First Report of Sphaeropsis Rot of Apple Caused by Sphaeropsis pyriputrescens in New York

In March 2012, decayed ‘Empire’ apple fruit (Malus × domestica Borkh.) were sampled from apples grown in Albion (Orleans County) in New York State and stored in bins for 6 months under controlled atmosphere at a commercial packinghouse. At the packinghouse following storage prior to be packed, the fruit were completely rotten, spongy to firm, and light brown without pycnidia. All fruit rots originated from either stem-end or calyx-end infections but no wound infections were observed. The incidence of fruit with these symptoms in the total decay was relatively low (0.1%). To isolate the causal agent, small fragments of fruit flesh from 12 decayed fruit were cut and placed on potato dextrose agar (PDA) acidified with 0.1% lactic acid. The plates were incubated at 20°C for 4 days and sub-cultured on PDA to obtain a pure culture. The colonies initially appeared with dense hyaline mycelium and later turned light yellow to yellow, and black pycnidia formed after about 2 weeks of incubation under a 24-h fluorescent light at 20°C. Conidia were light brown to brown, clavate to subglobose to irregular, and 15 × 8 μm on average. The fungus was identified as Sphaeropsis pyriputrescens Xiao & J.D. Rogers based on the morphology of the fungus (3). The identity of a representative isolate was further confirmed by analysis of nucleotide sequences of the internal transcribed spacer (ITS) regions amplified using the primers ITS1/ITS4. A BLAST search in GenBank showed that the sequence had 99% homology to an S. pyriputrescens sequence (Accession No. GQ374241). One representative isolate was tested for pathogenicity on apple fruit. Organic ‘Red Delicious’ apple fruit were surface-disinfected in 0.6% sodium hypochlorite solution for 5 min, rinsed twice with deionized water, and air-dried. Each fruit was wounded with a sterilized finish-nail head (3 mm in depth and 4 mm in diameter) and inoculated by placing a 4-mm-diameter plug from the leading edge of a 4-day-old PDA culture on the wound. Control fruit were treated with sterile PDA plugs. The inoculation site was covered with two layers of moist cheesecloth to avoid dehydration. There were four 10-fruit replicates for each treatment, and fruit were placed in plastic crispers and stored at 4°C for 4 weeks. The experiments were conducted twice. Sphaeropsis rot developed on all inoculated fruit, while no decays appeared on the control fruit. Koch's postulates were fulfilled by reisolating the fungus from the decayed fruit. Sphaeropsis rot is a recently reported postharvest fruit rot disease of apple and pear (1,3). The disease was first observed on ‘d'Anjou’ pears, and later more serious economic losses were observed in apples in Washington State (1). The disease has also since been reported in British Columbia, Canada (2). To the best of our knowledge, this is the first report of the occurrence of Sphaeropsis rot caused by S. pyriputrescens on apple in New York or in any region outside of the Pacific Northwest in North America. References: (1) Y. K. Kim and C. L. Xiao. Plant Dis. 92:940, 2008. (2) P. L. Sholberg et al. Plant Dis. 93:843, 2009. (3) C. L. Xiao et al. Plant Dis. 88:223, 2004.

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Preharvest Applications of Fungicides for Control of Sphaeropsis Rot in Stored Apples

Plant Health Progress ◽

10.1094/php-2013-0919-01-rs ◽

2013 ◽

Vol 14 (1) ◽

pp. 9

Author(s):

Y. K. Kim ◽

C. L. Xiao

Keyword(s):

Mycelial Growth ◽

Apple Fruit ◽

Fruit Rot ◽

Economic Losses ◽

In Vitro Tests ◽

Conidial Suspension ◽

Growth Assay ◽

Rot Disease ◽

Sphaeropsis Rot

Sphaeropsis rot caused by Sphaeropsis pyriputrescens is a recently reported postharvest fruit rot disease of apple in Washington State and causes significant economic losses. Infection of apple fruit by the fungus occurs in the orchard, but decay symptoms develop during storage or in the market. The objective of this study was to evaluate preharvest fungicide applications to control Sphaeropsis rot. Thirty isolates of the fungus collected from various sources were tested for sensitivity to the registered fungicides Pristine, Topsin M, and Ziram using an in vitro mycelial growth assay. In the orchard, ‘Golden Delicious' apple fruit were inoculated with the conidial suspension of the fungus at 2 or 5 weeks before harvest, sprayed with fungicides within 2 weeks before harvest, and harvested and stored at 0°C for disease evaluation. All three fungicides effectively inhibited mycelial growth of the fungus in the in vitro tests. On apple fruit in four seasons, Pristine applied 1 week and Ziram applied 2 weeks before harvest significantly reduced incidence of Sphaeropsis rot compared to the nontreated control by 43 to 80% and 42 to 83%, respectively. In 4 years of testing, the performance of Topsin M was less consistent than that of Pristine and Ziram. Accepted for publication 18 July 2013. Published 19 September 2013.

