First Report of Fusarium oxysporum Causing Soft Fruit Rot Disease of Gray Jujube (Zizyphus jujuba) in China

Gray Jujube, Zizyphus jujuba Mill., is a fruit crop unique to China that produces small fruit of high nutritional value with potential health benefits (2). In mid-September 2011, a fruit rot affecting approximately 10% of gray jujube fruit was observed in Xinzheng Date Garden, Henan Province, China. The diseased fruits exhibited small, oval, pale reddish brown lesions that expanded into clear concentric rings. Over time, the superficial lesions developed into soft rot affecting the whole fruit that produced a pungent odor. A putative Fusarium sp. was isolated by a single spore isolations from conidiophores produced on the decaying fruit. The isolated colonies first appeared on potato dextrose agar (PDA) as white to light yellow, then turned light pink. Falciform macroconidia were produced on PDA and were straight to slightly curved, usually 3-septate, short or medium long, 15.0 to 28 × 2.5 to 4.0 μm, with a curved apical cell and foot shaped to pointed basal cell. Microconidia were produced in false heads on Synthetic Nutrient-poor Agar (SNA), and were oval, 0-septate, 5.0 to 9.5 × 1.5 to 2.8 μm. Phialides were cylindrical and ranged from 7.0 to 20.0 × 0.7 to 1.4 μm. Chlamydospores were produced singularly and in pairs (1). Pathogenicity of the putative Fusarium sp. was evaluated by surface-sterilizing fresh gray jujubes on a healthy tree field and inoculating by placing a mycelial plug of the Fusarium sp. culture in contact with the fruit. An equal number of fresh gray jujube fruits were placed in contact with non-colonized PDA plugs to serve as a control. Each jujube fruit was wounded three times to create three holes close together using a steel needle (0.5 mm diameter), before inoculation with an agar plug. All the branches with inoculated fruits were enclosed in a clear plastic bag to maintain humidity and prevent cross contamination. After 3 days, inoculated jujubes exhibited the similar symptoms to those originally observed on the naturally infected fruits. Colonies resembling the Fusarium sp. isolated from the original lesions were obtained from each of the symptomatic fruits. Fruit inoculated with un-colonized PDA plugs remained asymptomatic and no fungus was isolated from these fruit. Koch's postulates were repeated three times with the same results. Based on the morphological characteristics, the Fusarium sp. was identified as F. oxysporum (1). The identity of the isolate was confirmed to be F. oxysporum by DNA sequencing of the elongation factor 1-alpha (EF-1a) gene (GenBank Accession No. KC796007), which was 99% homologous to those of other F. oxysporum isolates (JF430187 and JF430188). To our knowledge, this is the first report of F. oxysporum causing soft rot in fresh gray jujubes in Henan. This disease affects the yield and quality of fresh gray jujubes and potentially may threaten the jujube industry. References: (1) J. F. Leslie and B. A. Summerell. The Fusarium Laboratory Manual, 2006. (2) J. Sheng et al. Acta Hortic. 620:203, 2003.

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First Report of Fusarium proliferatum Causing Fruit Rot of Winter Jujube (Zizyphus jujuba) in Storage in China

Plant Disease ◽

10.1094/pdis-12-11-1035-pdn ◽

2012 ◽

Vol 96 (6) ◽

pp. 913-913 ◽

Cited By ~ 3

Author(s):

M. Zhang ◽

Y. Wang ◽

C. Y. Wen ◽

H. Y. Wu

Keyword(s):

