scholarly journals Combination of Hot Water and Ethanol to Control Postharvest Decay of Peaches and Nectarines

Plant Disease ◽  
1997 ◽  
Vol 81 (12) ◽  
pp. 1405-1409 ◽  
Author(s):  
Dennis A. Margosan ◽  
Joseph L. Smilanick ◽  
Gilbert F. Simmons ◽  
Delmer J. Henson
Keyword(s):  
Brown Rot ◽  
Hot Water ◽  
Monilinia Fructicola ◽  
Rhizopus Stolonifer ◽  
Postharvest Decay ◽  
Control Fruit ◽  
Extensive Evaluation

Spores of Monilinia fructicola or Rhizopus stolonifer were immersed in water or 10% ethanol (EtOH) for 1, 2, 4, or 8 min at temperatures of 46 or 50°C to determine exposure times that would produce 95% lethality (LT95). EtOH reduced the LT95 by about 90%. Peaches and nectarines infected with M. fructicola were immersed in hot water alone or with EtOH to control decay. EtOH significantly increased the control of brown rot compared to water alone. Immersion of fruit in water at 46 or 50°C for 2.5 min reduced the incidence of decayed fruit from 82.8% to 59.3 and 38.8%, respectively. Immersion of fruit in 10% ethanol at 46 or 50°C for 2.5 min further reduced decay to 33.8 and 24.5%, respectively. Decay after triforine (1,000 μg ml-1) treatment was 32.8%. Two treatments, 10% EtOH at 50°C for 2.5 min and 20% EtOH at 46°C for 1.25 min, were selected for extensive evaluation. The flesh of EtOH-treated fruit was significantly firmer, approximately 4.4 N force, than that of control fruit among seven of nine cultivars evaluated. No other factor evaluated was significantly influenced by heated EtOH treatments. The EtOH content of fruit treated with 10 or 20% EtOH was approximately 520 and 100 μg g-1 1 day and 14 days after treatment, respectively.

scholarly journals Fumigation of Fruit with Short-Chain Organic Acids to Reduce the Potential of Postharvest Decay

Plant Disease ◽  
1998 ◽  
Vol 82 (6) ◽  
pp. 689-693 ◽  
Author(s):  
P. L. Sholberg
Keyword(s):  
Formic Acid ◽  
Fungal Pathogens ◽  
Citrus Fruit ◽  
Penicillium Expansum ◽  
Monilinia Fructicola ◽  
Rhizopus Stolonifer ◽  
Pome Fruit ◽  
Fruit Peel ◽  
Postharvest Decay ◽  
Fruit Decay

Vapors of acetic (1.9 or 2.5 μl/liter), formic (1.2 μl/liter), and propionic (2.5 μl/liter) acids were tested for postharvest decay control on 8 cherry, 14 pome, and 3 citrus fruit cultivars. Surfacesterilized fruit were inoculated with known fungal pathogens by drying 20-μl drops of spore suspension on marked locations on each fruit, placing at 10°C to equilibrate for approximately 24 h, and fumigating by evaporating the above acids in 12.7-liter airtight fumigation chambers for 30 min. Immediately after fumigation, the fruit were removed, aerated, aseptically injured, and placed at 20°C until decay occurred. All three fumigants controlled Monilinia fructicola, Penicillium expansum, and Rhizopus stolonifer on cherry. Formic acid increased fruit pitting on six of eight cultivars and was the only organic acid to increase blackening of cherry stems when compared to the control. Decay of pome fruit caused by P. expansum was reduced from 98% to 16, 4, or 8% by acetic, formic, and propionic acids, respectively, without injury to the fruit. Decay of citrus fruit by P. digitatum was reduced from 86 to 11% by all three acids, although browning of the fruit peel was observed on grapefruit and oranges fumigated with formic acid.

scholarly journals 272 CONTROL OF BROWN ROT OF PEACHES AND APRICOTS WITH HOT WATER AND CONTROLLED-ATMOSPHERE STORAGE

HortScience ◽  
1994 ◽  
Vol 29 (5) ◽  
pp. 469a-469
Author(s):  
Salah E. Youssef ◽  
Elizabeth J. Mitcham
Keyword(s):  
Brown Rot ◽  
Titratable Acidity ◽  
Hot Water ◽  
Soluble Solids ◽  
Monilinia Fructicola ◽  
Controlled Atmosphere ◽  
Controlled Atmosphere Storage ◽  
Atmosphere Storage ◽  
Better Than

