were placed aseptically on PAR-V8 selective medium (1), and isolation plates were placed at 20°C in the dark for up to 7 days. P. cactorum was recovered from six plants. Isolates produced characteristic asexual and sexual structures directly on the isolation plates (i.e., papillate sporangia on sympodial sporangiophores and oospores with paragynous antheridia) (2). A single hypha of an isolate from each plant was transferred to fresh PAR-V8, and pure cultures were stored on cornmeal agar in glass vials at 15°C in the dark. All six isolates from the Lexington County field and nine other isolates of P. cactorum from strawberry (three from South Carolina, three from North Carolina, and three from Florida) were tested for sensitivity to mefenoxam on fungicide-amended medium. Mefenoxam was added to 10% clarified V8 juice agar (cV8A) after autoclaving so the concentration in the medium was 100 ppm. Agar plugs from active colonies were transferred to mefenoxam-amended and nonamended cV8A (three replicates per treatment), plates were placed at 25°C in the dark for 3 days, and linear mycelium growth was measured. All six isolates from Lexington County were highly resistant to mefenoxam with mycelium growth relatively unrestricted on mefenoxam-amended medium (73 to 89% of that on nonamended medium). In comparison, the other nine isolates were sensitive to mefenoxam with mycelium growth severely restricted by 100 ppm of mefenoxam (0 to 7% of that on nonamended medium). To our knowledge, this is the first report of mefenoxam resistance in P. cactorum on strawberry or any other crop in the United States and elsewhere. Because mefenoxam is the primary fungicide used to manage Phytophthora crown rot in the southeastern United States, resistance may limit use of this fungicide in strawberry production. References: (1) A. J. Ferguson and S. N. Jeffers. Plant Dis. 83:1129, 1999. (2) E. Seemüller. Crown rot. Pages 50–51 in: Compendium of Strawberry Diseases, 2nd ed. J. L. Maas, ed. The American Phytopathological Society, St. Paul, MN, 1998.

Plant Disease ◽  
2018 ◽  
Vol 102 (3) ◽  
pp. 686
Author(s):  
M. S. Wiseman ◽  
T. Bonar ◽  
M. I. Gordon ◽  
M. Serdani ◽  
M. L. Putnam

Plant Disease ◽  
2014 ◽  
Vol 98 (5) ◽  
pp. 692-692 ◽  
Author(s):  
D. Fernández-Ortuño ◽  
A. Grabke ◽  
P. K. Bryson ◽  
R. J. Rouse ◽  
P. Rollins ◽  
...  

Botrytis cinerea Pers. is the causal agent of gray mold and one of the most economically important plant-pathogenic fungi affecting strawberry (Fragaria × ananassa). Control of gray mold mainly depends on the use of site-specific fungicides, including the phenylpyrrole fludioxonil. This fungicide is currently registered in combination with cyprodinil in form of Switch 62.5WG (Syngenta Crop Protection, Greensboro, NC) for gray mold control of small fruits in the United States. In June 2013, strawberries affected with symptoms resembling gray mold were observed despite the application of Switch in one field located in Federalsburg, MD, and one located near Chesnee, SC. Ten single-spore isolates, each from a different fruit, were obtained from each location and confirmed to be B. cinerea using cultural and molecular tools as described previously (3). In vitro sensitivity to fludioxonil (Scholar SC, 20.4% [v/v] active ingredient, Syngenta Crop Protection, Greensboro, NC) was determined using a conidial germination assay as previously described (4). Eight of the 20 isolates (six from Maryland and two from South Carolina) were moderately resistant to fludioxonil, i.e., they grew on medium amended with 0.1 μg/ml fludixonil and showed residual growth at 10 μg/ml (4). The in vitro assay was repeated obtaining the same results. To assess in vivo sensitivity on fungicide-treated fruit, commercially grown strawberries were rinsed with water, dried, and sprayed 4 h prior to inoculation with either water or 2.5 ml/liter of Scholar SC to runoff using a hand mister. Fruit was stab-wounded with a sterile syringe and inoculated with a 30-μl droplet of conidia suspension (106 spores/ml) of either two sensitive or four resistant isolates (two isolates from Maryland and two isolates from South Carolina). Each isolate/treatment combination consisted of 24 mature but still firm strawberry fruit with three 8-fruit replicates. The fruit were kept at 22°C and lesion diameters were measured after 4 days of inoculation. The sensitive isolates developed gray mold symptoms on nontreated (2.5 cm lesion diameter) but not on Scholar SC-treated fruit. The resistant isolates developed gray mold on both, the water-treated control (2.3 cm lesion diameter), and the fungicide-treated fruit (1.8 cm lesion diameter). The experiment was performed twice. To our knowledge this is the first report of fludioxonil resistance in B. cinerea from strawberry fields in Maryland and South Carolina. Resistance to fludioxonil is still rare in the United States and has only been reported in B. cinerea isolates from a Virginia strawberry field (1). The increase in occurrence of resistance to fludioxonil may be a result of increased use of Switch following reports of resistance to other chemical classes in this pathogen in southern strawberry fields (2). References: (1) D. Fernández-Ortuño et al. Plant Dis. 97:848, 2013. (2) D. Fernández-Ortuño et al. Plant Dis. 96:1198, 2012. (3) D. Fernández-Ortuño et al. Plant Dis. 95:1482, 2011. (4) R. W. S. Weber and M. Hahn. J. Plant Dis. Prot. 118:17, 2011.