Apical Cell ◽

Morphological Characteristics ◽

Fusarium Proliferatum ◽

Fruit Rot ◽

Distilled Water ◽

First Report ◽

Pale Yellow ◽

Agar Plug ◽

Jujube Fruit ◽

Zizyphus Jujuba

Winter jujube, Zizyphus jujuba Mill., is a Chinese crop with fruit that has an extremely high nutritional value (4). In early November 2010, a severe fruit rot affecting ~20% of 1,000 kg of winter jujube fruit was observed in a storehouse in Zhengzhou, Henan province, China. The same fruit rot symptoms were found in two supermarkets in Zhengzhou in late November 2010 in ~10% of 100 kg of fruit in one supermarket and 25% of 50 kg of fruit in the other. Symptoms first appeared as small, round, pale yellow brown lesions on the fruits, 1 to 3 mm in diameter, then developed into 5- to 10-mm, sunken, brown spots, each with a pale brown margin. Three Fusarium isolates (DZF001 to DZF003) showing similar morphological characteristics were isolated from three specimens (collected from one storehouse and two supermarkets) by surface sterilizing small pieces of necrotic fruit tissue for 1 min in 2% NaOCl, washing the tissue pieces three times with sterile distilled water, and plating the pieces on potato dextrose agar (PDA). Fungal colonies for each isolate were white to light pink, and the adaxial side of each culture was pale yellow. Macroconidia were produced in pale orange sporodochia and were slender, relatively straight, three to five septa, 29.0 to 55.2 × 2.5 to 4.0 μm, with a curved apical cell and a poorly developed basal cell. Microconidia were produced in chains or false heads on synthetic nutrient-poor agar, clavate with a planar base, aseptate, and 4.5 to 8.0 × 2.5 to 3.5 μm. Conidiophores terminated in verticils of two to three phialides or monophialides. Chlamydospores were absent. The cultural and morphological characteristics were similar to those of Fusarium proliferatum (1,2). The identity of the three fungal isolates was confirmed to be F. proliferatum by DNA sequencing of the internal transcribed spacer (ITS) rDNA region (GenBank Accession Nos. JN889713 to JN889715), which were 99 to 100% homologous to those of other F. proliferatum isolates (GU066714, HQ113948, and GU363955); and the elongation factor 1-alpha (EF-1a) gene (JN889713 to JN889715), which was 99% homologous to those of other F. proliferatum isolates (FJ538244, FJ895277, and GQ848536) (3). Pathogenicity tests were conducted on 20 winter jujube fruits using a mycelial plug harvested from the periphery of a 7-day-old colony of strain DZF001, and placed on the surface of the fruit after the inoculated area of the fruit had been surface sterilized with 75% ethanol for 2 min; an equal number of fresh winter jujube fruits treated with non-colonized plugs of PDA served as the control treatment. Each jujube fruit was pricked three times with an insect needle to create three holes close together before inoculation with an agar plug. Each fruit was then enclosed in a clear plastic box with a cup of sterile distilled water to maintain high relative humidity, and held at 25°C. Symptoms similar to those originally observed on the naturally infected fruit were observed 3 days after inoculation, and the same fungus was reisolated from each of the symptomatic fruits; control fruits remained asymptomatic and no fungus was isolated from the control fruit. Koch's postulates were repeated three times with the same results. To our knowledge, this is the first report of F. proliferatum causing rot of winter jujube fruit in China. References: (1) K. Chehri et al. Saudi J. Biol. Sci. 18:341, 2011. (2) J. F. Leslie and B. A. Summerell. The Fusarium Laboratory Manual, Blackwell Publishing, 2006. (3) H. T. Phan. Studies Mycol. 50:261, 2004. (4) J. Sheng et al. Acta Hort. 620:203, 2003.

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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 Fruit Rot Caused by Fusarium luffae in Muskmelon in China

Plant Disease ◽

10.1094/pdis-12-21-2666-pdn ◽

2022 ◽

Author(s):

Xianping Zhang ◽

Xuedong Cao ◽

Qingqing Dang ◽

Yongguang Liu ◽

Xiaoping Zhu ◽

...

Keyword(s):

