scholarly journals First Report of Nectria haematococca Stem Girdling of Greenhouse Peppers in Florida

Plant Disease ◽  
2001 ◽  
Vol 85 (4) ◽  
pp. 446-446 ◽  
Author(s):  
E. Lamb ◽  
E. Rosskopf ◽  
R. M. Sonoda
Keyword(s):  
South Florida ◽  
Fruit Rot ◽  
Nectria Haematococca ◽  
Single Spore ◽  
Agar Block ◽  
First Report ◽  
Half Strength ◽  
Stem Lesions ◽  
First Time ◽  
Stem Girdling

Nectria haematococca Berk. & Broome causing stem girdling of three cultivars of greenhouse pepper, Capsicum annuum (cvs. Kelvin, Cubico, and Grizzly), was found for the first time in a single greenhouse in south Florida in March 1999. Approximately 10% of the plants were affected at first report increasing to over 40% within 3 months. Black lesions occurred at nodes where the plant was pruned or where fruit had been harvested. No mycelium or perithecia were noted in association with the lesions. All tissue above a lesion appeared normal until the lesion girdled the stem, causing the tissue above the lesion to wilt and die. The plant appeared unaffected below the lesion. The pathogen was isolated on half-strength Difco potato-dextrose agar (½ DPDA). Reddish perithecia developed readily in culture. Two single spore isolates of the pathogen obtained from two naturally infected plants (cultivar Kelvin) were used to satisfy Koch's postulates. Five plants of Kelvin were inoculated with each isolate by inserting a 4-mm agar block of the pathogen grown for 5 days on ½ DPDA into the stem. Five plants of the same cultivar were similarly treated with fungus-free ½ DPDA. Plants were grown under greenhouse conditions after inoculation. In four plants, black lesions similar to those seen in the commercial greenhouse developed within 1 week. In one plant, the portions of the plants above the point of inoculation wilted after 5 days. The upper parts of the plants appeared healthy until lesions girdled the stems. The plants treated with fungus-free agar remained healthy. The fungus was re-isolated from the margins of lesions on the inoculated plants. The pathogen has been reported to cause stem lesions and fruit rot of pepper in greenhouses in England (1) and Canada (2). Fruit symptoms were not observed in the Florida greenhouse. Stem symptoms were again reported from the same greenhouse in the following season. References: (1) J. T. Fletcher. Plant Pathol. 43:225–222, 1994. (2) W. R. Jarvis. Can. Plant Dis. Surv. 74:131–134, 1994.

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

Plant Disease ◽  
2011 ◽  
Vol 95 (9) ◽  
pp. 1190-1190 ◽  
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.

scholarly journals First report of Fusarium incarnatum causing fruit rot of litchi in China

Plant Disease ◽  
2021 ◽  
Author(s):  
Zhaoyin Gao ◽  
Jiaobao Wang ◽  
Zhengke Zhang ◽  
Min Li ◽  
Deqiang Gong ◽  
...  
Keyword(s):  
Southern China ◽  
Fusarium Species ◽  
Morphological Characteristics ◽  
Fruit Rot ◽  
Conidial Suspension ◽  
Single Spore ◽  
Internal Transcribed Spacer Region ◽  
First Report ◽  
Litchi Fruit ◽  
His3 Gene