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Eurytrema procyonis in a Raccoon (Procyon lotor) from New York State—A First Report

Journal of Wildlife Diseases ◽

10.7589/0090-3558-25.2.270 ◽

1989 ◽

Vol 25 (2) ◽

pp. 270-272 ◽

Cited By ~ 3

Author(s):

Susan E. Wade ◽

Wayne I. Anderson ◽

Jeffrey D. Kidder

Keyword(s):

New York ◽

Procyon Lotor ◽

New York State ◽

York State ◽

First Report

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First Report of Pepper Fruit Rot Caused by Fusarium concentricum in China

Plant Disease ◽

10.1094/pdis-03-13-0325-pdn ◽

2013 ◽

Vol 97 (12) ◽

pp. 1657-1657 ◽

Cited By ~ 6

Author(s):

J. H. Wang ◽

Z. H. Feng ◽

Z. Han ◽

S. Q. Song ◽

S. H. Lin ◽

...

Keyword(s):

Fusarium Species ◽

Fruit Rot ◽

Post Inoculation ◽

Distilled Water ◽

Conidial Suspension ◽

Average Growth ◽

First Report ◽

Control Fruit ◽

Pepper Fruit ◽

Fruit Samples

Pepper (Capsicum annuum L.) is an important vegetable crop worldwide. Some Fusarium species can cause pepper fruit rot, leading to significant yield losses of pepper production and, for some Fusarium species, potential risk of mycotoxin contamination. A total of 106 diseased pepper fruit samples were collected from various pepper cultivars from seven provinces (Gansu, Hainan, Heilongjiang, Hunan, Shandong, Shanghai, and Zhejiang) in China during the 2012 growing season, where pepper production occurs on approximately 25,000 ha. Pepper fruit rot symptom incidence ranged from 5 to 20% in individual fields. Symptomatic fruit tissue was surface-sterilized in 0.1% HgCl2 for 1 min, dipped in 70% ethanol for 30 s, then rinsed in sterilized distilled water three times, dried, and plated in 90 mm diameter petri dishes containing potato dextrose agar (PDA). After incubation for 5 days at 28°C in the dark, putative Fusarium colonies were purified by single-sporing. Forty-three Fusarium strains were isolated and identified to species as described previously (1,2). Morphological characteristics of one strain were identical to those of F. concentricum. Aerial mycelium was reddish-white with an average growth rate of 4.2 to 4.3 mm/day at 25°C in the dark on PDA. Pigments in the agar were formed in alternating red and orange concentric rings. Microconidia were 0- to 1-septate, mostly 0-septate, and oval, obovoid to allantoid. Macroconidia were relatively slender with no significant curvature, 3- to 5-septate, with a beaked apical cell and a foot-shaped basal cell. To confirm the species identity, the partial TEF gene sequence (646 bp) was amplified and sequenced (GenBank Accession No. KC816735). A BLASTn search with TEF gene sequences in NCBI and the Fusarium ID databases revealed 99.7 and 100% sequence identity, respectively, to known TEF sequences of F. concentricum. Thus, both morphological and molecular criteria supported identification of the strain as F. concentricum. This strain was deposited as Accession MUCL 54697 (http://bccm.belspo.be/about/mucl.php). Pathogenicity of the strain was confirmed by inoculating 10 wounded, mature pepper fruits that had been harvested 70 days after planting the cultivar Zhongjiao-5 with a conidial suspension (1 × 106 spores/ml), as described previously (3). A control treatment consisted of inoculating 10 pepper fruits of the same cultivar with sterilized distilled water. The fruit were incubated at 25°C in a moist chamber, and the experiment was repeated independently in triplicate. Initially, green to dark brown lesions were observed on the outer surface of inoculated fruit. Typical soft-rot symptoms and lesions were observed on the inner wall when the fruit were cut open 10 days post-inoculation. Some infected seeds in the fruits were grayish-black and covered by mycelium, similar to the original fruit symptoms observed at the sampling sites. The control fruit remained healthy after 10 days of incubation. The same fungus was isolated from the inoculated infected fruit using the method described above, but no fungal growth was observed from the control fruit. To our knowledge, this is the first report of F. concentricum causing a pepper fruit rot. References: (1) J. F. Leslie and B. A. Summerell. The Fusarium Laboratory Manual. Blackwell Publishing, Ames, IA, 2006. (2) K. O'Donnell et al. Proc. Nat. Acad. Sci. USA 95:2044, 1998. (3) Y. Yang et al. 2011. Int. J. Food Microbiol. 151:150, 2011.