Phylogenetic Analyses ◽

Apical Cell ◽

Morphological Characteristics ◽

Fruit Rot ◽

Likelihood Method ◽

Correct Identification ◽

Pathogenicity Test ◽

Fusarium Spp ◽

First Report ◽

The Core

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 muskmelon fruit, including Fusarium spp.. Fusarium spp. are the most important pathogen, affecting muskmelon fruit yield and quality (Wang et al. 2011). In August 2020, fruit rot symptoms were observed on ripening muskmelons (cv. Tianbao) in several fields in Jiyang District, Jinan City of Shandong Province, China. The incidences of infected muskmelon ranged from 15% to 30% and caused an average 20% yield loss. Symptoms appeared as pale brown, water-soaked lesions that were irregular in shape, with the lesion sizes ranging from a small spot (1 to 2 cm) to decay of the entire fruit. The core and surface of infected fruit were colonized and covered with white mycelia. Two infected muskmelons were collected from two fields, 3.5 km apart. Tissues removed from inside 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), 3 to 5 septate, falcate, with a pronounced dorsiventral curvature macroconidia with tapered apical cell, and foot-shaped basal cell, measuring 20 to 40 × 3.5 to 4.5 μm. Microconidia and chlamydospores were not observed. These morphological characteristics were consistent with the description of F. luffae (Wang et al., 2019). Because these isolates had similar morphology, two representative isolates (XP11 and XP12) were selected for multilocus phylogenetic analyses. DNA was extracted from the representative isolates using a CTAB method. Nucleotide sequences of the internal transcribed spacers (ITS) (White et al. 1990), calmodulin (CAM), RNA polymerase II second largest subunit (RPB2), translation elongation factor 1-α gene (TEF1) (Xia et al. 2019) were amplified using specific primers, sequenced, and deposited in GenBank (ITS: MW391509 and MW391510, CAM: MW392789 and MW392790, RPB2: MW392797 and MW392798, TEF1: MW392793 and MW392794). Alignments of a combined dataset of ITS, CAM, RPB2 and TEF1 were made using MAFFT v. 7, and phylogenetic analyses were conducted in MEGA v. 7.0 using the maximum likelihood method. The muskmelon isolates (XP11 and XP12) clustered together with the F. luffae reference strain LC12167 (99% bootstrap). To perform a pathogenicity test, 10 μl of conidial 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 expanded from the core towards the surface of the fruit, then white mycelia were produced on the surface. Ten isolations were re-isolated from the infected tissues and confirmed to fulfill Koch’s postulates. No symptoms were observed on the control muskmelons. To our knowledge, this is the first report of fruit rot caused by F. luffae in 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 Fusarium solani Fruit Rot of Pumpkin (Cucurbita pepo) in Trinidad

Plant Disease ◽

10.1094/pdis-93-5-0547b ◽

2009 ◽

Vol 93 (5) ◽

pp. 547-547

Author(s):

S. N. Rampersad

Keyword(s):

Fusarium Solani ◽

Cucurbita Pepo ◽

Morphological Characteristics ◽

Soft Rot ◽

The United States ◽

Fruit Rot ◽

Laboratory Manual ◽

First Report ◽

Pathogenicity Tests ◽

Negative Controls

Trinidad is a major exporter of pumpkins (Cucurbita pepo L.) to other Caribbean countries, Canada, and the United States. Producers and exporters have reported 50 to 80% yield losses because of soft rot and overnight collapse of fruit at the pre- and postharvest stages. Severe fruit rot occurred in fields in Victoria County in South Trinidad between April and May 2006 (mid-to-late dry season) with an increase in the severity and number of affected fruit in the rainy season (July to December). Symptoms began as water-soaked lesions on the fruit of any age at the point of contact with the soil. The disease progressed to a soft rot with leakage and whole fruit collapse. A dark brown, soft decay also developed at the base of the main vines. Fusarium solani was isolated on selective fusarium agar and potato dextrose agar (PDA) (1) after 7 to 10 days of incubation at 25°C. The pathogen was identified by morphological characteristics and pathogenicity tests. Colonies were fast growing with white aerial mycelia and a cream color on the reverse side; hyphae were septate and hyaline, conidiophores were unbranched, and microconidia were abundant, thin walled, hyaline, fusiform to ovoid, generally one to two celled, and 8 to 10 × 2 to 4 μm. Macroconidia were hyaline, two to three celled, moderately curved, thick walled, and 25 to 30 × 4 to 6 μm. Pathogenicity tests for 10 isolates were conducted on 2-week-old pumpkin seedlings (cv. Jamaican squash; seven plants per isolate) and mature pumpkin fruit (2). Briefly, seedlings were inoculated by dipping their roots in a spore suspension (1 × 104 spores per ml) for 20 min. The plants were repotted in sterile potting soil. For negative controls, plant roots were dipped in sterile water. After the rind of fruit was swabbed with 70% ethanol followed by three rinses with sterile distilled water, 0.4-cm-diameter agar plugs of the isolates were inserted into wounds made with a sterile 1-cm-diameter borer. Sterile PDA plugs served as negative controls. Fruit were placed in sealed, clear, plastic bags. Inoculated plants and fruit were placed on greenhouse benches (30 to 32°C day and 25 to 27°C night temperatures) and monitored over a 30-day period. Tests were repeated once. Inoculated fruit developed a brown, spongy lesion that expanded from the initial wound site over a period of approximately 17 days after inoculation. White mycelia grew diffusely over the lesion. Inoculated plants developed yellow and finally necrotic leaves and lesions developed on stems at the soil line approximately 21 days after inoculation. No symptoms developed on the control plants. The fungus was reisolated from symptomatic tissue, fulfilling Koch's postulates. To my knowledge, this is the first report of Fusarium fruit rot of pumpkin in Trinidad. References: (1) J. Leslie and B. Summerell. Page 1 in: The Fusarium Laboratory Manual. Blackwell Publishing, Oxford, 2006. (2) W. H. Elmer. Plant Dis. 80:131, 1996.