Litchi (Litchi chinensis Sonn.) is an indigenous tropical and subtropical fruit in Southern China with an attractive appearance, delicious taste, and good nutritional value (Jiang et al. 2003). In March 2020, brown rots were observed on nearly ripe litchi fruits (cv. Guihuaxiang) in an orchard of Lingshui county, Hainan province of China (18.615877° N, 109.948871° E). About 5% fruits were symptomatic in the field, and the disease caused postharvest losses during storage. The initial infected fruits had no obvious symptoms on the outer pericarp surfaces, but appeared irregular, brown to black-brown lesions in the inner pericarps around the pedicels. Then lesions expanded and became brown rots. Small tissues (4 mm × 4 mm) of fruit pericarps were cut from symptomatic fruits, surface-sterilized in 1% sodium hypochlorite for 3 min, rinsed in sterilized water three times, plated on potato dextrose agar (PDA) and incubated at 28℃ in the darkness. Morphologically similar colonies were isolated from 85% of 20 samples after 4 days of incubation. Ten isolates were purified using a single-spore isolation method. The isolates grown on PDA had abundant, fluffy, whitish to yellowish aerial mycelia, and the reverse side of the Petri dish was pale brown. Morphological characteristics of conidia were further determined on carnation leaf-piece agar (CLA) (Leslie et al. 2006). Macroconidia were straight to slightly curved, 3- to 5-septates with a foot-shaped basal cell, tapered at the apex, 2.70 to 4.43 µm × 18.63 to 37.58 µm (3.56 ± 0.36 × 28.68 ± 4.34 µm) (n = 100). Microconidia were fusoid to ovoid, 0- to 1-septate, 2.10 to 3.57 µm × 8.18 to 18.20 µm (2.88 ± 0.34 × 11.71 ± 1.97 µm) (n = 100). Chlamydospores on hyphae singly or in chains were globose, subglobose, or ellipsoidal. Based on cultural features and morphological characteristics, the fungus was identified as a Fusarium species (Leslie et al. 2006). To further confirm the pathogen, DNA was extracted from the 7-day-old aerial mycelia of three isolates (LZ-1, LZ-3, and LZ-5) following Chohan et al. (2019). The sequences of the internal transcribed spacer region of rDNA (ITS), translation elongation factor-1 alpha (tef1) gene, and histone H3 (his3) gene were partially amplified using primers ITS1/ITS4, EF1-728F/EF1-986R, and CYLH3F/CYLH3R, respectively (Funnell-Harris et al. 2017). The nucleotide sequences were deposited in GenBank (ITS: 515 bp, MW029882, 533 bp, MW092186, and 465 bp, MW092187; tef1: 292 bp, MW034437, 262 bp, MW159143, and 292 bp, MW159141; his3: 489 bp, MW034438, 477 bp, MW159142, and 474 bp, MW159140). The ITS, tef1, and his3 genes showed 99-100% similarity with the ITS (MH979697), tef1 (MH979698), and his3 (MH979696) genes, respectively of Fusarium incarnatum (TG0520) from muskmelon fruit. The phylogenetic analysis of the tef1 and his3 gene sequences showed that the three isolates clustered with F. incarnatum. Pathogenicity tests were conducted by spraying conidial suspension (1×106 conidia/ml) on wounded young fruits in the orchid. Negative controls were sprayed with sterilized water. Fruits were bagged with polythene bags for 24 hours and then unbagged for 10 days. Each treatment had 30 fruits. The inoculated fruits developed symptoms similar to those observed in the orchard and showed light brown lesions on the outer pericarp surfaces and irregular, brown to black-brown lesions in the inner pericarps, while the fruits of negative control remained symptomless. The same fungus was successfully recovered from symptomatic fruits, and thus, the test for the Koch’s postulates was completed. F. semitectum (synonym: F. incarnatum) (Saha et al. 2005), F. oxysporum (Bashar et al. 2012), and F. moniliforme (Rashid et al. 2015) have been previously reported as pathogens causing litchi fruit rots in India and Bangladesh. To our knowledge, this is the first report of Fusarium incarnatum causing litchi fruit rot in China.

scholarly journals First Report of White Leaf Spot Caused by Pseudocercosporella capsellae on Brassica juncea in Australia

Plant Disease ◽  
2005 ◽  
Vol 89 (10) ◽  
pp. 1131-1131 ◽  
Author(s):  
L. Eshraghi ◽  
M. P. You ◽  
M. J. Barbetti
Keyword(s):  
Brassica Juncea ◽  
Oilseed Rape ◽  
Western Australia ◽  
Leaf Spot ◽  
Oilseed Crop ◽  
Single Spore ◽  
First Report ◽  
White Leaf ◽  
Humidity Chamber ◽  
Stem Lesions

Brassica juncea (L.) Czern & Coss (mustard) has potential as a more drought-tolerant oilseed crop than the Brassica napus, and the first two canola-quality B. juncea cultivars will be sown as large strip trials across Australia in 2005. This will allow commercial evaluation of oil and meal quality and for seed multiplication for the commercial release Australia-wide in 2006. Inspection of experimental B. juncea field plantings at Beverley (32°6′30″S, 116°55′22″E), and Wongan Hills (30°50′32″S, 116°43′33″E), Western Australia in September 2004 indicated the occurrence of extensive leaf spotting during B. juncea flowering. Symptoms of this disease included as many as 15 or more grayish white-to-brownish spot lesions per leaf, often with a distinct brown margin. Some elongate grayish stem lesions were also observed as reported earlier for B. napus oilseed rape (1). When affected materials were incubated in moist chambers for 48 h, abundant conidia typical of Pseudocercosporella capsellae (Ellis & Everh.) Deighton were observed that matched the descriptions of conidia given by Deighton (2) and those on B. napus in Western Australia (1). Five single-spore cultures from lesions were grown on water agar (WA) where the colonies characteristically produced purple-pink pigment in the agar after 2 weeks growth in an incubator maintained at 20°C with a 12-h photoperiod (3). Since agar cultures of P. capsellae rarely produce conidia (3), this observation helped with the verification of the cultures. Mycelial inoculum from these cultures was used to inoculate cotyledons of 50 7-day-old plants of B. juncea to satisfy Koch's postulates. Small pieces of mycelia were teased out from the surface of the growing margin of potato dextrose agar (PDA) cultures and inoculated onto both lobes of each cotyledon and plants incubated in a 100% humidity chamber for 48 h within a controlled environment room maintained at 20/15°C (day/night) with a 12-h photoperiod. After 2 weeks, lesions 5 to 8 mm in diameter were observed on the cotyledons. There were no symptoms on control plants that were treated with water only. Lesions on infected cotyledons incubated on moist filter paper for 24 h produced abundant cylindrical conidia showing 2 to 3 septa measuring 42.9 to 71.4 μm long and 2.9 to 3.1 μm wide. Single-spore isolations from these conidia produced typical P. capsellae colonies showing purple-pink pigments in WA, and dark, compacted, and slow-growing colonies with a dentate margin on PDA. White leaf spot caused by P. capsellae is an important disease of crucifers worldwide, but to our knowledge, this is the first report of P. capsellae on B. juncea in Australia. In Western Australia, P. capsellae occurs on B. napus oilseed rape (1) and in 1956, 1984, and 1987, it was recorded on B. rapa, B. oleracea, and B. chinensis, respectively (4), and on the same range of Brassica hosts in other regions of Australia. References: (1) M. J. Barbetti and K. Sivasithamparam. Aust. Plant Pathol.10:43, 1981. (2) F. C. Deighton. Commonw. Mycol. Inst. Mycol. Pap. 133:42, 1973. (3) S. T. Koike. Plant Dis. 80:960, 1996. (4) R. G. Shivas. J. R. Soc. West. Aust. 72:1, 1989.

