First Report of Fruit Rot on Plum Caused by Monilinia fructicola at Alcalá del Río (Seville), Southwestern Spain

Monilinia fructicola, causal agent of brown rot, is one of the most important fungal pathogens of stone fruit. In the summer of 2011, Japanese plum fruit of ‘Larry Ann’ (Prunus salicina Lindl) showing symptoms of fruit rot disease were detected and collected from trees in an experimental field at Alcalá del Río (Seville), southwestern Spain. Fruit rot lesions were brown, sunken, and covered with grayish brown tufts or pustules. The majority of infected fruit became dry and mummified on the trees after 30 days. Symptoms were similar to those caused by three Monilinia species, M. laxa, M. fructigena, and M. fructicola (2). Pieces of infected tissue, previously disinfested in 0.6% NaOCl, were placed on potato dextrose agar (PDA) amended with 50 μg of streptomycin per liter and incubated at 22°C with a 12-h photoperiod for 15 days. The isolates produced abundant, grayish white mycelium, which after sporulation became hazel in color, and colonies displayed concentric rings. Colonies produced scarce conidia, which were arranged in branched, monilioid chains. Conidia were one celled, hyaline, ellipsoid to lemon shaped, and measured 15.42 ± 1.91 × 8.02 ± 0.9 μm. The morphological data and growth rates match the description of M. fructicola (Winter) Honey (2–4). Fungal identification was confirmed by PCR using genomic DNA extracted from the mycelia of pure cultures. The DNA was amplified with a common reverse primer and three specific forward primers obtained from a sequence-characterized, amplified region that distinguishes between M. fructicola, M. fructigena, and M. laxa. The size of the amplified fragment (a product of 535 bp) fit with the one described for M. fructicola (2). To confirm the pathogenicity of the isolate, mature ‘Larry Ann’ and ‘Sungold’ plum fruits (six fruits per cultivar) were inoculated by placing an agar plug from the edge of an actively growing colony on PDA directly on the fruit surface. After 5 days of incubation, typical brown rot symptoms developed on inoculated fruit and the fungus was successfully reisolated, thus fulfilling Koch's postulates. No symptoms appeared on control fruit. To our knowledge, this is the first report of M. fructicola on plums in southwestern Spain. M. fructicola is a quarantined pathogen in Europe and has been reported on imported apricot and nectarine (1) and peach in several European countries (3,4). References: (1) E. Bosshard et al. Plant Dis. 90:1554, 2006. (2) M. J. Côté. Plant Dis. 88:1219, 2004. (3) A. De Cal and I. Gell. Plant Dis. 93:763, 2009. (4). C. Pellegrino et al. Plant Dis. 93:668, 2009.

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First Report of Brown Rot of Stone Fruit Caused by Monilinia fructicola in Italy

Plant Disease ◽

10.1094/pdis-93-6-0668a ◽

2009 ◽

Vol 93 (6) ◽

pp. 668-668 ◽

Cited By ~ 39

Author(s):

C. Pellegrino ◽

M. L. Gullino ◽

A. Garibaldi ◽

D. Spadaro

Keyword(s):