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First Report of Fruit Rot of Pumpkin Caused by Fusarium solani f. sp. cucurbitae in Arkansas

Plant Disease ◽

10.1094/pdis-93-6-0669b ◽

2009 ◽

Vol 93 (6) ◽

pp. 669-669 ◽

Cited By ~ 1

Author(s):

V. L. Castroagudin ◽

J. C. Correll ◽

R. D. Cartwright

Keyword(s):

Fusarium Solani ◽

Disease Incidence ◽

Apical Cell ◽

Causal Agent ◽

Fruit Rot ◽

Monthly Precipitation ◽

Pathogenicity Test ◽

Fusarium Spp ◽

First Report ◽

Fusarium Sp

During 2008, fruit rot of pumpkin (Cucurbita pepo L.) occurred on several cultivars in commercial fields in northeast and northwest Arkansas. Disease incidence ranged from 50 to 75% of the fruit, which were unmarketable. Symptoms included large (>10 cm), brown, corky lesions where the fruit was in contact with the soil. Initially, the lesions were water soaked. A cross section of the symptomatic fruit rind revealed a dry, brown, spongy rot with a light brown halo. Lesions finally became soft and wet, causing infected fruit to collapse. Masses of white mycelia surrounded advanced lesions. No rot symptoms were observed on the vines. Fusarium spp. were isolated from symptomatic fruit. Macroconidia obtained from field-infected fruit and pure potato dextrose agar (PDA) cultures of the predominant Fusarium sp. were morphologically similar. The straight, cylindrical, and robust macroconidia contained between five and seven septa. The apical cell was rounded and blunt and the basal cell was rounded. All three morphological types were tested for pathogenicity on mature fruit of cv. Sorcerer. Fruit were surface disinfected in 70% ethanol. Wounds were made (4 mm deep) in the fruit surface with a cork borer. Three wounds per isolate per fruit were inoculated with a PDA plug colonized with mycelium from a 3-day-old culture. Three replicated wounds were inoculated per isolate and four replicate fruit were used. After inoculation, the wounds were covered with saran wrap. The fruit were incubated at approximately 24°C and evaluated after 7 days. An uncolonized PDA plug was used as a negative control. After 7 days, only the predominant Fusarium sp. produced typical lesions, which were brown, water soaked, and approximately 3 cm in diameter. Fusarium spp. were recovered from the inoculated lesions. The colonies on PDA and macroconidia of the pathogenic Fusarium sp. were morphologically similar to the isolate inoculated and the ones recovered from field lesions. DNA was extracted from the same three isolates used in the pathogenicity test. A portion of the translation elongation factor 1α (TEF) gene was sequenced to verify the identity of the pathogenic isolates. On the basis of a comparison of the Fusarium-ID database at Pennsylvania State University (3), the pathogenic isolates had a 100% match with Fusarium solani f. sp. cucurbitae race 1, teleomorph Nectria haematococca mating population I, isolate NRRL 22098. F. solani f. sp cucurbitae was previously identified as the causal agent of crown and foot rot and a fruit rot of cucurbits and responsible for outbreaks on pumpkin fruit in Connecticut, Missouri, New York, and Ohio from 2001 to 2003 and again in Ohio in 2005 (2). In 2008, a higher average total of monthly precipitation was recorded late in the growing season in Arkansas, (13.7 cm in August and 23.7 cm in September). Although F. equiseti has previously been reported as a fruit rot pathogen of pumpkin in Arkansas (1), to our knowledge, this is the first report of F. solani f. sp cucurbitae as causal agent of pumpkin fruit rot in the state. Reference: (1) J. C. Correll et al. Plant Dis. 75:751, 1991. (2) W. H. Elmer et al. Plant Dis. 91:1142, 2007. (3) D. M. Geiser et al. Eur. J. Plant Pathol. 110:473, 2004.