scholarly journals First Report of Brown Rot Caused by Monilinia fructicola on Nectarine in Serbia

Plant Disease ◽  
2013 ◽  
Vol 97 (1) ◽  
pp. 147-147 ◽  
Author(s):  
J. Hrustić ◽  
M. Mihajlović ◽  
B. Tanović ◽  
G. Delibašić ◽  
I. Stanković ◽  
...  
Keyword(s):  
Prunus Persica ◽  
Its Region ◽  
Fruit Rot ◽  
Economic Losses ◽  
Morphological Identification ◽  
Single Spore ◽  
Daily Growth ◽  
Causal Organism ◽  
First Report ◽  
Apple Fruits

In August 2011, nectarine (Prunus persica (L.) Batsch var. nucipersica (Suckow) C. K. Schneid) fruit originated from Oplenac region with symptoms of fruit rot was collected at a green market in Belgrade. Fruit had large, brown, sunken lesions covered with grayish brown tufts. Symptoms resembled those caused by species of Monilinia including M. laxa, M. fructigena, or M. fructicola (2). In order to isolate the causal organism, small superficial fragments of pericarp were superficially disinfected with commercial bleach and placed on potato dextrose agar (PDA). The majority (32 out of 33) isolates formed rosetted non-sporulating colonies with lobed margins resembling those of M. laxa. However, one isolate (Npgm) produced an abundant, grayish-white colony with even margins and concentric rings of sporogenous mycelium, resembling those described for M. fructicola (2). Conidia were one-celled, hyaline, ellipsoid to lemon shaped, 7.38 to 14.76 × 4.92 to 9.84 μm, and borne in branched monilioid chains. The average daily growth on PDA at 24°C was 10.9 mm. A single-spore isolate of Npgm was identified as M. fructicola based on the morphology of colony and conidia, temperature requirements, and growth rate (2). Morphological identification was confirmed by an amplified product of 535 bp using genomic DNA extracted from the mycelium of pure culture and species-specific PCR for the detection of M. fructicola (2). The ribosomal internal transcribed spacer (ITS) region of rDNA of Npgm was amplified and sequenced using primers ITS1/ITS4. Sequence analysis of ITS region revealed 100% nucleotide identity between the isolate Npgm (GenBank Accession No. JX127303) and 17 isolates of M. fructicola from different parts of the world, including four from Europe (FJ411109, FJ411110, GU967379, JN176564). Pathogenicity of the isolate Npgm was confirmed by inoculating five surface-disinfected mature nectarine and five apple fruits by placing a mycelial plug under the wounded skin of the fruit. Nectarine and apple fruits inoculated with sterile PDA plugs served as a negative controls. After a 3-day incubation at 22°C, inoculated sites developed brown lesions and the pathogen was succesfully reisolated. There were no symptoms on the control nectarine or apple fruits. M. fructicola is commonly present in Asia, North and South America, New Zealand, and Australia, while in the EPPO Region the pathogen is listed as an A2 quarantine organism (3). In Europe, the first discovery of M. fructicola was reported in France and since then, it has been found in Hungary, Switzerland, the Czech Republic, Spain, Slovenia, Italy, Austria, Poland, Romania, Germany, and Slovakia (1). Most recently, M. fructicola was found on stored apple fruits in Serbia (4). To our knowledge, this is the first report of M. fructicola decaying peach fruit in Serbia. These findings suggest that the pathogen is spreading on its principal host plants and causing substantial economic losses in the Serbian fruit production. References: (1) R. Baker et al. European Food Safety Authority. Online publication. www.efsa.europa.eu/efsajournal . EFSA J. 9:2119, 2011. (2) M. J. Côté. Plant Dis. 88:1219, 2004. (3) OEPP/EPPO. EPPO A2 list of pests recommended for regulation as quarantine pests. Version 2009-09. http://www.eppo.org/QUARANTINE/listA2.htm . (4). M. Vasic et al. Plant Dis. 96:456, 2012.