Plant Disease ◽  
2021 ◽  
Author(s):  
Charles Krasnow ◽  
Nancy Rechcigl ◽  
Jennifer Olson ◽  
Linus Schmitz ◽  
Steven N. Jeffers

Chrysanthemum (Chrysanthemum × morifolium) plants exhibiting stem and foliage blight were observed in a commercial nursery in eastern Oklahoma in June 2019. Disease symptoms were observed on ~10% of plants during a period of frequent rain and high temperatures (26-36°C). Dark brown lesions girdled the stems of symptomatic plants and leaves were wilted and necrotic. The crown and roots were asymptomatic and not discolored. A species of Phytophthora was consistently isolated from the stems of diseased plants on selective V8 agar (Lamour and Hausbeck 2000). The Phytophthora sp. produced ellipsoid to obpyriform sporangia that were non-papillate and persistent on V8 agar plugs submerged in distilled water for 8 h. Sporangia formed on long sporangiophores and measured 50.5 (45-60) × 29.8 (25-35) µm. Oospores and chlamydospores were not formed by individual isolates. Mycelium growth was present at 35°C. Isolates were tentatively identified as P. drechsleri using morphological characteristics and growth at 35°C (Erwin and Ribeiro 1996). DNA was extracted from mycelium of four isolates, and the internal transcribed spacer (ITS) region was amplified using universal primers ITS 4 and ITS 6. The PCR product was sequenced and a BLASTn search showed 100% sequence similarity to P. drechsleri (GenBank Accession Nos. KJ755118 and GU111625), a common species of Phytophthora that has been observed on ornamental and vegetable crops in the U.S. (Erwin and Ribeiro 1996). The gene sequences for each isolate were deposited in GenBank (accession Nos. MW315961, MW315962, MW315963, and MW315964). These four isolates were paired with known A1 and A2 isolates on super clarified V8 agar (Jeffers 2015), and all four were mating type A1. They also were sensitive to the fungicide mefenoxam at 100 ppm (Olson et al. 2013). To confirm pathogenicity, 4-week-old ‘Brandi Burgundy’ chrysanthemum plants were grown in 10-cm pots containing a peat potting medium. Plants (n = 7) were atomized with 1 ml of zoospore suspension containing 5 × 103 zoospores of each isolate. Control plants received sterile water. Plants were maintained at 100% RH for 24 h and then placed in a protected shade-structure where temperatures ranged from 19-32°C. All plants displayed symptoms of stem and foliage blight in 2-3 days. Symptoms that developed on infected plants were similar to those observed in the nursery. Several inoculated plants died, but stem blight, dieback, and foliar wilt were primarily observed. Disease severity averaged 50-60% on inoculated plants 15 days after inoculation. Control plants did not develop symptoms. The pathogen was consistently isolated from stems of symptomatic plants and verified as P. drechsleri based on morphology. The pathogenicity test was repeated with similar results. P. drechsleri has a broad host range (Erwin and Ribeiro 1996; Farr et al. 2021), including green beans (Phaseolus vulgaris), which are susceptible to seedling blight and pod rot in eastern Oklahoma. Previously, P. drechsleri has been reported on chrysanthemums in Argentina (Frezzi 1950), Pennsylvania (Molnar et al. 2020), and South Carolina (Camacho 2009). Chrysanthemums are widely grown in nurseries in the Midwest and other regions of the USA for local and national markets. This is the first report of P. drechsleri causing stem and foliage blight on chrysanthemum species in the United States. Identifying sources of primary inoculum may be necessary to limit economic loss from P. drechsleri.