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First Report of Leaf Blight of Japanese Yew Caused by Pestalotiopsis microspora in Korea

Plant Disease ◽

10.1094/pdis-08-13-0821-pdn ◽

2014 ◽

Vol 98 (5) ◽

pp. 691-691 ◽

Cited By ~ 2

Author(s):

Y. H. Jeon ◽

W. Cheon

Keyword(s):

Dna Sequences ◽

Apical Cell ◽

Morphological Characteristics ◽

Leaf Blight ◽

Economic Damage ◽

Leaf Margin ◽

Conidial Suspension ◽

First Report ◽

Pestalotiopsis Microspora ◽

Large Trees

Worldwide, Japanese yew (Taxus cuspidata Sieb. & Zucc.) is a popular garden tree, with large trees also being used for timber. In July 2012, leaf blight was observed on 10% of Japanese yew seedling leaves planted in a 500-m2 field in Andong, Gyeongsangbuk-do Province, South Korea. Typical symptoms included small, brown lesions that were first visible on the leaf margin, which enlarged and coalesced into the leaf becoming brown and blighted. To isolate potential pathogens from infected leaves, small sections of leaf tissue (5 to 10 mm2) were excised from lesion margins. Eight fungi were isolated from eight symptomatic trees, respectively. These fungi were hyphal tipped twice and transferred to potato dextrose agar (PDA) plates for incubation at 25°C. After 7 days, the fungi produced circular mats of white aerial mycelia. After 12 days, black acervuli containing slimy spore masses formed over the mycelial mats. Two representative isolates were further characterized. Their conidia were straight or slightly curved, fusiform to clavate, five-celled with constrictions at the septa, and 17.4 to 28.5 × 5.8 to 7.1 μm. Two to four 19.8- to 30.7-μm-long hyaline filamentous appendages (mostly three appendages) were attached to each apical cell, whereas one 3.7- to 7.1-μm-long hyaline appendage was attached to each basal cell, matching the description for Pestalotiopsis microspora (2). The pathogenicity of the two isolates was tested using 2-year-old plants (T. cuspidata var. nana Rehder; three plants per isolate) in 30-cm-diameter pots filled with soil under greenhouse conditions. The plants were inoculated by spraying the leaves with an atomizer with a conidial suspension (105 conidia/ml; ~50 ml on each plant) cultured for 10 days on PDA. As a control, three plants were inoculated with sterilized water. The plants were covered with plastic bags for 72 h to maintain high relative humidity (24 to 28°C). At 20 days after inoculation, small dark lesions enlarged into brown blight similar to that observed on naturally infected leaves. P. microspora was isolated from all inoculated plants, but not the controls. The fungus was confirmed by molecular analysis of the 5.8S subunit and flanking internal transcribed spaces (ITS1 and ITS2) of rDNA amplified from DNA extracted from single-spore cultures, and amplified with the ITS1/ITS4 primers and sequenced as previously described (4). Sequences were compared with other DNA sequences in GenBank using a BLASTN search. The P. microspora isolates were 99% homologous to other P. microspora (DQ456865, EU279435, FJ459951, and FJ459950). The morphological characteristics, pathogenicity, and molecular data assimilated in this study corresponded with the fungus P. microspora (2). This fungus has been previously reported as the causal agent of scab disease of Psidium guajava in Hawaii, the decline of Torreya taxifolia in Florida, and the leaf blight of Reineckea carnea in China (1,3). Therefore, this study presents the first report of P. microspora as a pathogen on T. cuspidata in Korea. The degree of pathogenicity of P. microspora to the Korean garden evergreen T. cuspidata requires quantification to determine its potential economic damage and to establish effective management practices. References: (1) D. F. Farr and A. Y. Rossman, Fungal Databases, Syst. Mycol. Microbiol. Lab. Retrieved from http://nt.ars-grin.gov/fungaldatabases/ (2) L. M. Keith et al. Plant Dis. 90:16, 2006. (3) S. S. N. Maharachchikumbura. Fungal Diversity 50:167, 2011. (4) T. J. White et al. PCR Protocols. Academic Press, San Diego, CA, 1990.