scholarly journals First Report of Gliocephalotrichum bulbilium Causing Fruit Rot of Posthavest Mangosteen in China

Plant Disease ◽  
2014 ◽  
Vol 98 (7) ◽  
pp. 994-994 ◽  
Author(s):  
Y. X. Li ◽  
W. X. Chen ◽  
A. Y. Liu ◽  
Q. L. Chen ◽  
S. J. Feng
Keyword(s):  
Its Region ◽  
The United States ◽  
Psidium Guajava ◽  
Morphological Characters ◽  
Fruit Rot ◽  
Diseased Plant ◽  
Garcinia Mangostana ◽  
Single Spore ◽  
Tropical Fruit ◽  
First Report

Mangosteen (Garcinia mangostana L., Guttiferae) is a tropical fruit renowned for its pleasant taste, rich nutrition, and medicinal value. Little research about mangosteen diseases during storage and transport has been reported. In June of 2012, fruit rots on mangosteens imported from Thailand were observed in Guangzhou, China. In infected fruits, pericarps showed an increased firmness, were discolored to deep pink, and the edible aril became brown and rotten. In order to search for the etiological agent of this rot symptom, infected mangosteens were analyzed. Diseased mangosteen tissues were surface-sterilized with 70% alcohol, then with 0.1% HgCl2, dipped in sterilized water three times, and placed onto potato dextrose agar (PDA) at 26°C. The fungi isolated from tissues of the pericarp and aril were similar in morphology and grew rapidly, covering the plate surface (9 mm diameter) after 2 to 3 days of incubation at 26°C. The morphological characters of 10 single-spore isolates were observed. These isolates showed light yellow to light brown fertile colonies on PDA. On corn meal agar (CMA), conidiophores were erect, arising from wide hyphae; they were composed of a basal stipe ending in a penicillate conidiogenous apparatus with directly subtending sterile stipe extensions ranging from 74.5 to 195.0 μm long. Conidia were unicellular, smooth, oblong to elliptical, 6.3 to 8.5 × 2.5 to 3.0 μm, and accumulated in a mucilaginous mass. Chlamydospores were multicellular, dark brown, regular in shape and thick-walled, and 40.0 to 52.5 μm in diameter. On the basis of these morphological characters, these isolates were identified as Gliocephalotrichum bulbilium (2). To confirm the identity of this fungus, genomic DNA of two isolates was extracted, and fragments of ITS region and β-tubulin gene were amplified by PCR, sequenced, and compared with sequences of Gliocephalotrichum species available in NCBI GenBank. Both DNA regions (GenBank Accession Nos. KF716166 and KF716168) had sequence similarities of 99% and 97%, respectively, to other G. bulbilium sequences at GenBank. Pathogenicity tests were conducted on three detached fruits for two isolates. Fruits were inoculated using 5-mm mycelial disks with conidia taken from 3-day-old cultures of G. bulbilium isolate Gb1 and Gb10 grown on PDA. Controls were inoculated with PDA disks only. All treated fruits were kept individually in a humid chamber at 26°C. Tests were repeated twice. Three days after inoculation, white mycelial growth for Gb was observed at inoculation sites. Eight days after inoculation, mycelium of Gb nearly covered the fruit, causing fruit rot, and the pericarp became hard and light in color. The control fruit did not rot. G. bulbilium was re-isolated from diseased plant tissue, thus fulfilling Koch's postulates. G. bulbilium has been reported causing postharvest fruit rot of rambutan (Nephelium lappaceum) and guava (Psidium guajava) in some locations (3,4). Moreover, the fungus caused cranberry fruit rot in the United States (1). To our knowledge, this is the first report of G. bulbilium causing postharvest fruit rot of mangosteen in China. It is uncertain whether the fungus infected mangosteen in Thailand and was carried to China due to commercial relationship. References: (1) C. Constantelos et al. Plant Dis. 95:618, 2011. (2) C. Decock et al. Mycologia 98:488, 2006. (3) L. M. Serrato-Diaz et al. Plant Dis. 96:1225, 2012. (4) A. Sivapalan et al. Australas. Plant Pathol. 27:274, 1998.

scholarly journals First Report of Fusarium solani Causing Fruit Rot of Sweet Pepper in Trinidad

Plant Disease ◽  
2010 ◽  
Vol 94 (11) ◽  
pp. 1375-1375 ◽  
Author(s):  
H. A. Ramdial ◽  
S. N. Rampersad
Keyword(s):  
Fusarium Solani ◽  
Disease Incidence ◽  
Sweet Pepper ◽  
Fruit Rot ◽  
Universal Primers ◽  
Distilled Water ◽  
Sequence Comparisons ◽  
Agar Block ◽  
First Report ◽  
Plant Pathol