Plant Disease ◽  
2021 ◽  
Author(s):  
Samara A. Oliveira ◽  
Daniel M. Dlugos ◽  
Paula Agudelo ◽  
Steven N. Jeffers

Root-knot nematodes (RKNs), Meloidogyne spp., are some of the most economically important pathogens of cultivated plants. Meloidogyne javanica is one of the most destructive RKN species and is well known for its broad host range and the severe damage it causes to plant roots (Perry et al. 2009). In Feb 2018, four mature dead and dying hybrid lavender plants (Lavandula ×intermedia ‘Phenomenal’) were collected in Edgefield County, South Carolina, and suspected of having Phytophthora root and crown rot (Dlugos and Jeffers 2018). Greenhouse-grown plants had been transplanted in Dec 2016 and Jan 2017 into a sandy loam soil on a site that had been fallow or in pasture for over 30 years. Some plants began to turn gray and die in summer 2017, and approximately 40% of 1230 plants were symptomatic or dead by Feb 2018. Phytophthora spp. were not isolated from the collected plants but were isolated from plants collected on subsequent visits. Instead, all four plants had small, smooth galls on the roots. Lavender roots were examined microscopically (30-70×), and egg masses of RKNs were observed on the galls. Mature, sedentary RKN females were handpicked from galled roots, and perineal patterns of 10 specimens were examined and identified as M. javanica. Juveniles and eggs were extracted from lavender roots by the method of Coolen and D’herde (1972). To confirm species identification, DNA was extracted from 10 individual juveniles, and a PCR assay was conducted using species-specific primers for M. javanica, Fjav/Rjav (Zijlstra et al. 2000). A single amplicon was produced with the expected size of approximately 720 bp, which confirmed identity as M. javanica. To determine pathogenicity, M. javanica from lavender roots were inoculated onto susceptible tomato plants for multiplication, and severe gall symptoms occurred on tomato roots 60 days later. Nematodes were extracted from tomato roots and inoculated onto healthy, rooted cuttings of ‘Phenomenal’ lavender plants growing in pots of soilless medium in a greenhouse. Plants were inoculated with 0, 1000, 2000, 5000, or 10000 eggs and juveniles of M. javanica. Five single-plant replicates were used for each treatment, and plants were randomized on a greenhouse bench. Plants were assessed 60 days after inoculation, and nematodes were extracted from roots and counted. The reproduction factor was 0, 43.8, 40.9, 9.1, 7.7, and 2.6 for initial nematode populations 0, 1000, 2000, 5000, and 10000, respectively, which confirmed pathogenicity (Hussey and Janssen 2002). Meloidogyne javanica also was recovered in Mar 2018 from galled roots on a ‘Munstead’ (L. angustifolia) lavender plant from Kentucky (provided by the Univ. of Kentucky Plant Disease Diagnostic Laboratories), and an unidentified species of Meloidogyne was isolated in Aug 2020 from a ‘Phenomenal’ plant grown in Florida. COI mtDNA sequences from the SC (MZ542457) and KY (MZ542458) populations were submitted to Genbank. M. javanica previously was found associated with field-grown lavender (hybrid and L. angustifolia) in Brazil, but pathogenicity was not studied (Pauletti and Echeverrigaray 2002). To our knowledge, this is the first report of M. javanica pathogenic to L. ×intermedia in the USA, and the first time RKNs have been proven to be pathogenic to Lavandula spp. following Koch’s Postulates. Further studies are needed to investigate the geographic distribution of M. javanica on lavender and the potential threat this nematode poses to lavender production in the USA.