Peaches and apricots were obtained at harvest. One-half were inoculated with the brown rot organism (Monilinia fructicola) and incubated overnight before immersion in 52C water for 2.5 and 2 minutes, respectively. Fruit were placed in storage at SC in air, 2% O2 and 15% CO2, or 17% O2 and 15% CO2 for 5 or 15 days before ripening at 20C. For peach, controlled atmosphere (CA) had no influence on decay while hot water significantly reduced decay incidence and severity. For apricot, after 15 days cold storage, both hot water and controlled atmosphere storage reduced decay incidence and severity. CA with 2% O2 and 15% CO2 controlled decay better than 17% O2 and 15% CO2. Growth and sporulation of Monilinia fructicola in air and CA was also evaluated in vitro. The combination of heat and CA controlled decay better than either treatment alone. The hot water treatment resulted in minor surface injury on peaches while apricots were not injured. Fruit were evaluated after storage for firmness, soluble solids, and titratable acidity. Accumulation of ethanol and acetaldehyde as a result of CA storage was monitored.

scholarly journals First Report of Brown Rot Caused by Monilinia fructicola in Sweet Cherry in Maryland

Plant Disease ◽  
2013 ◽  
Vol 97 (1) ◽  
pp. 145-145 ◽  
Author(s):  
F. Chen ◽  
X. Liu ◽  
G. Schnabel
Keyword(s):  
Sweet Cherry ◽  
Prunus Avium ◽  
Brown Rot ◽  
Causal Agent ◽  
Monilinia Fructicola ◽  
Conidial Suspension ◽  
Sterile Water ◽  
Tomato Sauce ◽  
Control Fruit ◽  
Petri Dishes

Monilinia fructicola (G. Wint.) Honey is the most important causal agent of brown rot of stone fruits in North America. In July 2010, 20 sweet cherry fruit (Prunus avium) of unknown variety with symptoms resembling brown rot were collected from one commercial orchard in Maryland. Each cherry fruit came from a different tree. Symptoms included necrotic areas up to 10 mm in diameter with brown conidia and conidiophores developing from the infection center. Spores from nine symptomatic fruit collected each from different trees of a single orchard were suspended in sterile water, spread onto the surface of 1% agar plates, and incubated at 22°C. After 12 h, single, germinated spores were transferred onto 9-cm petri dishes with potato dextrose agar (PDA). Nine fungal colonies, each from a different fruit, were investigated in three replicates for cultural characteristics on separate petri dishes containing PDA. They were very similar in morphology and grew 12.4 mm per day on average at 22°C, forming branched, monilioid chains of grayish colonies with concentric rings and little sporulation. Rich sporulation was observed on tomato sauce medium (250 ml tomato sauce and 20 g agar in 750 ml water). The lemon-shaped spores had an average size of 15 × 10 μm, which is consistent with M. fructicola. Two colonies were randomly selected to identify the pathogen to the species level using a PCR technique based on cytochrome b sequence amplifications (2). Resulting gel electrophoresis patterns were consistent with M. fructicola. Koch's postulates were fulfilled by inoculating 15 mature sweet cherry fruits of cv. Bing with a conidial suspension (105 spores/ml) of one of the single-spore isolates from cherry. Fruit were stab-inoculated at a point to a depth of 2 mm using a sterile needle. A 10-μl droplet was placed on each wound; control fruit received sterile water without conidia. After 3 days of incubation at room temperature in airtight plastic bags, the inoculated fruit developed typical brown rot symptoms with lesions that were 20.6 mm in diameter. The developing spores on inoculated fruit were confirmed to be M. fructicola. All control fruit remained healthy. The entire detached fruit experiment was repeated 1 week later. M. fructicola is assumed to be the main causal agent of brown rot of sweet cherry in the northeastern United States, but recent studies show that M. laxa is also causing the disease on sweet cherry in many northeastern states (1). For this reason, it is important to delineate species for accurate disease assessments. This study confirms assumptions that M. fructicola is a causal agent of sweet cherry in Maryland. References: (1) K. D. Cox et al. Plant Dis. 12:1584. 2011. (2) J.-M. Hily et al. Pest Manag. Sci. 67:385, 2011.

scholarly journals First Report of Brown Rot of Peach Caused by Monilinia fructicola in Southeastern China

Plant Disease ◽  
2011 ◽  
Vol 95 (2) ◽  
pp. 225-225 ◽  
Author(s):  
M. J. Hu ◽  
Y. Chen ◽  
S. N. Chen ◽  
X. L. Liu ◽  
L. F. Yin ◽  
...  
Keyword(s):  
Dna Sequences ◽  
Prunus Persica ◽  
Morphological Characteristics ◽  
Brown Rot ◽  
Its Sequences ◽  
Monilinia Fructicola ◽  
Southeastern China ◽  
Fujian Province ◽  
First Report ◽  
Control Fruit