In Trinidad, sweet pepper (Capsicum annuum L.) is an important crop that is produced for local markets and regional export. From February to April 2010, severe fruit rot was observed in 9 of 11 commercial fields located in North Trinidad in the major production areas of North and South Aranguez. All fields were in the late harvesting stage and the most commonly grown cultivars were Aristotle and Canape. Disease incidence for each field was estimated to be 80% with a yield loss of 40 to 60%. Symptoms appeared on mature red fruits but growers reported that disease can also occur on green fruit. Symptoms began as soft lesions that turned dark brown to black. Lesions usually originated at the calyx end of the fruit and extended down the sides. Fruits were surface sterilized by rinsing with 70% ethanol for 2 min, followed by three rinses with sterile distilled water. Two 4-mm3 blocks of tissue from the opposite sides of fruit lesions were transferred to water agar and incubated for 5 to 7 days at 25 ± 1°C. A 4-mm3 agar block consisting of the leading mycelial edge was then transferred to potato dextrose agar (PDA) and incubated under the same conditions. Colonies on PDA were fast growing with white, fluffy, aerial mycelia; hyphae were septate and hyaline; conidiophores were unbranched; microconidia were abundant, thin walled, hyaline, ovoid, one to two celled, and measured 6 to 10 × 2 to 4 μm. Macroconidia were hyaline, three to four celled, curved, thick walled, and measured 20 to 30 × 4 to 6 μm. PCR amplification was carried out utilizing universal primers ITS4/5 and translation elongation factor primers EF1/2 (2). Sequence comparisons of the internal transcribed spacer (ITS) region (HM157262) and EF-1α gene (HQ014854) with cognate sequences available in GenBank and the FUSARIUM-ID databases revealed 100 and 99.6% sequence identity, respectively, to Fusarium solani (Mart.) Sacc. Pathogenicity tests were conducted by drop inoculating 10-μl of spore suspension (106 spores/ml) of each of four isolates on wounded and unwounded sites of mature sweet pepper fruits (five per isolate of cvs. Aristotle, Canape, Century, Destra, and Paladin). Control fruits were inoculated with sterile distilled water. Inoculated fruits were kept at 25 ± 1°C in loosely sealed plastic containers and monitored for the onset of symptoms for 6 days. The experiment was conducted twice. Lesions (8.0 to 15.2 mm in diameter) developed on wounded fruit of Aristotle, Canape, and Century. No symptoms were seen on Destra, Paladin, or the water controls. No symptoms developed on nonwounded fruits. Koch's postulates were fulfilled by reisolating the pathogen from infected tissues. Fruit rot caused by F. solani has been reported to be a serious constraint to sweet pepper production in Canada (4), the United Kingdom (1), and New Zealand (3). To our knowledge, this is the first report of Fusarium fruit rot of sweet pepper in Trinidad. References: (1) J. T. Fletcher. Plant Pathol. 43:225, 1994. (2) D. M. Geiser et al. Eur. J. Plant Pathol. 110:473, 2004. (3) J. L. Tyson. Aust. Plant Pathol. 30:375, 2001. (4) R. Utkhede and S. Mathur. Plant Dis. 87:100, 2003.

scholarly journals First Report of Anthracnose Fruit Rot Caused by Colletotrichum fioriniae on Litchi in China

Plant Disease ◽  
2020 ◽  
Author(s):  
Jin-Feng Ling ◽  
Aitian Peng ◽  
Zide Jiang ◽  
Pinggen Xi ◽  
Xiaobing Song ◽  
...  
Keyword(s):  
Species Complex ◽  
Morphological Characteristics ◽  
Morphological Characterization ◽  
Fruit Rot ◽  
Single Spore ◽  
Potential Threat ◽  
First Report ◽  
Fruit Cracking ◽  
Pure Cultures ◽  
Colletotrichum Spp