2017 ◽  
Vol 18 (1) ◽  
pp. 28-34 ◽  
Author(s):  
Chandrasekar (Shaker) S. Kousik ◽  
Pingsheng Ji ◽  
Daniel S. Egel ◽  
Lina M. Quesada-Ocampo

About 50% of the watermelons in the United States are produced in the southeastern states, where optimal conditions for development of Phytophthora fruit rot prevail. Phytophthora fruit rot significantly limits watermelon production by causing serious yield losses before and after fruit harvest. Efficacy of fungicide rotation programs and Melcast-scheduled sprays for managing Phytophthora fruit rot was determined by conducting experiments in Phytophthora capsici-infested fields at three locations in southeastern United States (North Carolina, South Carolina, and Georgia). The mini seedless cultivar Wonder and seeded cultivar Mickey Lee (pollenizer) were used. Five weekly applications of fungicides were made at all locations. Significant fruit rot (53 to 91%, mean 68%) was observed in the nontreated control plots in all three years (2013 to 2015) and across locations. All fungicide rotation programs significantly reduced Phytophthora fruit rot compared with nontreated controls. Overall, the rotation of Zampro alternated with Orondis was highly effective across three locations and two years. Rotations of Actigard followed by Ranman+Ridomil Gold, Presidio, V-10208, and Orondis, or rotation of Revus alternated with Presidio were similarly effective. Use of Melcast, a melon disease-forecasting tool, may occasionally enable savings of one spray application without significantly impacting control. Although many fungicides are available for use in rotations, under very heavy rain and pathogen pressure, the fungicides alone may not offer adequate protection; therefore, an integrated approach should be used with other management options including well-drained fields.


Plant Disease ◽  
2000 ◽  
Vol 84 (11) ◽  
pp. 1250-1250 ◽  
Author(s):  
M. E. Matheron ◽  
M. Porchas

In March 2000, plants began to die within two garbanzo (Cicer arietinum L.) fields about 48 km apart in southwestern Arizona. Initial symptoms included wilting of leaves and stem necrosis on individual branches, followed by entire plant necrosis and death. White mycelium was present on plant stems near the soil surface. In one field, small black irregularly shaped sclerotia (1 mm in diameter) were present on the infected stem surface along with the white mycelia, whereas in the other field the associated sclerotia were of similar shape but larger (5 to 6 mm in diameter). Isolation from diseased garbanzo stem tissue from the respective fields yielded Sclerotinia minor, which produced small sclerotia when cultured on potato-dextrose agar and S. sclerotiorum, which produced the typical larger sclerotia of this species. To fulfill Koch's postulates, healthy plants and associated soil from a garbanzo field with no evidence of infection by Sclerotinia were removed with a shovel and transferred into a series of 8-liter plastic pots. After transporting back to the laboratory, some of the plants were inoculated by wounding stems with a 5-mm-diameter cork borer, placing an agar disk containing either S. minor or S. sclerotiorum onto each wound, securing the agar disk to the stem with plastic tape, then incubating the plants at 25°C for 7 days. Control plants were treated similarly except that agar disks did not contain Sclerotinia. Stems inoculated with S. minor or S. sclerotiorum developed symptoms of wilt and necrosis, including the appearance of white mycelium and sclerotia on the stem surface, whereas control plants remained healthy. S. minor or S. sclerotiorum were recovered from garbanzo stems inoculated with the respective species of the pathogen. Sclerotinia leaf drop, which can be caused by S. minor or S. sclerotiorum on lettuce in Arizona, had been observed in both fields previously. Garbanzo fields in Arizona usually are watered by furrow irrigation. Disease was most severe in areas of the garbanzo fields that were heavily irrigated with resultant wetting of tops of plant beds. Proper management of irrigation water and avoidance of establishing a garbanzo planting in fields following lettuce could help reduce future losses from these pathogens. S. minor previously had been reported as a pathogen on Cicer arietinum from the island of Sardinia (2); however, this is apparently the first report of the pathogen on garbanzo other than in Sardinia. S. sclerotiorum has been reported as a pathogen on this host in several countries including the United States (California) (1) but not previously in the state of Arizona. References: (1) I. W. Buddenhagen, F. Workneh, and N. A. Bosque-Perez. Int. Chickpea Newsl. 19:9–10, 1988. (2) F. Marras. Rev. Appl. Mycol. 43:112, 1964.