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First Report of Fusarium pernambucanum Causing Fruit Rot of Muskmelon in China

Plant Disease ◽

10.1094/pdis-07-21-1520-pdn ◽

2021 ◽

Author(s):

Xianping Zhang ◽

Jiwen Xia ◽

Jiakui Liu ◽

Dan Zhao ◽

Lingguang Kong ◽

...

Keyword(s):

Phylogenetic Analyses ◽

Apical Cell ◽

Morphological Characteristics ◽

Fruit Rot ◽

Likelihood Method ◽

Correct Identification ◽

Pathogenicity Test ◽

First Report ◽

The Core ◽

Representative Isolate

Muskmelon (Cucumis melo L.) is one of the most widely cultivated and economically important fruit crops in the world. However, many pathogens can cause decay of muskmelons; among them, Fusarium spp. is the most important pathogen, affecting fruit yield and quality (Wang et al. 2011). In May 2017, fruit rot symptoms were observed on ripening muskmelons (cv. Jipin Zaoxue) in several fields in Liaocheng of Shandong Province, China. Symptoms appeared as brown, water-soaked lesions, irregularly circular in shape, with the lesion size ranging from a small spot (1 to 2 cm) to the decay of the entire fruit. The core and the surface of the infected fruit were covered with white to rose-reddish mycelium. Two infected muskmelons were collected from each of two fields, 10 km apart. Tissues from the inside of the infected fruit were surface disinfected with 75% ethanol for 30 s, and cultured on potato dextrose agar (PDA) at 25 °C in the dark for 5 days. Four purified cultures were obtained using the single spore method. On carnation leaf agar (CLA), macroconidia had a pronounced dorsiventral curvature, falcate, 3 to 5 septa, with tapered apical cell, and foot-shaped basal cell, measuring 19 to 36 × 4 to 6 μm. Chlamydospores were abundant, 5.5–7.5 μm wide, and 5.5–10.5 μm long, ellipsoidal or subglobose. No microconidia were observed. These morphological characteristics were consistent with the descriptions of F. pernambucanum (Santos et al. 2019). Because these isolates had similar morphology, one representative isolate was selected for multilocus phylogenetic analyses. DNA was extracted from the representative isolate using the CTAB method. The nucleotide sequences of the internal transcribed spacers (ITS) (White et al. 1990), translation elongation factor 1-α gene (TEF1), RNA polymerase II second largest subunit gene (RPB2), calmodulin (CAM) (Xia et al. 2019) were amplified using specific primers, sequenced, and deposited in GenBank (MN822926, MN856619, MN856620, and MN865126). Based on the combined dataset of ITS, TEF1, RPB2, CAM, alignments were made using MAFFT v. 7, and phylogenetic analyses were processed in MEGA v. 7.0 using the maximum likelihood method. The studied isolate (XP1) clustered together with F. pernambucanum reference strain URM 7559 (99% bootstrap). To perform pathogenicity test, 10 μl of spore suspensions (1 × 106 conidia/ml) were injected into each muskmelon fruit using a syringe, and the control fruit was inoculated with 10 μl of sterile distilled water. There were ten replicated fruits for each treatment. The test was repeated three times. After 7 days at 25 °C, the interior of the inoculated muskmelons begun to rot, and the rot lesion was expanded from the core towards the surface of the fruit, then white mycelium produced on the surface. The same fungus was re-isolated from the infected tissues and confirmed to fulfill the Koch’s postulates. No symptoms were observed on the control muskmelons. To our knowledge, this is the first report of F. pernambucanum causing of fruit rot of muskmelon in China. Considering the economic value of the muskmelon crop, correct identification can help farmers select appropriate field management measures for control of this disease.