Anthracnose fruit rot of litchi (Litchi chinensis Sonn.), caused by Colletotrichum spp., has been mainly associated with the C. acutatum species complex and C. gloeosporioides species complex (Farr and Rossman 2020). In June 2010, isolates of the C. acutatum species complex were isolated together with the C. gloeosporioides species complex from anthracnose lesions on litchi fruits (cv. Nuomici) obtained from a litchi orchard in Shenzhen (N 22.36°, E 113.58°), China. The symptoms typically appeared as brown lesions up to 25 mm in diameter, causing total fruit rot and sometimes fruit cracking. Based on the number of isolates we collected, the C. acutatum species complex appears less frequently on infected fruit compared to the C. gloeosporioides species complex. Since only the C. gloeosporioides species complex has been reported in China (Qi 2000; Ann et al. 2004), we focused on the C. acutatum species complex in this study. Pure cultures of fungal isolates were obtained by single-spore isolation. The isolate GBLZ10CO-001 was used for morphological characterization, molecular and phylogenetic analysis, and pathogenicity testing. Colonies were cultured on potato dextrose agar (PDA) at 25 ℃ for 7 days, circular, raised, cottony, gray or pale orange, with reverse carmine, and 39.6 to 44.7 mm in diameter. Conidia were 13.5 to 19 × 4 to 6 µm (mean ± SD = 15.9 ± 1.1 × 5.2 ± 0.3 µm, n = 50) in size, hyaline, smooth-walled, aseptate, straight, fusiform to cylindrical with both ends acute. Appressoria were 5.5 to 13.5 × 4.5 to 7.5 µm (mean ± SD = 7.6 ± 1.6 × 6.0 ± 0.7 µm, n = 50) in size, subglobose to elliptical, sometimes clavate or irregular, smooth-walled, with entire edge, sometimes undulate, pale to medium brown. These morphological characteristics were consistent with the descriptions of several Colletotrichum species belonging to the C. acutatum species complex, including C. fioriniae (Shivas and Tan 2009; Damm et al. 2012). For molecular identification, genomic DNA was extracted and the ribosomal internal transcribed spacer (ITS), partial sequences of the β-tubulin (TUB2), actin (ACT), glyceraldehyde-3-phosphate dehydrogenase (GAPDH), chitin synthase 1 (CHS-1), and histone3 (HIS3) genes were amplified and sequenced using the primer pairs ITS4/ITS5, T1/Bt2b, ACT512F/ACT783R, GDF1/GDR1, CHS-79F/CHS-354R, and CYLH3F/CYLH3R, respectively (White et al. 1990; Damm et al. 2012). The resulting sequences were submitted to GenBank (ITS: MN527186, TUB2: MT740310, ACT: MN532321, GAPDH: MN532427, CHS-1: MT740311, HIS3: MT740312). BLAST searches showed 98.70%-100% identity to the sequences of the C. fioriniae ex-holotype culture CBS 128517. The phylogram reconstructed from the combined dataset using MrBayes 3.2.6 (Ronquist et al. 2012) showed that isolate GBLZ10CO-001 clustered with C. fioriniae with high posterior probability. Koch’s postulates were performed in the field to confirm pathogenicity. Isolate GBLZ10CO-001 was grown on PDA (25 ℃ for 7 days) to produce conidia. In June 2014, litchi fruits (cv. Nuomici) were sprayed with conidial suspensions (106 conidia/ml), with sterile water as blank controls, and each treatment inoculated at least 15 fruits. Inoculated fruits were covered by an adhesive-bonded fabric bag until the trial ended. After 31 days, typical symptoms were observed, while control fruits remained asymptomatic. The fungus was re-isolated from diseased fruits and identified as C. fioriniae according to the methods described above. To our knowledge, this is the first report of anthracnose fruit rot on litchi caused by C. fioriniae, one species of the C. acutatum species complex, in China. For the difficulty in distinguishing anthracnose caused by C. fioriniae from the C. gloeosporioides species complex just by the symptoms, and mixed infection usually occurring in the field, further investigations are required to reliably assess the potential threat posed by C. fioriniae for litchi production in China.

scholarly journals First Report of Ceratocystis changhui Causing Postharvest Fruit Rot of Peach in Kunming, China

Plant Disease ◽  
2020 ◽  
Author(s):  
Xue Li ◽  
Ruiqi Zhang ◽  
Kecheng Xu ◽  
Jie Li ◽  
Yu Zhang ◽  
...  
Keyword(s):  
Phylogenetic Trees ◽  
Prunus Persica ◽  
Management Strategies ◽  
Its Region ◽  
Its Sequences ◽  
Fruit Rot ◽  
Single Spore ◽  
Early Maturity ◽  
Potato Dextrose Agar Medium ◽  
First Report