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First Report of Stemphylium botryosum Causing Leaf Blight of Kiwi in the Province Imathia, Northern Greece

Plant Disease ◽

10.1094/pdis-92-4-0650b ◽

2008 ◽

Vol 92 (4) ◽

pp. 650-650 ◽

Cited By ~ 1

Author(s):

T. Thomidis ◽

T. J. Michailides

Keyword(s):

Apical Cell ◽

Morphological Characteristics ◽

Leaf Blight ◽

Width Ratio ◽

Northern Greece ◽

Cell Width ◽

Koch’S Postulates ◽

First Report ◽

Stemphylium Botryosum ◽

Koch's Postulates

In Greece, kiwi (Actinidia deliciosa) is mostly found in the northern part of the country where approximately 440,000 ha are grown. In the summer of 2006, a Stemphylium sp. was frequently isolated from leaves of kiwi (cv. Hayward) grown in the province of Imathia. Symptomatic leaves were covered with irregular, necrotic, brown areas. Lesions had a distinct margin that, in some cases, covered a wide part of the diseased leaves. Intense symptoms were frequently observed and associated with defoliation. This Stemphylium sp. was consistently isolated from diseased leaves onto potato dextrose agar (PDA) after surface sterilization with 0.1% chlorine solution. On the basis of morphological characteristics of mycelia, dimensions (length 20 to 29 μm and width 14 to 21 μm) and mean length/width ratio (1.42 μm) of conidia, and width and apical cell width of condiophores, the fungus was identified as Stemphylium botryosum (Wallr.) (2,3) Koch's postulates were completed in the laboratory by inoculating leaves of kiwi (cv. Hayward) with an isolate of S. botryosum originated from a symptomatic leaf of a Hayward kiwi. Twenty leaves were surface sterilized by dipping them into 0.1% chlorine solution for 2 to 3 min, washing in sterile distilled water, and allowing them to dry in a laminar flow hood. A leaf was then placed into a petri plate containing a wet, sterilized paper towel. Inoculation was made by transferring a 5-mm-diameter mycelial disc from the margins of a 7-day-old culture onto the center of each leaf surface. Petri plates were closed and incubated at 25°C with 12 h of light for 6 days. Koch's postulates were satisfied when the same S. botryosum was reisolated from 100% of inoculated leaves that developed symptoms similar to those observed in the vineyards. Leaves inoculated with a PDA plug alone (with no S. botryosum) did not develop any symptoms. Previously, Alternaria alternata was reported as the causal agent of a leaf spot pathogen of kiwi (1,4). To our knowledge, this is the first report of the occurrence of S. botryosum causing leaf blight of kiwi in Greece and worldwide. This pathogen can cause a high level of defoliation in diseased plants. References: (1) L. Corazza et al. Plant Dis. 83:487, 1999. (2) M. B. Ellis. Dematiaceous Hyphomycetes. Mycology Institute. London, England, 1971. (3) E. G. Simmons. Mycologia 61:1, 1969. (4) C. Tsahouridou and C. C. Thanassoulopoulos. Plant Dis. 84:371, 2000

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First Report of a Fruit Rot of Pumpkin Caused by Acidivorax avenae subsp. citrulli in Georgia

Plant Disease ◽

10.1094/pdis.1999.83.2.199b ◽

1999 ◽

Vol 83 (2) ◽

pp. 199-199 ◽

Cited By ~ 31

Author(s):

D. B. Langston ◽

R. D. Walcott ◽

R. D. Gitaitis ◽

F. H. Sanders

Keyword(s):