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First Report of Diaporthe hongkongensis Causing Fruit rot on Peach (Prunus persica) in China

Plant Disease ◽

10.1094/pdis-07-20-1505-pdn ◽

2021 ◽

Author(s):

Zhou Zhang ◽

Zheng Bing Zhang ◽

Yuan Tai Huang ◽

FeiXiang Wang ◽

Wei Hua Hu ◽

...

Keyword(s):

Prunus Persica ◽

Fruit Rot ◽

Hunan Province ◽

Post Inoculation ◽

Distilled Water ◽

Conidial Suspension ◽

Internal Transcribed Spacer Region ◽

First Report ◽

Representative Isolate ◽

Rot Disease

Peach [Prunus persica (L.) Batsch] is an important deciduous fruit tree in the family Rosaceae and is a widely grown fruit in China (Verde et al., 2013). In July and August 2018, a fruit rot disease was observed in a few peach orchards in Zhuzhou city, the Hunan Province of China. Approximately 30% of the fruit in more than 400 trees was affected. Symptoms displayed were brown necrotic spots that expanded, coalesced, and lead to fruit being rotten. Symptomatic tissues excised from the margins of lesions were surface sterilized in 70% ethanol for 10 s, 0.1% HgCl2 for 2 min, rinsed with sterile distilled water three times, and incubated on potato dextrose agar (PDA) at 26°C in the dark. Fungal colonies with similar morphology developed, and eight fungal colonies were isolated for further identification. Colonies grown on PDA were grayish-white with white aerial mycelium. After an incubation period of approximately 3 weeks, pycnidia developed and produced α-conidia and β-conidia. The α-conidia were one-celled, hyaline, fusiform, and ranged in size from 6.0 to 8.4 × 2.1 to 3.1 μm, whereas the β-conidia were filiform, hamate, and 15.0 to 27.0 × 0.8 to 1.6 μm. For molecular identification, total genomic DNA was extracted from the mycelium of a representative isolate HT-1 and the internal transcribed spacer region (ITS), β-tubulin gene (TUB), translation elongation factor 1-α gene (TEF1), calmodulin (CAL), and histone H3 gene (HIS) were amplified and sequenced (Meng et al. 2018). The ITS, TUB, TEF1, CAL and HIS sequences (GenBank accession nos. MT740484, MT749776, MT749778, MT749777, and MT749779, respectively) were obtained and in analysis by BLAST against sequences in NCBI GenBank, showed 99.37 to 100% identity with D. hongkongensis or D. lithocarpus (the synonym of D. hongkongensis) (Gao et al., 2016) (GenBank accession nos. MG832540.1 for ITS, LT601561.1 for TUB, KJ490551.1 for HIS, KY433566.1 for TEF1, and MK442962.1 for CAL). Pathogenicity tests were performed on peach fruits by inoculation of mycelial plugs and conidial suspensions. In one set, 0.5 mm diameter mycelial discs, which were obtained from an actively growing representative isolate of the fungus on PDA, were placed individually on the surface of each fruit. Sterile agar plugs were used as controls. In another set, each of the fruits was inoculated by application of 1 ml conidial suspension (105 conidia/ml) by a spray bottle. Control assays were carried out with sterile distilled water. All treatments were maintained in humid chambers at 26°C with a 12-h photoperiod. The inoculation tests were conducted twice, with each one having three fruits as replications. Six days post-inoculation, symptoms of fruit rot were observed on inoculated fruits, whereas no symptoms developed on fruits treated with agar plugs and sterile water. The fungus was re-isolated and identified to be D. hongkongensis by morphological and molecular methods, thus fulfilling Koch’s Postulates. This fungus has been reported to cause fruit rot on kiwifruit (Li et al. 2016) and is also known to cause peach tree dieback in China (Dissanayake et al. 2017). However, to our knowledge, this is the first report of D. hongkongensis causing peach fruit rot disease in China. The identification of the pathogen will provide important information for growers to manage this disease.