The peach (Prunus persica (L) Batsch) is a predominant commercially grown stone fruit in China (Lee et al. 1990). Ceratocystis changhui is an aggressive pathogen causing typical black rot symptoms on corms of taro (Colocasia esculenta) (Liu et al. 2018), it has not been reported on other hosts. During the summer and autumn of 2013, a postharvest fruit rot disease was observed on several peaches at a farmer's market (N 25°02′; E 102°42′) in Kunming City, Yunnan Province, China. The incidence of the disease varied from 5 to 20%. Necrotic spots were first observed on the infected peach fruit (Prunus persica cv. shuimitao). The spots enlarged gradually and developed into a brown, water-soaked and rotted lesion. Eventually, the whole fruit became soft, rotted and covered with a gray-brown mycelium (Fig. 1 A, B). The isolates were obtained from the symptomatic tissues incubated on slices of fresh carrot root (Moller et al. 1968). After 5 to 10 days of incubation, perithecia and mycelium were observed growing on carrot slices. Spore masses were removed from the apices of perithecia, transferred to potato dextrose agar medium (PDA) and incubated at 25°C for 5 to 10 days, followed by single-spore isolation. All eight single-spore isolates from peach fruits obtained in this study were deposited in the State Key Laboratory for Conservation and Utilization of Bio-Resources in Yunnan, Yunnan Agricultural University, China. In culture, mycelium was initially white, gradually turned to greyish-green or brown (Fig. 1E, F). Measurements were made 7 days after the formation of perithecia. Perithecia (Fig. 1G) were black, globose, 185.71 to 305.56 μm × 142.86 to 264.29 µm and showed a long black neck, 600 to 957.14 µm (Fig. 1H). Ascospores (Fig. 1I) were helmet-hat shaped and 2.86 to 6.67 µm ×3.81 to 4.76 µm. Cylindrical conidia (Fig. 1J) 6.67 to 38. 95 µm × 2.86 to7.62 µm were observed. Chlamydospore (Fig. 1K), 8.57 to 13.33 μm × 5.71 to 9.52 μm, were ovoid or obpyriform, smooth. To further verify pathogen identity the internal transcribed spacer (ITS) region of rDNA was amplified using primers ITS1F and ITS4 (Thorpe et al. 2005), and the total genomic DNA from the mycelia of five isolates was extracted using a CTAB method (Lee &Taylor 1990). The nucleotide sequences have been blasted and deposited in the GenBank database. Analysis of the ITS sequences from the isolates T1-1yp, T1-2yp, T2-1yp (GenBank accession no. KY580895-KY580897) showed 99% to 100% similarity with isolates C. changhui CMW43272 (KY643886), CMW43281 (KY643884), CMW46112 (KY643891) and CMW46113 (KY643892) from taro in China. Phylogenetic trees based on the maximum-likelihood (ML) method were constructed using MEGA 7. ITS sequences of other Ceratocystis spp. were attained from NCBI for comparative analysis (Liu et al. 2018), and Davidsoniella virescens (CMW11164) served as outgroup. The robustness of ML tree was evaluated with 1,000 bootstrap (BS) values. The pathogen was identified as C. changhui based on the phylogenetic analysis (Fig. 2). Three isolates (T1-1yp, T1-2yp, T2-1yp) were used for pathogenicity. Nine Prunus persica cv. yingzuitao fruits at early maturity (8 points out of 10) were wound inoculated with 200μL conidia suspension of the fungus (approximately 2.0 × 106 conidia / mL). Degreasing cotton dipped in sterile water was used to raise the humidity in preservation boxes. Boxes were incubated for 10 days at 25°C. Three peaches as controls were treated only with sterile distilled water in the same way. Symptoms of sunken lesions and fruit rot were observed two days after inoculation, and measured at 1.8 to 3.2 cm from the inoculation point within 5 days (Fig. 1C: right, D). The same pathogen was re-isolated from them confirming Koch’s postulates. Control peaches remained symptomless. This fungus was morphologically and phylogenetically identified as C. changhui. To our knowledge, this is the first report of C. changhui on postharvest peach in Yunnan, China. The disease will affect quality and taste of peach, so it is critical to deploy appropriate management strategies to limit the fungus spread.

scholarly journals First Report of Pestalotiopsis virgatula Causing Pestalotiopsis Fruit Rot on Rambutan in Hawaii

Plant Disease ◽  
2008 ◽  
Vol 92 (5) ◽  
pp. 835-835 ◽  
Author(s):  
L. M. Keith
Keyword(s):  
Tap Water ◽  
Aerial Mycelium ◽  
Internal Transcribed Spacers ◽  
Fruit Rot ◽  
Basal Cells ◽  
Mature Fruit ◽  
Single Spore ◽  
First Report ◽  
Nephelium Lappaceum ◽  
Diseased Fruit