In 2009 and 2010, peaches (Prunus persica) with brown rot symptoms were collected from Zhejiang Plant Protection State Research Farm and a commercial orchard in Fujian Province in southeastern China. Affected fruit showed brown decay with zones of sporulation. Single-spore isolates from the diseased fruit were cultured on potato dextrose agar. After incubation at 25°C in the dark for 5 days, colonies were gray with concentric rings of sporulation. Mean mycelial growth of isolates MZ09-2a from Zhejiang Province and 0907-a from Fujian Province was 4.46 ± 0.58 and 7.05 ± 0.81 cm after 4 and 7 days of incubation, respectively. Lemon-shaped conidia were formed in branched, monilioid chains and mean size was 14.6 (9.6 to 21.6) × 10.3 (7.2 to 13.2) μm. Mean conidial germination was 97 ± 1% with one straight germ tube per conidium. These characteristics were consistent with descriptions of Monilinia fructicola (G. Wint.) Honey (3). Morphology-based species identification was confirmed by sequencing and analysis of ribosomal internal transcribed spacer (ITS) sequences. A 496-bp fragment including ITS 1 and 2 and the gene encoding the 5.8S small subunit of the ribosomal RNA from isolates MZ09-2a and 0907-a was amplified using the universal primer pair ITS1/ITS4 (4) and sequenced. Nucleotide sequences of both isolates were identical. Blast searches of the ITS sequences in GenBank showed the highest similarity (100%) with sequences of M. fructicola isolates from China (FJ515894), Italy (FJ411109), and Spain (EF207423). The isolates were also identified as M. fructicola using the Monilinia spp. PCR detection protocol based on sequence-characterized amplification region marker DNA sequences (2). Pathogenicity was confirmed by inoculating surface-sterilized, mature cv. Zhonghua 2 peaches with mycelial plugs of representative isolates. Fruit was stabbed at two points with a 5-mm-diameter sterile cork borer, mycelial plugs (5 mm in diameter) were removed from the periphery of a 4-day-old colony of each isolate and placed upside down into each wound; control fruit received water agar. Inoculated fruit developed typical brown rot symptoms with sporulating fungi while control fruit remained healthy after 3 days of incubation at 22°C in a moist chamber. Pathogens were reisolated from the inoculated fruit and confirmed to be M. fructicola on the basis of morphological characteristics. To our knowledge, this is the first report of M. fructicola in Zhejiang and Fujian provinces. Both provinces are located more than 1,000 km south of Beijing, Hebei, and Shandong provinces, where M. fructicola had been reported previously (1). References: (1) J. Y. Fan et al. Acta Phytophylacica Sin. (in Chinese) 34:289, 2007. (2) I. Gell et al. J. Appl. Microbiol. 103:2629, 2007. (3) G. C. M. van Leeuwen and H. A. van Kesteren. Can. J. Bot. 76:2041, 1998. (4) T. J. White et al. Page 315 in: PCR Protocols: A Guide to Methods and Applications. M. A. Innis et al., eds., Academic Press, San Diego, 1990.

scholarly journals Overexpression of a Redox-Regulated Cutinase Gene, MfCUT1, Increases Virulence of the Brown Rot Pathogen Monilinia fructicola on Prunus spp.

2010 ◽  
Vol 23 (2) ◽  
pp. 176-186 ◽  
Author(s):  
Miin-Huey Lee ◽  
Chiu-Min Chiu ◽  
Tatiana Roubtsova ◽  
Chien-Ming Chou ◽  
Richard M. Bostock
Keyword(s):  
Gene Expression ◽  
Redox Regulation ◽  
Brown Rot ◽  
Gus Expression ◽  
Apple Fruit ◽  
Gus Activity ◽  
Monilinia Fructicola ◽  
Gus Reporter ◽  
Flanking Regions ◽  
Prunus Spp

A 4.5-kb genomic DNA containing a Monilinia fructicola cutinase gene, MfCUT1, and its flanking regions were isolated and characterized. Sequence analysis revealed that the genomic MfCUT1 carries a 63-bp intron and a promoter region with several transcription factor binding sites that may confer redox regulation of MfCUT1 expression. Redox regulation is indicated by the effect of antioxidants, shown previously to inhibit MfCUT1 gene expression in cutin-induced cultures, and in the present study, where H2O2 enhanced MfCUT1 gene expression. A β-glucuronidase (GUS) reporter gene (gusA) was fused to MfCUT1 under the control of the MfCUT1 promoter, and this construct was then used to generate an MfCUT1-GUS strain by Agrobacterium spp.-mediated transformation. The appearance of GUS activity in response to cutin and suppression of GUS activity by glucose in cutinase-inducing medium verified that the MfCUT1-GUS fusion protein was expressed correctly under the control of the MfCUT1 promoter. MfCUT1-GUS expression was detected following inoculation of peach and apple fruit, peach flower petals, and onion epidermis, and during brown rot symptom development on nectarine fruit at a relatively late stage of infection (24 h postinoculation). However, semiquantitative reverse-transcriptase polymerase chain reaction provided sensitive detection of MfCUT1 expression within 5 h of inoculation in both almond and peach petals. MfCUT1-GUS transformants expressed MfCUT1 transcripts at twice the level as the wild type and caused more severe symptoms on Prunus flower petals, consistent with MfCUT1 contributing to the virulence of M. fructicola.