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First Report of Brown Rot Caused by Monilinia fructicola Affecting Peach Orchards in Slovenia

Plant Disease ◽

10.1094/pdis-94-9-1166a ◽

2010 ◽

Vol 94 (9) ◽

pp. 1166-1166 ◽

Cited By ~ 15

Author(s):

A. Munda ◽

M. Viršček Marn

Keyword(s):

Prunus Persica ◽

Brown Rot ◽

Fruit Rot ◽

Morphological Identification ◽

Monilinia Fructicola ◽

Conidial Suspension ◽

Stone Fruits ◽

The European Union ◽

First Report ◽

Representative Isolate

Monilinia fructicola, the causal agent of brown rot, is a destructive fungal pathogen that affects mainly stone fruits (Prunoideae). It causes fruit rot, blossom wilt, twig blight, and canker formation and is common in North and South America, Australia, and New Zealand. M. fructicola is listed as a quarantine pathogen in the European Union and was absent from this region until 2001 when it was detected in France. In August 2009, mature peaches (Prunus persica cv. Royal Glory) with brown rot were found in a 5-year-old orchard in Goriška, western Slovenia. Symptoms included fruit lesions and mummified fruits. Lesions were brown, round, rapidly extending, and covered with abundant gray-to-buff conidial tufts. The pathogen was isolated in pure culture and identified based on morphological and molecular characters. Colonies on potato dextrose agar (PDA) incubated at 25°C in darkness had an average daily growth rate of 7.7 mm. They were initially colorless and later they were light gray with black stromatal plates and dense, hazel sporogenous mycelium. Colony margins were even. Sporulation was abundant and usually developed in distinct concentric zones. Limoniform conidia, produced in branched chains, measured 10.1 to 17.7 μm (mean = 12.1 μm) × 6.2 to 8.6 μm (mean = 7.3 μm) on PDA. Germinating conidia produced single germ tubes whose mean length ranged from 251 to 415 μm. Microconidia were abundant, globose, and 3 μm in diameter. Morphological characters resembled those described for M. fructicola (1). Morphological identification was confirmed by amplifying genomic DNA of isolates with M. fructicola species-specific primers (2–4). Sequence of the internal transcribed spacer (ITS) region (spanning ITS1 and ITS 2 plus 5.8 rDNA) of a representative isolate was generated using primers ITS1 and ITS4 and deposited in GenBank (Accession No. GU967379). BLAST analysis of the 516-bp PCR product revealed 100% identity with several sequences deposited for M. fructicola in NCBI GenBank. Pathogenicity was tested by inoculating five mature surface-sterilized peaches with 10 μl of a conidial suspension (104 conidia ml–1) obtained from one representative isolate. Sterile distilled water was used as a control. Peaches were wounded prior to inoculation. After 5 days of incubation at room temperature and 100% relative humidity, typical brown rot symptoms developed around the inoculation point, while controls showed no symptoms. M. fructicola was reisolated from lesion margins. Peach and nectarine orchards in a 5-km radius from the outbreak site were surveyed in September 2009 and M. fructicola was confirmed on mummified fruits from seven orchards. The pathogen was not detected in orchards from other regions of the country, where only the two endemic species M. laxa and M. fructigena were present. To our knowledge, this is the first report of M. fructicola associated with brown rot of stone fruits in Slovenia. References: (1) L. R. Batra. Page 106 in: World Species of Monilinia (Fungi): Their Ecology, Biosystematics and Control. J. Cramer, Berlin, 1991. (2) M.-J. Côté et al. Plant Dis. 88:1219, 2004. (3) K. J. D. Hughes et al. EPPO Bull. 30:507, 2000. (4) R. Ioos and P. Frey. Eur. J. Plant Pathol. 106:373, 2000.

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Control of Sphaeropsis Rot in Stored Apple Fruit Caused by Sphaeropsis pyriputrescens with Postharvest Fungicides

Plant Disease ◽

10.1094/pdis-04-11-0273 ◽

2011 ◽

Vol 95 (9) ◽

pp. 1075-1079 ◽

Cited By ~ 5

Author(s):

C. L. Xiao ◽

Y. K. Kim ◽

R. J. Boal

Keyword(s):