Polyclonal Antibodies ◽

Pcr Amplification ◽

Tween 80 ◽

Soft Rot ◽

Fruit Rot ◽

Identification System ◽

Banding Patterns ◽

First Report ◽

Microbial Identification ◽

Necrotic Spots

In September 1998, a fruit rot was reported affecting pumpkin (Cucurbita pepo) in a commercial field in Terrell Co., Georgia. Symptoms on the surface of fruit occurred as round, necrotic spots or cracks a few millimeters in diameter. With age, the tissue surrounding these lesions became soft and wrinkled. A soft rot expanded into the flesh of the pumpkin, originating from the lesions observed on the surface. In time, infected pumpkins totally collapsed. V-shaped, necrotic lesions occurred at the margin of the leaf and extended inward toward the mid-rib. Samples were collected from the field and bacteria were isolated from fruit and leaf lesions onto King's medium B (1). The bacterium isolated was rod shaped, gram negative, nonflourescent, oxidase positive, Tween 80 positive, carboxymethyl cellulose positive, β-OH butyrate positive, and malonate negative. The bacterium reacted positively with polyclonal antibodies specific for the watermelon fruit blotch pathogen Acidivorax avenae subsp. citrulli and was identified as A. avenae subsp. citrulli by MIDI (Microbial Identification System, Newark, DE) according to statistical analysis of fatty acid data. Results from polymerase chain reaction (PCR) amplification of the bacterium isolated from pumpkin yielded 360-bp fragments that, when digested with the restriction enzyme HaeIII, had DNA banding patterns identical to those of stock A. avenae subsp. citrulli DNA. Koch's postulates were completed successfully with 2-week-old watermelon seedlings. This is the first report of A. avenae subsp. citrulli causing fruit rot of pumpkin in Georgia. Reference: (1) E. O. King et al. J. Lab. Clin. Med. 44:301, 1954.

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First Report of Strawberry Fruit Rot Caused by Alternaria tenuissima in Korea

Plant Disease ◽

10.1094/pdis.2001.85.5.563b ◽

2001 ◽

Vol 85 (5) ◽

pp. 563-563 ◽

Cited By ~ 5

Author(s):

H. B. Lee ◽

C.-J. Kim ◽

S. H. Yu

Keyword(s):

Fruits And Vegetables ◽

Morphological Characteristics ◽

West Germany ◽

Fruit Rot ◽

Conidial Suspension ◽

Strawberry Fruit ◽

Alternaria Tenuissima ◽

First Report ◽

The Usa ◽

Dark Green

A strawberry (Fragaria × ananassa Duch.) fruit rot disease has been observed in several vinyl-house fields at Nonsan and Taejon, Chungnam district, Korea, especially following moist and cool conditions in the spring and again in September. Over the past 7 years, incidence of the disease has ranged from 0.2 to 2.0%. Early symptoms on fruits were characterized by small, irregular lesions, which were slightly sunken and appeared light green to black in color as sporulation began. Conidia were 25 to 55 μm long by 10 to 17 μm wide; beaks, when present, were 2 to 3 μm wide and up to 40 μm long; and conidiophores were 20 to 110 μm long by 3 to 5 μm wide. Older lesions were circular, largely sunken, firm, and dark-green to almost black because of abundant sporulation. The fungus isolated from infected fruit tissues was identified as Alternaria tenuissima (Fries) Wiltshire, based on the morphological characteristics of the conidia and conidiophores. Pathogenicity tests were conducted by inoculating slightly wounded, ripe (red) and immature (green) fruits with a conidial suspension (1 × 106 conidia/ml). Twenty-four ripe and immature fruits were inoculated with each of six isolates in duplicate and placed in a moist chamber for 48 h at 25°C and then transferred to vinyl-house field. After 7 to 10 days fruit rot symptoms were visible on the inoculated fruits and appeared nearly identical to lesions observed in the field, although there were differences in aggressiveness among isolates. Control fruits sprayed with distilled water did not develop any symptoms. Green fruits were generally more resistant to infection than ripe ones. The causal fungus was easily reisolated from lesions on inoculated strawberries. Alternaria fruit rot of strawberries has been reported from the USA, UK, and West Germany (2). Howard and Albregts (1) first reported a strawberry fruit rot caused by A. tenuissima in Florida, but the disease is generally not considered important. However, occasionally losses from this disease have been extensive in Korea. To the authors' knowledge, this is the first report of strawberry fruit rot caused by Alternaria tenuissima in Korea. References: (1) C. M. Howard and E. E. Albregts. Phytopathology 63:638–639, 1973. (2) A. L. Snowdon. Pages 250–252 in: A Color Atlas of Post-Harvest Diseases and Disorders of Fruits and Vegetables. Vol. 1. 1990. Wolfe Scientific, London.