scholarly journals Efeito da irradiação UV-C no controle da podridão parda (Monilinia fructicola) e da podridão mole (Rhizopus stolonifer) em pós-colheita de pêssegos

2007 ◽  
Vol 32 (5) ◽  
pp. 393-399 ◽  
Author(s):  
Eliane Bassetto ◽  
Lilian Amorim ◽  
Eliane A. Benato ◽  
Fabrício P. Gonçalves ◽  
Silvia A. Lourenço
Keyword(s):  
Monilinia Fructicola ◽  
Rhizopus Stolonifer ◽  
Uv C

Este trabalho teve por objetivo avaliar o efeito da irradiação UV-C no controle in vitro de Monilinia fructicola e Rhizopus stolonifer e no controle das doenças causadas por estes fungos em pêssegos inoculados com ferimento. No experimento in vitro, avaliou-se o crescimento micelial dos fungos em meio BDA após a exposição nas doses de UV-C de 0, 0,26, 0,52, 1,04, 3,13, 5,22, 10,44, 15,66, e 31,32 kJ.m-2 num equipamento com quatro lâmpadas com taxa de fluência de 1,74 mW.cm-2. Nos experimentos in vivo, os frutos foram tratados com irradiação UV-C de forma protetora e curativa. No tratamento protetor, os frutos foram expostos a 1,04 kJ.m-2 por 1 min. e foram inoculados imediatamente após e 16, 24 e 40 h após. No tratamento curativo, os frutos foram inoculados, incubados e irradiados com doses de UV-C de 0, 1,04, 5,22, 10,44, 15,66 e 31,32 kJ.m². Avaliou-se a incidência das doenças e a severidade da podridão parda. No experimento in vitro, apenas as doses aplicadas durante 1 e 10 min. de exposição reduziram o crescimento micelial de M. fructicola enquanto que a aplicação da luz UV-C entre 10-15 minutos reduziu o crescimento micelial de R. stolonifer e a dose aplicada durante 30 minutos inibiu completamente o crescimento micelial deste fungo. Não houve efeito protetor da luz UV-C no controle das doenças. Não houve controle curativo da podridão parda. A irradiação UV-C foi eficiente no controle curativo da podridão mole e o tempo de exposição de 10 min. foi o que apresentou melhor resultado.

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

Plant Disease ◽  
2010 ◽  
Vol 94 (9) ◽  
pp. 1166-1166 ◽  
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.

scholarly journals Identification and Characterization of Benzimidazole Resistance in Monilinia fructicola from Stone Fruit Orchards in California

2003 ◽  
Vol 69 (12) ◽  
pp. 7145-7152 ◽  
Author(s):  
Zhonghua Ma ◽  
Michael A. Yoshimura ◽  
Themis J. Michailides
Keyword(s):  
Dna Sequences ◽  
Point Mutations ◽  
Brown Rot ◽  
Stone Fruit ◽  
Monilinia Fructicola ◽  
Tubulin Gene ◽  
Benzimidazole Fungicides ◽  
Specific Pcr ◽  
Allele Specific ◽  
Fruit Orchards

ABSTRACT Low and high levels of resistance to the benzimidazole fungicides benomyl and thiophanate-methyl were observed in field isolates of Monilinia fructicola, which is the causative agent of brown rot of stone fruit. Isolates that had low levels of resistance (hereafter referred to as LR isolates) and high levels of resistance (hereafter referred to as HR isolates) were also cold and heat sensitive, respectively. Results from microsatellite DNA fingerprints showed that genetic identities among the populations of sensitive (S), LR, and HR isolates were very high (>0.96). Analysis of DNA sequences of theβ -tubulin gene showed that the LR isolates had a point mutation at codon 6, causing a replacement of the amino acid histidine by tyrosine. Codon 198, which encodes a glutamic acid in S and LR isolates, was converted to a codon for alanine in HR isolates. Based on these point mutations in the β-tubulin gene, allele-specific PCR assays were developed for rapid detection of benzimidazole-resistant isolates of M. fructicola from stone fruit.

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