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

1965 ◽  
Vol 16 (2) ◽  
pp. 141 ◽  
Author(s):  
PT Jenkins

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.

Plant Disease ◽  
2010 ◽  
Vol 94 (9) ◽  
pp. 1166-1166 ◽  
Author(s):  
A. Munda ◽  
M. Viršček Marn

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.


2012 ◽  
Vol 75 (10) ◽  
pp. 1883-1889 ◽  
Author(s):  
RAPHAEL SANZIO PIMENTA ◽  
JULIANA F. MOREIRA da SILVA ◽  
JEFFREY S. BUYER ◽  
WOJCIECH J. JANISIEWICZ

Enophytic fungi were isolated from plum (Prunus domestica) leaves, identified with ITS1 and ITS4 primers, and their antagonistic activity was tested against Monilinia fructicola, which causes brown rot, blossom blight, and twig blight of stone fruits, and Colletotrichum gloeosporioides, which causes anthracnose on a variety of fruit crops. The production of antifungal compounds was determined in agar-diffusion and volatile inverted-plate tests. A total of 163 fungi were recovered from 30 plum trees, representing 22 cultivars. Twenty-nine morphotypes were detected, but only 14 species were identified genetically. The most frequently isolated species was Phaeosphaeria nodorum, constituting 86.5% of the total isolates. Four isolates produced inhibitory volatiles to M. fructicola; however, no isolate produced volatiles inhibitory to C. gloeosporioides. The volatiles produced by these fungi were identified as ethyl acetate, 3-methyl-1-butanol, acetic acid, 2-propyn-1-ol, and 2-propenenitrile. The fungal volatiles inhibited growth and reduced width of the hyphae, and caused disintegration of the hyphal content. This is the first study describing fungal endophytes in stone fruits. The P. nodorum strains producing inhibitory volatiles could play a significant role in reduction of M. fructicola expansion in plum tissues. Potential of these strains for biological control of this pathogen on stone fruits warrants further investigation.


Plant Disease ◽  
2009 ◽  
Vol 93 (6) ◽  
pp. 668-668 ◽  
Author(s):  
C. Pellegrino ◽  
M. L. Gullino ◽  
A. Garibaldi ◽  
D. Spadaro

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.


1969 ◽  
Vol 20 (2) ◽  
pp. 317 ◽  
Author(s):  
PF Kable

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.


Plant Disease ◽  
2020 ◽  
Vol 104 (2) ◽  
pp. 576-576
Author(s):  
A. C. Q. Brito ◽  
J. F. Mello ◽  
J. C. B. Vieira ◽  
M. P. S. Câmara ◽  
J. D. P. Bezerra ◽  
...  

1972 ◽  
Vol 23 (6) ◽  
pp. 1035 ◽  
Author(s):  
PF Kable

Brown rot caused severe losses on the Murrumbidgee Irrigation Areas in nine of 36 seasons. Slight to moderate losses were more frequent. The influence of weather on incidence of brown rot losses was examined. Losses did not occur unless there was rain when fruits were ripe. Losses never resulted from long damp periods occurring prior to the commencement of harvest. Rain causing surface wetness on ripe fruit of duration in excess of 10 hr was necessary before losses occurred. Severity of losses increased with duration of wetness, losses being most likely and most severe when the duration of surface wetness approached or exceeded 20 hr. The probability of losses increased with increasing number of long rain-induced damp periods during the harvest period. Dews appeared to have little influence on brown rot incidence. Temperatures during damp periods were generally in a range suitable for infection. The most common weather patterns associated with long rain-induced damp periods are described. Losses from fruit rot increase for some 3-5 days after the damp period causing infection, then gradually decline. Springtime brown rot infection was not a prerequisite for fruit rot.