Fungal Pathogens ◽

Brown Rot ◽

Stone Fruit ◽

Fruit Rot ◽

Brown Spot ◽

Morphological Identification ◽

Monilinia Fructicola ◽

Stone Fruits ◽

First Report ◽

Sequence Characterized Amplified Region

Monilinia fructicola, causal agent of brown rot, is one of the most important fungal pathogens of stone fruit. M. fructicola is a quarantined pathogen in Europe. During the summer of 2008 in 15 orchards located in Piedmont (northern Italy), 12,500 stone fruits (cherries, apricots, peaches, nectarines, and plums) were stored in cold chambers at 4 and 6°C and monitored for 8 weeks for the presence of Monilinia spp. M. fructicola was detected on 0.5% of nectarines (cvs. Sweet Red and Orion) that originated from two orchards in Lagnasco. Symptoms appeared on the fruit during storage, starting 3 weeks after harvest. Fruit rot lesions were brown, sunken, and covered with grayish tufts. The majority of infected fruit became dry and mummified. Brown rot symptoms were similar to those caused by endemic M. fructigena and M. laxa. Symptoms began with a small, circular, brown spot, and the rot spread rapidly. At the same time, numerous, small, grayish stromata developed. Finally, the whole surface of the fruit was covered by conidial tufts. Tissues were excised from diseased stone fruits and cultured on potato dextrose agar (PDA) amended with 25 μg of streptomycin per liter. The isolates produced abundant mycelium on PDA at 20 ± 2°C. Colonies were initially gray, but after sporulation, they became hazel, showing concentric rings (sporulation is sparse in M. laxa or M. fructigena). Conidia were one-celled, ellipsoid, hyaline, 15.2 × 10.1 μm, and produced in branched monilioid chains (2). Preliminary morphological identification of fungi resembling M. fructicola was confirmed by PCR using genomic DNA extracted from the mycelia of pure cultures. The DNA was amplified with a common reverse primer and three species-specific forward primers (3) obtained from a sequence characterized amplified region and a product of 535 bp, diagnostic for the species M. fructicola, was obtained. BLAST analysis of the amplified sequence (GenBank Accession No. FI569728) showed 96% similarity to the sequence of a M. fructicola isolated from Canada (GenBank Accession No. AF506700), 15% similarity to M. laxa ATCC11790 (GenBank Accession No. AF506702), and 35% similarity to a M. fructigena sequence isolated in Italy (GenBank Accession No. AF506701). Moreover, two sequences obtained through the amplification of ribosomal region ITS1-5.8S-ITS2, showing 100% similarity to the same ribosomal sequence of M. fructicola, were deposited in GenBank (Accession Nos. FJ411109 and FJ411110). The pathogen was detected on some mummified fruit from the same orchards in November of 2008. Pathogenicity was tested by spraying 103 conidia/ml on 10 surface-sterilized artificially wounded nectarines per strain of M. fructicola. After 5 days of incubation at 20 ± 2°C, typical, brown, rot symptoms developed on inoculated fruit. M. fructicola was reisolated from the inoculated fruit on PDA. Symptoms did not appear on control fruit. To our knowledge, this is the first report of M. fructicola in Italy. Its occurrence in Europe has been reported sporadically in Austria and France, and in 2006, it was detected in Hungary and Switzerland on peaches and nectarines imported from Italy and Spain (1,4). References: (1) E. Bosshard et al. Plant Dis. 90:1554, 2006. (2) R. J. W. Byrde and H. J. Willetts. The Brown Rot Fungi of Fruit: Their Biology and Control. Pergamon Press, Oxford, 1977. (3) M. J. Coté et al. Plant Dis. 88:1219, 2004. (4) M. Petròczy and L. Palkovics. Plant Dis. 90:375, 2006.

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

Plant Disease ◽

10.1094/pdis-94-9-1166a ◽

2010 ◽

Vol 94 (9) ◽

pp. 1166-1166 ◽

Cited By ~ 15

Author(s):

A. Munda ◽

M. Viršček Marn

Keyword(s):

Prunus Persica ◽

Brown Rot ◽

Fruit Rot ◽

Morphological Identification ◽

Monilinia Fructicola ◽

Conidial Suspension ◽

Stone Fruits ◽

The European Union ◽

First Report ◽

Representative Isolate

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

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First Report of Brown Rot Caused by Monilinia fructicola on Apple in Italy

Plant Disease ◽

10.1094/pdis-09-12-0869-pdn ◽

2013 ◽

Vol 97 (5) ◽

pp. 689-689 ◽

Cited By ~ 6

Author(s):

C. Martini ◽

A. Spadoni ◽

M. Mari

Keyword(s):