Mycelial Growth ◽

Disease Incidence ◽

Apple Fruit ◽

Conidial Germination ◽

Fruit Rot ◽

Mitigation Measures ◽

The Mean ◽

Rot Disease ◽

Sphaeropsis Rot

Sphaeropsis rot caused by Sphaeropsis pyriputrescens is a recently reported postharvest fruit rot disease of apple grown in Washington State. The objective of this study was to develop chemical-based mitigation measures for Sphaeropsis rot in stored apple fruit. To determine in vitro sensitivity of S. pyriputrescens to the three registered postharvest fungicides thiabendazole, fludioxonil, and pyrimethanil, 30 isolates of S. pyriputrescens obtained from various sources were tested for mycelial growth and conidial germination on fungicide-amended media. Golden Delicious apple fruit were inoculated with the pathogen in the orchard at 2 or 5 weeks before harvest. After harvest, fruit were either nontreated or dipped in thiabendazole, fludioxonil, or pyrimethanil solutions, stored at 0°C, and monitored for decay development for up to 9 months after harvest. The mean effective concentration of a fungicide that inhibits mycelial growth or spore germination by 50% relative to the nonamended control (EC50) values of thiabendazole, fludioxonil, and pyrimethanil on mycelial growth were 0.791, 0.0005, and 2.829 μg/ml, respectively. Fludioxonil and pyrimethanil also were effective in inhibiting conidial germination of the fungus with EC50 values of 0.02 μg/ml for fludioxonil and 5.626 μg/ml for pyrimethanil. All three postharvest fungicides applied at label rates immediately after harvest were equally effective in controlling Sphaeropsis rot in stored apple fruit, reducing disease incidence by 92 to 100% compared with the nontreated control. The results indicated that Sphaeropsis rot may be effectively controlled by the currently registered postharvest fungicides thiabendazole, fludioxonil, and pyrimethanil.

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First Report of Fruit Rot Disease on Pomelo Caused by Lasiodiplodia theobromae in China

Plant Disease ◽

10.1094/pdis-03-11-0214 ◽

2011 ◽

Vol 95 (9) ◽

pp. 1190-1190 ◽

Cited By ~ 5

Author(s):

M. Luo ◽

Z. Y. Dong ◽

S. Y. Bin ◽

J. T. Lin

Keyword(s):

Its Region ◽

Fruit Rot ◽

Economic Losses ◽

Single Spore ◽

Lasiodiplodia Theobromae ◽

First Report ◽

Potted Plants ◽

Diseased Fruit ◽

Long Time ◽

Water Plants

Pomelo (Citrus grandis) is widely cultivated in MeiZhou Guangdong Province of China. In 2008, a disease on pomelo fruit caused significant economic losses by affecting fruit quality. Diseased fruit was collected in December 2008 from MeiZhou Guangdong, surface sterilized in 75% ethanol for 1 min and internal necrotic tissue was transferred to potato dextrose agar (PDA) and incubated at 28°C for 5 days. Three single-spore isolates were obtained from different fruit and identified as Lasiodiplodia theobromae (Pat.) Griffon & Maubl. (synonyms Diplodia natalensis Pole-Evans and Botryodiplodia theobromae Pat.; teleomorph Botryosphaeria rhodina (Cooke) Arx) on the basis of morphological and physiological features. The fungus produced dark brown colonies (initially grayish) on PDA. Young hyphae were hyaline and aseptate, whereas mature hyphae were septate with irregular branches. Cultures of L. theobromae produced globular or irregular pycnidia abundantly on PDA (pH 3.5) at 28°C after 1 month. Mature conidia of L. theobromae were 20 to 26 × 12 to 15.5 μm, subovoid to ellipsoid-ovoid, initially hyaline and nonseptate, remaining hyaline for a long time, and finally becoming dark brown and one septate with melanin deposits on the inner surface of the wall arranged longitudinally giving a striate appearance to the conidia. The internal transcribed spacer (ITS) region of the rDNA was amplified from gDNA using primers ITS1 (5′-TCCGATGGTGAACCTGCGG-3′) and ITS4 (5′-TCCTCCGCTTATTGATATGC-3′) (1). Amplicons were 542 bp long (GenBank Accession No. JF693024) and had 100% nucleotide identity with the corresponding sequence (GenBank Accession No. EU860391) of L. theobromae isolated from a Pinus sp. (2). To satisfy Koch's postulates, six asymptomatic fruit on potted plants were sprayed until runoff with a spore suspension (1 × 106 spores/ml) prepared from 30-day-old cultures of one isolate. Control fruit received water. Plants were covered with sterile wet gauze to maintain high humidity. Fruit spot symptoms similar to those on diseased field fruit appeared after 15 days on all inoculated fruits. L. theobromae was reisolated from all inoculated test fruit. No symptoms were observed on the fruit of control plants. To our knowledge, this is the first report of L. theobromae causing disease on pomelo fruit in China. This pathogen has also been previously reported to be economically important on a number of other hosts by mostly affecting the leaves. References: (1) J. C. Batzer et al. Mycologia 97:1268, 2005. (2) C. A. Pérez et al. Fungal Divers. 41:53,2010.