Author(s):  
G. M. Waterhouse

Abstract A description is provided for Phytophthora syringae. Information is included on the disease caused by the organism, its transmission, geographical distribution, and hosts. HOSTS: On Syringa vulgaris, Castanea saliva, Cereus martianus, C. tetracanthus, Citrus spp., Foeniculum vulgare, Malus pumila, Prunus armeniaca, P. cerasus, P. persica, Pyrus communis and Pyrus sp. Also pathogenic to the following hosts on inoculation; Aesculus hippocastanum, Alnus glutinosa, Chionanthus virginica, Corylus avellana, Crataegus oxyacantha, Jasminum nudiflorum, Ligustrum vulgare, Prunus domestica and Quercus spp. DISEASE: Causing twig blight and wilt of lilac. Also on apple and pear and other woody Rosaceae causing fruit rot and collar rot; on sweet chestnut and beech causing root rot; on citrus causing fruit brown rot and twig and blossom blight; on fennel causing a leaf blight, and on cacti causing stem rot. GEOGRAPHICAL DISTRIBUTION: Europe (Belgium, Czechoslovakia, Denmark, Eire, Great Britain, France, Greece, Germany, Holland, Italy, Portugal, Romania, Sicily, Sweden, U.S.S.R., Yugoslavia); North America (Canada, U.S.A.); Asia (? India) and New Zealand. (CMI Map 174) TRANSMISSION: Soil borne, common in orchard soils and persisting in arable land for as long as 15 years after orchards have been ploughed up (42: 75), but not present in soils under cultivation for as long as 138 years (38: 213). Pathogenicity to lilac was unimpaired after storage for 2 years in bog soil (1: 399). Disseminated by water (6: 668) and in irrigation canals and reservoirs supplying citrus groves in California during winter and spring (39: 24).


Plant Disease ◽  
2012 ◽  
Vol 96 (4) ◽  
pp. 590-590 ◽  
Author(s):  
F. T. Arroyo ◽  
M. Camacho ◽  
A. Daza

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.


Plant Disease ◽  
2014 ◽  
Vol 98 (7) ◽  
pp. 1009-1009 ◽  
Author(s):  
L. F. Yin ◽  
G. K. Chen ◽  
S. N. Chen ◽  
S. F. Du ◽  
G. Q. Li ◽  
...  

Cherry is widely planted in China, from Liaoning, Beijing, Hebei, Shandong, Zhejiang, Jiangsu, and Anhui provinces (eastern China), to Shaanxi, Sichuan, Chongqing, and Guizhou provinces (western China). The brown rot fungus Monilinia fructigena causes considerable production losses in cherry production in Liaoning Province (3). In May 2013, Chinese sour cherry (Prunus pseudocerasus) cv. Wupi displaying symptoms of brown rot was found in an orchard in Chongqing municipality. Diseased cherry fruit had a brown rot sporulating with grayish, conidial tufts. The fruit later succumbed to the soft rot or shivered and became a mummy. Single-spore isolations on PDA resulted in colonies with concentric rings of pigmented mycelium with lobbed margins. Conidia were broadly ellipsoid to subglobose, occasionally even globose, with an average size of 16 × 12.7 μm. Multiple germ tubes were produced from each conidium, a germination pattern unique to Monilia mumecola (1,2,4). The pathogen identity was confirmed by multiplex PCR as described by Hu et al. (2). The PCR resulted in a 712-bp amplicon, which is diagnostic of M. mumecola. Further sequencing of the internal transcribed spacer (ITS) region 1 and 2 and 5.8S gene further indicated 100% identity with that of M. mumecola isolates from China (Accession No. HQ908786) and from Japan (AB125613, AB125614, and AB125620). Koch's postulates were confirmed by inoculating mature cherry fruit with mycelia plugs. Inoculated fruit were placed in a sterilized moist chamber, and incubated at 22°C with 12 h light/dark cycle. Inoculated fruit developed typical brown rot symptoms only 2 days after inoculation, while the control fruit, inoculated with a sterile PDA plug, remained healthy. The pathogen isolated from inoculated symptomatic fruit was confirmed to be M. mumecola based on morphological characteristics and germination pattern. It should be noted that the conidia on inoculated fruit showed an average size of 20 × 15.3 μm, significantly bigger than that of from PDA, and most produced more than three germ tubes. The inoculation experiments were performed in triplicates. M. mumecola was first reported as the causal agent of brown rot of mume in Japan in 2004 (1). Later studies demonstrated that it is also pathogen on other stone fruits, e.g., peach, nectarine (2), and apricot (4). To our knowledge, this is the first report of cherry brown fruit rot caused by M. mumecola, and the first report of M. mumecola in Chongqing municipality. References: (1) Y. Harada et al. J. Gen. Plant Pathol. 70:297, 2004. (2) M. J. Hu et al. Plos One 6(9): e24990, 2011. (3) Z. H. Liu et al. J. Fruit Sci. 29:423, 2012. (4) L. F. Yin et al. Plant Dis. 98:694, 2014.


Plant Disease ◽  
2021 ◽  
Vol 105 (1) ◽  
pp. 220
Author(s):  
S. I. Ismail ◽  
K. Ahmad Dahlan ◽  
S. Abdullah ◽  
D. Zulperi

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