Fungal Pathogens ◽

Brown Rot ◽

Its2 Region ◽

Monilinia Fructicola ◽

Malt Extract ◽

Conidial Suspension ◽

First Report ◽

Molecular Features ◽

Sterile Needle ◽

Emilia Romagna Region

Monilinia fructicola (G. Wint.) Honey, the causal agent of brown rot, is one of the most important fungal pathogens of stone fruit but may also affect pome fruits. The pathogen is common in North America, Oceania, South America, and Asia. It is a quarantined pathogen in Europe (3), but was recently detected in apple from the Czech Republic, Germany, and Serbia (1,2,4). In January 2012, during a survey for fungal postharvest pathogens, stored apple (Malus domestica Borkh.) belonging to the cultivars Gala and Pink Lady showing brown rot symptoms were observed in the Emilia Romagna region, Italy. Typical decay spots were circular and brown, tending toward black. Decayed tissues remained firm, and numerous grayish pustules containing spores appeared on rotted areas. The pathogen was isolated on V8 juice agar and culture plates were incubated at 25°C in darkness for 5 days. A conidial suspension was spread on malt extract agar and single spores were selected. The colonies were morphologically identified as M. fructigena. Two colonies developing a gray mass of spores in concentric rings with the reverse side black were further studied by molecular tools. The colony margins were even and the conidia were one-celled, limoniform, hyaline, and 12.1 to 17.4 × 8.4 to 11.2 μm. The ribosomal ITS1-5.8S-ITS2 region was PCR-amplified from genomic DNA obtained from mycelium using primers ITS1 and ITS4. A BLAST search in GenBank revealed the highest similarity (99%) to M. fructicola sequences (GenBank Accession Nos. HQ893748.1 and FJ515894.1). Pathogenicity was confirmed using surface-sterilized mature ‘Gala’ apples, wounded with a sterile needle, and inoculated with an isolate conidial suspension (103 spores/ml). A 20 μl droplet was placed in the wound; control fruits received sterile water without conidia. After 5 days of incubation at 20°C in plastic containers with high humidity, typical symptoms of brown rot developed on inoculated fruits, while control fruits remained symptomless. The fungus isolated from inoculated fruit exhibited the same morphological and molecular features shown by the original isolates. To our knowledge, this is the first report of the fungus M. fructicola on apple in Italy. Further studies are necessary to determine geographic distribution, prevalence and economic importance of this quarantine organism in Italy. References: (1) J. Duchoslavovà et al. Plant Dis.91:907, 2007. (2) A. Grabke et al. Plant Dis. 95:772, 2011. (3) OEPP/EPPO. EPPO A2 list of pests recommended for regulation as quarantine pests. Version 2010-09. Retrieved from http://www.eppo.int/QUARANTINE/listA2.htm , 2010. (4) M. Vasic et al. Plant Dis. 96:456, 2012.

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Brown rot of stone fruits on the Murrumbidgee Irrigation Areas. II. Aetiology of the disease in Trevatt apricot trees

Australian Journal of Agricultural Research ◽

10.1071/ar9690317 ◽

1969 ◽

Vol 20 (2) ◽

pp. 317 ◽

Cited By ~ 6

Author(s):

PF Kable

Keyword(s):

Brown Rot ◽

Economic Importance ◽

Fruit Rot ◽

Monilinia Fructicola ◽

Stone Fruits

Blossom blight is of economic importance in apricots on the Murrumbidgee Irrigation Areas (MIA), but fruit rot is not. Monilinia fructicola generally does not overwinter effectively in apricot trees in the MIA, the inocula for primary infections coming from nearby peach plantations. Blighted blossoms in apricot trees, which flower a week before peaches, may provide inoculum for blighting of flowers in the latter crop. In apricot trees, unlike peach, there is a continuous infection chain from flowering till harvest. Inoculum may pass from apricot to peach in December and January, thus bridging a gap in the infection chain in peach. The infection chain in apricot is described. Latent and quiescent infections were observed. The implications of the exchange of inoculum between peach and apricot are discussed.