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First Report of a New Postharvest Fruit Rot on Apple Caused by Sphaeropsis pyriputrescens

Plant Disease ◽

10.1094/pdis.2004.88.2.223a ◽

2004 ◽

Vol 88 (2) ◽

pp. 223-223 ◽

Cited By ~ 14

Author(s):

C. L. Xiao ◽

J. D. Rogers ◽

R. J. Boal

Keyword(s):

Leading Edge ◽

Preliminary Evidence ◽

Apple Fruit ◽

Causal Agent ◽

Fruit Rot ◽

Postharvest Disease ◽

Fluorescent Light ◽

Pathogenicity Test ◽

First Report ◽

Golden Delicious

During March to July 2003, a postharvest fruit rot was observed on ‘Golden Delicious’, ‘Granny Smith’, and ‘Red Delicious’ apples (Malus × domestica Borkh.) sampled from commercial packinghouses in Washington State. Losses as high as 24% in storage bins were observed in July on ‘Red Delicious’. The disease started at the stem bowl area or the calyx end of the fruit. Decayed fruit was apparently not wounded. Decayed areas were brown and firm. Internal decayed flesh appeared yellowish brown. On ‘Red Delicious’ apples, decayed fruit was apparently discolored from red to brown. As the disease advanced, pycnidia of a fungus might form on the stem, sepals, or the surface of decayed fruit. Pycnidia were 0.3 to 0.7 mm in diameter, black, and partially immersed in decayed tissues. To isolate the causal agent, decayed fruit was lightly sprayed with 70% ethanol and air dried. Fragments of diseased tissue were removed from the margin of diseased and healthy tissue and plated on acidified potato dextrose agar (PDA). A fungus was consistently isolated from decayed fruit with the symptoms described above. On PDA, the colonies of the fungus first appeared with dense hyaline mycelium and later turned light yellow to yellow. Black pycnidia of the fungus formed on 2- to 3-week-old oatmeal agar cultures at 20°C under 12-h alternating cycles of fluorescent light and dark. The fungus was identified as Sphaeropsis pyriputrescens Xiao & J. D. Rogers, based on the description of the fungus (1). Voucher specimens were deposited at the WSU Mycological Herbarium. Two isolates of the fungus recovered from decayed apples were tested for pathogenicity on apple. Fruit of ‘Golden Delicious’ and ‘Gala’ were surface-disinfested for 5 min in 0.5% NaOCl, rinsed, and air dried. Fruit was wounded with a sterile 4-mm-diameter nail head. A 4-mm-diameter plug from the leading edge of a 3-day-old PDA culture or plain PDA (control) was placed in the wound of each of 10 replicate fruit for each isolate or control. Fruit was tray packed with polyethylene liners and stored in cardboard boxes in air at 3°C, and decay was evaluated 2 weeks after inoculation. Five decayed fruits from each treatment were selected for reisolation of the causal agent. The experiment was conducted twice. In a separate pathogenicity test, two isolates (one each from apple and pear) were included in the test. Fruit of ‘Red Delicious’ apple was prepared and inoculated as the same manner described above, but fruit was stored in air at 0°C. The experiment was conducted twice. All fruit that were inoculated with the fungus developed decay symptoms. No decay developed on fruit in the controls. The same fungus was reisolated from decayed fruit. This indicates that isolates from apple and pear were pathogenic to apple. S. pyriputrescens is the causal agent of a newly reported postharvest disease on ‘d'Anjou’ pears (1). To our knowledge, this is the first report of this fungus causing postharvest fruit rot on apple. We propose ‘Sphaeropsis rot’ as the name of this new disease on apple and pear. Preliminary evidence suggests that infection of fruit by this fungus occurred in the orchard prior to storage. Reference: (1) C. L. Xiao and J. D. Rogers. Plant Dis. 88:114, 2004.