Plant Disease ◽  
2008 ◽  
Vol 92 (12) ◽  
pp. 1708-1708 ◽  
Author(s):  
E. Coneva ◽  
J. F. Murphy ◽  
R. Boozer ◽  
N. Velásquez

In 2006, primocane stunted growth and crumbly berry development were observed on 4-year-old Kiowa and Apache blackberry cultivars grown at the Chilton Research and Extension Center, Clanton, AL. Samples from affected plants were tested for virus infection by ELISA kits (Agdia, Inc., Elkhart, IN) specific to each of 14 different viruses. Most samples tested positive for Tobacco ringspot virus (TRSV). TRSV was detected in blackberry samples from North Carolina and South Carolina (2). Bray et al. (1) studied the incidence of viruses in blackberry nursery stock in the United States and reported that 9% of the tested samples contained TRSV. Thus, a survey was conducted for TRSV incidence among commercial blackberry stands in eight counties in Alabama during July 2007. Blackberry plants were observed to express virus-like symptoms including chlorotic spots on leaves, leaf veinal chlorosis, stunting, and combinations thereof. Fruit-bearing plants sometimes had crumbly fruit symptoms characteristic of virus infection. Leaf samples that were collected from symptomatic and nonsymptomatic plants representing 14 cultivars were tested by TRSV ELISA (Agdia, Inc.). Of 180 blackberry samples, 68 tested positive for TRSV. Positive ELISA reactions for TRSV were on average 28 times greater than the reactions of known negative control samples considered negative for TRSV. Blackberry plants shown to be infected with TRSV during the 2007 survey were tested in July 2008 in an effort to confirm the presence of TRSV. Fifty-four percent of the samples tested positive by ELISA with the average positive ELISA value being 21 times higher than the average negative ELISA value for known negative control samples. To further confirm the occurrence of TRSV in Alabama-grown blackberry plants, leaf samples were tested by reverse transcription (RT)-PCR to amplify a 329-bp fragment of the viral coat protein gene (TRSV RNA 2 sequence accession no. NC_005096; primers TRSCP-F (5′-TCTGGCACTATAAGCGGAAG-3′) and TRSCP-R (5′-GAAAACATGGGAGGATGCAC-3′). A single band of the anticipated size was amplified (analyzed by agarose gel electorphoresis and visualized by ethidium bromide staining) from RNA samples extracted with a RNeasy Mini kit (Qiagen, Valencia, CA) from blackberry samples that tested positive for TRSV by ELISA and a known positive control. No amplified product resulted from a blackberry sample that tested negative for TRSV by ELISA. These results illustrate and confirm the presence of TRSV in blackberry leaf tissues grown in Alabama. To our knowledge, this is the first report of TRSV infection of blackberry plants in Alabama. References: (1) M. M. Bray et al. HortScience 40:874, 2005. (2) T. L. Guzmán-Baeny. Incidence, distribution, and symptom description of viruses in cultivated blackberry (Rubus subgenus Eubatus) in the southeastern United States. M.S. thesis, North Carolina State University, Raleigh, 2003.


Plant Disease ◽  
2011 ◽  
Vol 95 (11) ◽  
pp. 1479-1479 ◽  
Author(s):  
J. J. Riggins ◽  
S. W. Fraedrich ◽  
T. C. Harrington