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Spatial Patterns of Brown Rot Epidemics and Development of Microsatellite Markers for Analyzing Fine-Scale Genetic Structure of Monilinia fructicola Populations Within Peach Tree Canopies

Plant Health Progress ◽

10.1094/php-2012-0723-04-rs ◽

2012 ◽

Vol 13 (1) ◽

pp. 28 ◽

Cited By ~ 6

Author(s):

S. E. Everhart ◽

A. Askew ◽

L. Seymour ◽

T. C. Glenn ◽

H. Scherm

Keyword(s):

Microsatellite Markers ◽

Spatial Patterns ◽

Spatial Dynamics ◽

Brown Rot ◽

Fruit Rot ◽

Monilinia Fructicola ◽

Peach Tree ◽

Fine Scale ◽

Tree Canopies ◽

Diseased Fruit

To better understand the fine-scale spatial dynamics of brown rot disease and corresponding fungal genotypes, we analyzed three-dimensional spatial patterns of pre-harvest fruit rot caused by Monilinia fructicola in individual peach tree canopies and developed microsatellite markers for canopy-level population genetics analyses. Using a magnetic digitizer, high-resolution maps of fruit rot development in five representative trees were generated, and M. fructicola was isolated from each affected fruit. To characterize disease aggregation, nearestneighbor distances among symptomatic fruit were calculated and compared with appropriate random simulations. Within-canopy disease aggregation correlated negatively with the number of diseased fruit per tree (r = −0.827, P = 0.0009), i.e., aggregation was greatest when the number of diseased fruit was lowest. Sixteen microsatellite primers consistently amplified polymorphic regions in a geographically diverse test population of 47 M. fructicola isolates. None of the test isolates produced identical multilocus genotypes, and the number of alleles per locus ranged from 2 to 16. We are applying these markers to determine fine-scale population structure of the pathogen within and among canopies. Accepted for publication 23 May 2012. Published 23 July 2012.

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Sclerotinia laxa Aderh. & Ruhl: A cause of brown rot of stone fruits not previously recorded in Australia

Australian Journal of Agricultural Research ◽

10.1071/ar9650141 ◽

1965 ◽

Vol 16 (2) ◽

pp. 141 ◽

Cited By ~ 13

Author(s):

PT Jenkins

Keyword(s):

Brown Rot ◽

Fruit Rot ◽

Stone Fruits ◽

Prunus Domestica ◽

Cultural Characteristics ◽

First Report ◽

Brown Rot Fungus ◽

Twig Blight

A fungus with the cultural characteristics of Sclerotinia laxa Aderh. & Ruhl. has been determined as a cause of blossom and twig blight and fruit rot of stone fruits in southern Victoria. This is the first report of a brown rot species other than S. fructicola (Wint.) Rehm. occurring in Australia. European plum (Prunus domestica) is the host most severely affected, and there is evidence that the disease has spread from this host to adjacent cherry, peach, and apricot varieties. The distribution of S. laxa appears to be restricted to the Wandin, Tyabb, and Red Hill districts of southern Victoria. S. fructicola also is a cause of blossom blight and fruit rot in these districts, and is the only brown rot fungus which causes losses of stone fruits in the major canning fruit districts of northern Victoria.

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Fine-Scale Genetic Structure of Monilinia fructicola During Brown Rot Epidemics Within Individual Peach Tree Canopies

Phytopathology ◽

10.1094/phyto-03-14-0088-r ◽

2015 ◽

Vol 105 (4) ◽

pp. 542-549 ◽

Cited By ~ 8

Author(s):

S. E. Everhart ◽

H. Scherm

Keyword(s):

Genetic Structure ◽

Brown Rot ◽

Genotypic Diversity ◽

Fruit Rot ◽

Monilinia Fructicola ◽

Peach Tree ◽

Fine Scale ◽

High Genetic Diversity ◽

Pathogen Diversity ◽

Tree Canopies

The purpose of this study was to determine the fine-scale genetic structure of populations of the brown rot pathogen Monilinia fructicola within individual peach tree canopies to better understand within-tree plant pathogen diversity and to complement previous work on spatiotemporal development of brown rot disease at the canopy level. Across 3 years in a total of six trees, we monitored disease development, collected isolates from every M. fructicola symptom during the course of the season, and created high-resolution three-dimensional maps of all symptom and isolate locations within individual canopies using an electromagnetic digitizer. Each canopy population (65 to 173 isolates per tree) was characterized using a set of 13 microsatellite markers and analyzed for evidence of spatial genetic autocorrelation among isolates during the epidemic phase of the disease. Results showed high genetic diversity (average uh = 0.529) and high genotypic diversity (average D = 0.928) within canopies. The percentage of unique multilocus genotypes within trees was greater for blossom blight isolates (78.2%) than for fruit rot isolates (51.3%), indicating a greater contribution of clonal reproduction during the preharvest epidemic. For fruit rot isolates, between 54.2 and 81.7% of isolates were contained in one to four dominant clonal genotypes per tree having at least 10 members. All six fruit rot populations showed positive and significant spatial genetic autocorrelation for distance classes between 0.37 and 1.48 m. Despite high levels of within-tree pathogen diversity, the contribution of locally available inoculum combined with short-distance dispersal is likely the main factor generating clonal population foci and associated spatial genetic clustering within trees.