Rambutan (Nephelium lappaceum Linn.) is a tropical, exotic fruit that has a rapidly expanding niche market in Hawaii. Diseased rambutan fruit was commonly observed in orchards in the Hilo and Kona districts of Hawaii Island during 2006. In surveys conducted in January, symptoms appeared as dark brown-to-black spots on mature fruit and blackened areas at the base of spinterns (hair-like projections) of mature and immature fruits. Pieces of infected fruit (cv. R167) were surface sterilized for 2 min in 0.5% NaOCl, plated on potato dextrose agar, and incubated at 24 ± 1°C for 7 days. The fungus growing on PDA was pale buff with sparse, aerial mycelium and acervuli containing black, slimy spore masses. All isolates had five-celled conidia. Apical and basal cells were hyaline, while the three median cells were olivaceous; the upper two were slightly darker than the lower one. Conidia (n = 40) were 20.3 ± 0.1 × 6.8 ± 0.1 μm. There were typically three apical appendages averaging 16.8 ± 0.2 μm long. The average basal appendage was 3.8 ± 0.1 μm long. The fungus was initially identified as Pestalotiopsis virgatula (Kleb.) Stey. on the basis of conidial and cultural characteristics (3). The identification was confirmed by molecular analysis of the 5.8S subunit and flanking internal transcribed spacers (ITS1 and ITS2) of rDNA amplified from DNA extracted from single-spore cultures with the ITS1/ITS4 primers (1,4) and sequenced (GenBank Accession No. EU047943). To confirm pathogenicity, agar pieces, 3 mm in diameter, from 7-day old cultures were used as inoculum. Five mature fruit from rambutan cv. R134 were rinsed with tap water, surface sterilized with 0.5% NaOCl for 2 min, wounded with a needle head, inoculated in the laboratory, and maintained in a moist chamber for 7 days. Lesions resembling symptoms that occurred in the field were observed on fruit after 7 days. No symptoms were observed on fruit inoculated with agar media. The fungus reisolated from diseased fruit was identical to the original isolates, confirming Koch's postulates. The disease appears to be widespread in Hawaii. Preharvest symptoms may have the potential to affect postharvest fruit quality if fruits are not stored at the proper conditions. Pestalotiopsis spp. have been reported on rambutan in Malaysia, Brunei, and Australia (2). To my knowledge, this is the first report of P. virgatula causing fruit spots on rambutan in Hawaii. References: (1) G. Caetano-Annolles et al. Curr. Genet. 39:346, 2001. (2) D. F. Farr et al. Fungal Databases. Systematic Botany and Mycology Laboratory. On-line publication. ARS, USDA, 2007. (3) E. F. Guba. Monograph of Pestalotia and Monochaetia. Harvard University Press, Cambridge, MA, 1961. (4) T. J. White et al. PCR Protocols: A Guide to Methods and Applications. Academic Press, San Diego, CA. 1990.

scholarly journals First Report of Colletotrichum gloeosporioides Causing Anthracnose Fruit Rot of Trichosanthes kirilowii in China

Plant Disease ◽  
2007 ◽  
Vol 91 (5) ◽  
pp. 636-636 ◽  
Author(s):  
H. Y. Li ◽  
Z. F. Zhang
Keyword(s):  
Relative Humidity ◽  
Colletotrichum Gloeosporioides ◽  
Aerial Mycelium ◽  
Causal Agent ◽  
High Relative Humidity ◽  
Fruit Rot ◽  
Single Spore ◽  
Specific Primers ◽  
First Report ◽  
Trichosanthes Kirilowii

Trichosanthes kirilowii Maxim., a species within the gourd family, is cultivated in China for its edible seeds and medicinal roots. Since 2000, heavy losses due to fruit rot have been caused by a new disease with typical anthracnose symptoms, i.e., water-soaked, dark brown-to-black, sunken lesions. Signs of the suspected pathogen were usually seen on near-mature fruits and were especially evident after abundant rainfall. The lesions contained numerous black acervuli with black setae that produced abundant, salmon-colored spore masses under high relative humidity. Dark lesions on leaves and stems could also be found in the field that sometimes led to stem girdling and wilting. Conidia produced in acervuli were 14 to 20 × 3 to 6 μm, straight, cylindrical, hyaline, aseptate, with both ends rounded. Conidiophores were 13 to 22 × 4 to 6 μm, aseptate, and cylindrical, while the setae, usually with three to five septa, measured 60 to 86 × 5 to 6 μm. The pathogen was initially identified as Colletotrichum gloeosporioides on the basis of the morphology (2). In culture, the fungus produced a gray-to-black colony with whitish aerial mycelium on potato dextrose agar (PDA) medium. Pathogenicity was tested by inoculating the equator of 10 fruits of T. kirilowii with a 5-day-old mycelia plug from a single-spore colony (0.5 cm in diameter); fruits inoculated with the plugs of PDA medium served as the control. Inoculated fruits were covered with plastic for 24 h to maintain high relative humidity. After 4 days, 100% of the inoculated fruits showed symptoms identical to those observed on T. kirilowii fruit affected in the field, while all fruits inoculated with PDA medium remained free of symptoms. Reisolation of the fungus from fruit lesions confirmed that the causal agent was C. gloeosporioides. To confirm the pathogen to species, the C. gloeosporioides-specific primers CgInt/ITS4 and C. acutatum-specific primers CaInt2/ITS4 (1) were used to amplify the sequence of internal transcribed spacer regions. A fragment of approximately 500 bp was only amplified with primers CgInt/ITS4 and the sequence (GenBank Accession No. AM491334) was 98 to 100% matched to the sequences of several C. gloeosporioides isolates (e.g., GenBank Accession Nos. AJ301919, AB255249, AJ301908), whereas the sequence shares 86 and 91% identity to that of C. orbiculare (GenBank Accession No. AB042308) and C. acutatum (GenBank Accession No. AJ749675), respectively. Thus, we concluded that C. gloeosporioides is the causal agent of anthracnose fruit rot of T. kirilowii. To our knowledge, this is the first report of C. gloeosporioides infecting T. kirilowii. References: (1) A. E. Brown et al. Phytopathology 86:523, 1996. (2) B. C. Sutton. The Coelomycetes. CAB International Publishing, New York, 1980.

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