Laurel wilt is caused by the fungus Raffaelea lauricola T.C. Harrin., Aghayeva & Fraedrich and is lethal to redbay (Persea borbonia (L.) Spreng.), sassafras (Sassafras albidum (Nutt.) Nees), and other species in the Lauraceae (1). The fungus is carried by the redbay ambrosia beetle (Xyleborus glabratus Eichh.), which is native to Asia. After being discovered in Georgia in 2002 (1), X. glabratus and R. lauricola have spread rapidly, causing extensive redbay mortality in South Carolina, Georgia, Florida, and Mississippi (1,4). The disease has also been confirmed on sassafras in Florida, South Carolina (1), and Georgia. Questions remain as to whether laurel wilt will continue to spread on sassafras, which often occurs as scattered trees in the eastern United States. In June 2010, a homeowner reported that a sassafras tree north of Van Cleave, MS (30.668°N, 88.686°W) had begun wilting in late May. This landscape tree had three 10-m high stems (~20 cm in diameter at breast height). Dark staining in the xylem was observed around the entire circumference of all three stems and nearly all leaves were bronze colored and wilted. No ambrosia beetle tunnels were observed in the stems. No other symptomatic Lauraceae were encountered in the wooded area within 300 m. The nearest known location with laurel wilt on redbay was ~15 km away (4). A Lindgren funnel trap baited with manuka oil (2) was placed at the site in June and monitored biweekly until November, but no X. glabratus adults were captured. Chips from discolored xylem of the sassafras were surface sterilized, plated on cycloheximide-streptomycin malt agar, and R. lauricola was readily isolated (1). Identity of the fungus (isolate C2792 in collection of T. Harrington) was confirmed by using partial sequences of the 28S rDNA (3). The sassafras sequence was identical to that of all known sequences of R. lauricola in the United States, including GenBank No. EU123076 (the holotype isolate from redbay). To confirm pathogenicity, isolate C2792 was grown on malt extract agar and three redbay (average: 141 cm high and 12 mm in diameter at soil interface) and three sassafras (average: 170 cm high and 17 mm in diameter at soil interface) potted plants were wound inoculated with 0.2 ml of a spore suspension (4.9 × 106 conidia/ml) (1). Three control plants of each species were inoculated with sterile deionized water. After 8 weeks in a growth chamber at 26°C, all inoculated redbay and sassafras plants exhibited xylem discoloration above and below the inoculation point, two of the redbay and two of the sassafras had died, and the other plant of each species exhibited partial wilt (the main terminal or one or more branches). All control plants were asymptomatic. R. lauricola was reisolated from all inoculated symptomatic plants but not from controls. To our knowledge, this is the first report of laurel wilt on sassafras in Mississippi. Both redbay (4) and sassafras appear to be highly susceptible to the disease as it moves westward. Sassafras is less attractive than redbay to X. glabratus and it was thought that this might contribute to slowing the spread of laurel wilt once outside the range of redbay (2). Nonetheless, our observations confirm that sassafras can be infected where laurel wilt on redbay is not in the immediate vicinity. References: (1) S. W. Fraedrich et al. Plant Dis. 92:215, 2008. (2) J. L. Hanula et al. J. Econ. Entomol. 101:1276, 2008. (3) T. C. Harrington et al. Mycotaxon 111:337, 2010. (4) J. J. Riggins et al. Plant Dis. 94:634, 2010.


Plant Disease ◽  
2006 ◽  
Vol 90 (3) ◽  
pp. 380-380 ◽  
Author(s):  
C. L. Harmon ◽  
P. F. Harmon ◽  
T. A. Mueller ◽  
J. J. Marois ◽  
G. L. Hartman

Soybean rust caused by Phakopsora pachyrhizi H. Sydow & Sydow was first reported in the continental United States during 2004 (2). By 10 November 2005, the disease was confirmed in eight southern states (Florida, Georgia, Alabama, Mississippi, South Carolina, North Carolina, Louisiana, and Texas). Diagnoses have been based on visual observation of uredinia and urediniospores of the pathogen followed by polymerase chain reaction confirmation. On 10 November 2005, uredinia and telia were identified on leaves of kudzu (Pueraria lobata) in central Florida. Telia first were noted as dark brown-to-black flecks on the abaxial leaf surface intermingled with abundant tan-to-light brown uredinia. Of 200 leaves examined, 143 (72%) had telia. The number of telia ranged from a few (1/cm2) that were scattered to many (73/cm2). Telia were approximately the same diameter as uredinia, but were appressed to the leaf surface and pigmented. Twenty telia were excised from host tissue with the aid of a dissecting microscope and a 20 gauge hypodermic needle. Telia averaged 89 × 100 μm (n = 20, σ = 17 and 16 μm, respectively). Four telia were crushed and five teliospores from each averaged 4.3 × 8.3 μm (n = 20, σ = 0.5 and 0.9 μm, respectively). Pale yellowish brown-to-hyaline teliospores were similar in color to urediniospores. Observations matched descriptions by Ono et al. (1). To our knowledge, this is the first report of the telial stage of P. pachyrhizi in the United States. References: (1) Y. Ono et al. Mycol. Res. 96:825, 1992. (2) R. W. Schneider et al. Plant Dis. 89:774, 2005.


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