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Redox Climate in Quiescence and Pathogenicity of Postharvest Fungal Pathogens

10.32747/2003.7586466.bard ◽

2003 ◽

Author(s):

Richard M. Bostock ◽

Dov Prusky ◽

Martin Dickman

Keyword(s):

Redox Potential ◽

Fungal Pathogens ◽

High Efficiency ◽

Fluorescent Protein ◽

Brown Rot ◽

Hyphal Growth ◽

Fruit Rot ◽

Putative Virulence Factor ◽

Immature Fruit ◽

Related Compounds

Monilinia fructicola causes brown rot blossom blight and fruit rot in stone fruits. Immature fruit are highly resistant to brown rot but can become infected. These infections typically remain superficial and quiescent until they become active upon maturation of the fruit. High levels of chlorogenic acid (CGA) and related compounds occur in the peel of immature fruit but these levels decline during ripening. CGA inhibits cutinase expression, a putative virulence factor, with little or no effect on spore germination or hyphal growth. To better understand the regulation of cutinase expression by fruit phenolics, we examined the effect of CGA, caffeic acid (CA) and related compounds on the redox potential of the growth medium and intracellular glutathione (GSH) levels. The presence of CA in the medium initially lowered the electrochemical redox potential of the medium, increased GSH levels and inhibited cutinase expression. Conidia germinated in the presence of CA, CGA, or GSH produced fewer appressoria and had elongated germ tubes compared to the controls. These results suggest that host redox compounds can regulate fungal infectivity. In order to genetically manipulate this fungus, a transformation system using Agrobacterium was developed. The binary transformation vector, pPTGFPH, was constructed from the plasmid pCT74, carrying green fluorescent protein (GFP) driven by the ToxA promoter of Pyrenophora tritici-repentis and hygromycin B phosphotransferase (hph) under control of the trpC promoter of from Aspergillus nidulans, and the binary vector pCB403.2, carrying neomycin phosphotransferase (nptII) between the T-DNA borders. Macroconidia of M. fructicola were coincubated with A. tumefaciens strain LBA 4404(pPTGFPH) on media containing acetosyringone for two days. Hygromycin- and G418-resistant M. fructicola transformants were selected while inhibiting A. tumefaciens with cefotaxime. Transformants expressing GFP fluoresced brightly, and were formed with high efficiency and frequency of T-DNA integration frequency. The use of these transformants for in situ studies on stone fruit tissues is discussed.

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First Report of Brown Rot on Peach, Nectarine, Cherry, and Plum Fruits Caused by Monilinia fructicola in Bulgaria

Plant Disease ◽

10.1094/pdis-10-19-2094-pdn ◽

2020 ◽

Vol 104 (5) ◽

pp. 1561-1561

Author(s):

S. G. Bobev ◽

L. T. Angelov ◽

K. Van Poucke ◽

M. Maes

Keyword(s):

Brown Rot ◽

Monilinia Fructicola ◽

First Report

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First Report of Calonectria hongkongensis Causing Fruit Rot of Rambutan (Nephelium lappaceum)

Plant Disease ◽

10.1094/pdis-01-13-0008-pdn ◽

2013 ◽

Vol 97 (8) ◽

pp. 1117-1117 ◽

Cited By ~ 2

Author(s):

L. M. Serrato-Diaz ◽

E. I. Latoni-Brailowsky ◽

L. I. Rivera-Vargas ◽

R. Goenaga ◽

P. W. Crous ◽

...