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First Report of Blueberry Leaf Rust Caused by Thekopsora minima on Vaccinium corymbosum in Michigan

Plant Disease ◽

10.1094/pdis-12-10-0884 ◽

2011 ◽

Vol 95 (6) ◽

pp. 768-768 ◽

Cited By ~ 4

Author(s):

A. M. C. Schilder ◽

T. D. Miles

Keyword(s):

South Africa ◽

New York ◽

Leaf Rust ◽

Vaccinium Corymbosum ◽

Economic Losses ◽

Its2 Region ◽

Highbush Blueberry ◽

Alternate Host ◽

First Report ◽

Growing Seasons

Leaf rust symptoms have been noticed sporadically on northern highbush blueberry plants (Vaccinium corymbosum L.) in Michigan for the past 8 years. In 2009, leaf rust was seen in several cultivated blueberry fields and on greenhouse-grown blueberry plants in southwest Michigan. In 2010, leaf rust was widespread throughout western Michigan and particularly evident in the fall, sometimes resulting in premature defoliation. Cultivars Rubel, Jersey, Elliott, Liberty, and Brigitta were most commonly affected. Both the 2009 and 2010 growing seasons were characterized by above-average precipitation in early to mid-summer. Early symptoms on the adaxial leaf surface consisted of roughly circular yellow spots that later developed brown, necrotic centers. Older lesions were more angular and sometimes surrounded by a purplish border. In the fall, a “green island” effect was sometimes apparent around the lesions. On the abaxial side, numerous yellow-to-orange rust pustules (uredinia) were visible. Uredinia were dome shaped, erumpent, 100 to 400 μm in diameter, clustered, and sometimes coalescing. Urediniospores were broadly obovate with dark yellowish content and measured 19 to 25 × 16 to 20 μm (average 22 × 18 μm, n = 30). Spore walls were hyaline, echinulate, and 1.0 to 1.5 μm thick with obscure germ pores. Uredinia were examined with light and scanning electron microscopy for the presence of conspicuous ostiolar cells characteristic of Naohidemyces vaccinii (Wint.) Sato, Katsuya et Y. Hiratsuka, but none were observed. No telia or teliospores were observed. On the basis of morphology, the pathogen was identified as Thekopsora minima P. Syd. & Syd. (3,4) and a sample was deposited in the U.S. National Fungus Collection (BPI 881107). Genomic DNA was extracted from urediniospores of rust isolates from six different locations, and a 267-bp fragment of the ITS2 region was amplified and sequenced using the primers ITS3 and ITS4 (GenBank Accession No. HQ661383). All sequences were identical to each other and shared 99% identity (232 of 234 bp) with a T. minima isolate from South Africa (GenBank Accession No. GU355675). The alternate host, hemlock (mostly Tsuga canadensis L.) is a common and valuable conifer in the Michigan landscape. Hemlock trees were not examined for the presence of aecia but are assumed to play a role in the epidemiology of the disease in Michigan because leaf rust tends to be more severe near hemlock trees. Pucciniastrum vaccinii (G. Wint.) Jorst. was considered the causal agent of blueberry leaf rust until Sato et al. (1,4) identified three unique species. While T. minima has been reported on black huckleberry (Gaylussacia baccata [Wangenh.] K. Koch) in Michigan (4), to our knowledge, this is the first report of T. minima on highbush blueberry in the state. T. minima has been reported on highbush blueberry in Delaware and New York (4), Japan (2), and South Africa (3). The severity of the outbreak in 2010 warrants further research into economic losses, epidemiology, and management of the disease. References: (1) D. F. Farr and A. Y. Rossman. Fungal Databases. Systematic Botany and Mycology Laboratory, ARS, UDSA. Retrieved from http://nt.ars-grin.gov/fungaldatabases/ , 2010. (2) T. Kobayashi. Page 1227 in: Index of Fungi Inhabiting Woody Plants in Japan. Host, Distribution and Literature. Zenkoku-Noson-Kyoiku Kyokai Publishing Co., Tokyo, 2007. (3) L. Mostert et al. Plant Dis. 94:478, 2010. (4) S. Sato et al. Trans. Mycol. Soc. Jpn. 34:47, 1993.

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