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First Report of Fruit Rot of Melon Caused by Fusarium asiaticum in China

Plant Disease ◽

10.1094/pdis-08-20-1857-pdn ◽

2020 ◽

Author(s):

Fangmin Hao ◽

Quanyu Zang ◽

Weihong Ding ◽

Erlei Ma ◽

Yunping Huang ◽

...

Keyword(s):

Disease Incidence ◽

Elongation Factor ◽

Morphological Characteristics ◽

Its Region ◽

Fruit Rot ◽

Post Inoculation ◽

Basal Cells ◽

First Report ◽

Fusarium Asiaticum ◽

Sterile Needle

Melon (Cucumis melo L.) is a member of the Cucurbitaceae family, an important economical and horticultural crop, which is widely grown in China. In May 2020, fruit rot disease with water-soaked lesions and pink molds on cantaloupe melons was observed in several greenhouses with 50% disease incidence in Ningbo, Zhejiang Province in China. In order to know the causal agent, diseased fruits were cut into pieces, surface sterilized for 1 min with 1% sodium hypochlorite (NaClO), 2 min with 75% ethyl alcohol, rinsed in sterile distilled water three times (Zhou et al. 2018), and then placed on potato dextrose agar (PDA) medium amended with streptomycin sulfate (100 μg/ml) plates at 25°C for 4 days. The growing hyphae were transferred to new PDA plates using the hyphal tip method, putative Fusarium colonies were purified by single-sporing. Twenty-five fungal isolates were obtained and formed red colonies with white aerial mycelia at 25°C for 7 days, which were identified as Fusarium isolates based on the morphological characteristics and microscopic examination. The average radial mycelial growth rate of Fusarium isolate Fa-25 was 11.44 mm/day at 25°C in the dark on PDA. Macroconidia were stout with curved apical and basal cells, usually with 4 to 6 septa, and 29.5 to 44.2 × 3.7 to 5.2 μm on Spezieller Nährstoffarmer agar (SNA) medium at 25°C for 10 days (Leslie and Summerell 2006). To identify the species, the internal transcribed spacer (ITS) region and translational elongation factor 1-alpha (TEF1-α) gene of the isolates were amplified and cloned. ITS and TEF1-α was amplified using primers ITS1/ITS4 and EF1/EF2 (O’Donnell et al. 1998), respectively. Sequences of ITS (545 bp, GenBank Accession No. MT811812) and TEF1-α (707 bp, GenBank Acc. No. MT856659) for isolate Fa-25 were 100% and 99.72% identical to those of F. asiaticum strains MSBL-4 (ITS, GenBank Acc. MT322117.1) and Daya350-3 (TEF1-α, GenBank Acc. KT380124.1) in GenBank, respectively. A phylogenetic tree was established based on the TEF1-α sequences of Fa-25 and other Fusarium spp., and Fa-25 was clustered with F. asiaticum. Thus, both morphological and molecular characterizations supported the isolate as F. asiaticum. To confirm the pathogenicity, mycelium agar plugs (6 mm in diameter) removed from the colony margin of a 2-day-old culture of strain Fa-25 were used to inoculate melon fruits. Before inoculation, healthy melon fruits were selected, soaked in 2% NaClO solution for 2 min, and washed in sterile water. After wounding the melon fruits with a sterile needle, the fruits were inoculated by placing mycelium agar plugs on the wounds, and mock inoculation with mycelium-free PDA plugs was used as control. Five fruits were used in each treatment. The inoculated and mock-inoculated fruits were incubated at 25°C with high relative humidity. Symptoms were observed on all inoculated melon fruits 10 days post inoculation, which were similar to those naturally infected fruits, whereas the mock-inoculated fruits remained symptomless. The fungus re-isolated from the diseased fruits resembled colony morphology of the original isolate. The experiment was conducted three times and produced the same results. To our knowledge, this is the first report of fruit rot of melon caused by F. asiaticum in China.

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