Keyword(s):

Mycelial Growth ◽

Elongation Factor ◽

Type Specimen ◽

Fruit Rot ◽

Fluorescent Light ◽

Mycelium Growth ◽

Tropical Fruit ◽

First Report ◽

Nephelium Lappaceum ◽

Pure Cultures

Fruit rot of rambutan is a pre- and post-harvest disease problem of rambutan orchards. In 2011, fruit rot was observed at USDA-ARS orchards in Mayaguez, Puerto Rico. Infected fruit were collected and 1 mm2 tissue sections were surface disinfested with 70% ethanol followed by 0.5% sodium hypochlorite. Infected fruit were rinsed with sterile, deionized, double-distilled water and transferred to acidified potato dextrose agar (APDA). Plates were incubated at 25 ± 1°C for 6 days. Three isolates of Calonectria hongkongensis (Cah), CBS134083, CBS134084, and CBS134085, were identified morphologically using taxonomic keys (2,3). In APDA, colonies of Cah produced raw sienna to rust-colored aerial mycelial growth. Conidiophores of Cah had a penicillate arrangement of primary to quaternary branches of 2 to 6 phialides. Conidia (n = 50) were cylindrical, hyaline, 1-septate, rounded at both ends, and 44 to 52 μm × 3.5 to 4.5 μm. Conidiophores produced terminal and lateral stipe extensions with terminal sphaeropedunculate vesicles that were 8 to 12 μm wide. Subglobose to ovoid perithecia, 300 to 500 μm × 200 to 350 μm and orange to red-brown, were produced in groups of 3. Asci were clavate and contained 8 ascospores aggregated at the top of the ascus. Ascospores (n = 50) were hyaline, guttulate, fusoid with rounded ends, straight to curved, 1-septate with constriction at the septum, and 28 to 36 μm × 4 to 7 μm. For molecular identification, the ITS rDNA, fragments of β-tubulin (BT), histone H3 (HIS3), and elongation factor (EF1-α) genes were amplified by PCR, sequenced, and compared using BLASTn with Calonectria spp. submitted to the NCBI GenBank. The sequences of Cah submitted to GenBank include accessions KC342208, KC342206, and KC342207 for ITS; KC342217, KC342215, and KC342216 for BT; KC342211, KC342209, and KC342210 for HIS3; and KC342214, KC342212, and KC342213 for EF1α. The sequences were >99% or identical with the ex-type specimen of Cah CBS 114828 for all genes used. Pathogenicity tests were conducted on 5 healthy superficially sterilized fruits per isolate. Both scalpel-wounded and unwounded fruit tissues were inoculated with 5-mm mycelial disks from 8-day-old pure cultures grown in APDA. Untreated controls were inoculated with APDA disks only. Fruits were kept in a humid chamber for 8 days at 25°C under 12 h of fluorescent light. The test was repeated once. Three days after inoculation (DAI), white mycelial growth was observed on the fruit. Five DAI, the fruit changed color from red to brown and yellowish mycelia colonized 50 to 62% of the fruit surface. Eight DAI, all the fruit turned brown, the mycelium growth covered the entire fruit, and conidiophores were produced on spinterns (hairlike appendages). Fruit rot of spinterns, exocarp (skin), endocarp (aril), and light brown discoloration were observed inside the fruit. Untreated controls showed no symptoms of fruit rot and no fungi were reisolated from tissue. Cah was reisolated from diseased tissue, fulfilling Koch's postulates. Calonectria spp. (or their Cylindrocladium asexual states) have been associated with lychee decline syndrome in North Vietnam (1). Both fruits belong to the Sapindaceae family. To our knowledge, this is the first report of Cah causing fruit rot of rambutan. References: (1) L. M. Coates et al. Diseases of Longan, Lychee and Rambutan. Pages 307-325 in: Diseases of Tropical Fruit Crops. R. C. Ploetz, ed. CABI Publishing, Cambridge, MA, 2003. (2) P. W. Crous. Taxonomy and Pathology of Cylindrocladium (Calonectria) and Allied Genera. APS Press, St Paul, MN, 2002. (3) P. W. Crous, et al. Stud. Mycol. 50:415, 2004.

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