Monilinia fructicola, causal agent of fruit brown rot, is a quarantine pathogen in Europe (1). It presents a significant threat because of its aggressivity on flowers, shoots, and wood at low temperatures and propensity for sexual reproduction that increases potential for evolutionarily adaptation to new environments, hosts, and fungicides. It is common in North America, Japan, Australia, and South America. It occurs in orchards in France, has been detected but eradicated from Austria and Spain, and has been found on imported peach in Hungary (1,2). In Switzerland, we recently detected M. fructicola in supermarkets on imported fruit with brown rot symptoms similar to those caused by endemic M. fructigena and M. laxa. Preliminary identification was based on distinctive colony and conidial morphology on potato dextrose agar of fruit isolates. Specific identification was determined by polymerase chain reaction (PCR) (3) and sequencing the internal transcribed spacer (ITS) region. Koch's postulates were fulfilled by reproducing brown rot on healthy inoculated fruit. Surveys of imported fruit in markets (n = 42) using PCR revealed M. fructicola on all imported apricot and nectarine from the United States and France, but none on apricot, peach, plum, and cherry from Spain, France, Italy, or Turkey. Field surveys of apricot, peach, plum, prune, nectarine, and cherry orchards in 13 Swiss cantons were all negative (n = 71 in 2003 and 164 in 2005). This report demonstrates that imported fruit is a weak link in quarantine efforts and poses a potential threat. Transmission to local trees via highly dispersible, profuse spores from recycled packaging and disposal sites for discarded fruit has thus far not occurred but the risk deserves attention. Revised regulations for fruit treatment at points of entry and/or scrutiny of origin orchards may be warranted. References: (1) OEPP/EPPO. List of A2 pests regulated as quarantine pests in the EPPO region. Version 2005-09. Online publication with distribution map at http://www.eppo.org , 2005. (2) M. Petróczy and L. Palkovics. Plant Dis. 90:375, 2006. (3) K. J. D. Hughes et al. EPPO Bull. 30:507, 2000.
Switzerland joined the list of fireblight‐affected European countries in 1989. Vigorous and systematic steps were taken to limit the impact of the disease on fruit production and amenity plants. These efforts are codified in a Swiss law detailing prevention, eradication, control measures and issues of compensation. As with many Swiss legal directives, there is a defined coordination of federal and cantonal responsibilities and, in the case of fireblight, there is also an emphasis at all levels on personal responsibility of owners of susceptible objects (e.g. nurseries, orchards, host plants). Extension activities have been a key component in achieving compliance with disease management regulations and in obtained public support for control efforts. Agroscope FAW Wädenswil has taken a leading role in this respect through its website http://www.feuerbrand.ch.
Monilinia fructicola (G. Wint.), causal agent of brown rot on stone and pome fruits, is a quarantine pathogen in Europe (EPPO A2 quarantine pest). Since it was first discovered in French orchards in 2001, this pathogen has been officially identified from orchards in Austria (eradicated), Spain, Czech Republic, Italy, and Germany. M. fructicola has also been reported on imported fruit in Hungary and Switzerland (2). Orchard surveys in Switzerland in 2003 and 2005 found no evidence of natural infections (2). From July to August 2008, a large-scale survey of orchards was conducted in the primary apricot- (Prunus armeniaca Linn.) production region of Switzerland (Canton Valais). Apricots showing brown rot symptoms were collected from 57 different orchards at packinghouses (152 samples). In addition, mummies and fresh fruits showing brown rot symptoms were directly collected from three orchards (70 samples). All samples were tested using the PCR-based assay of Côté et al. (3). Ten apricots, originating from an orchard where the samples were directly collected from the trees, tested positive for M. fructicola. These apricots showed brown, sunken lesions covered with grayish pustules. The remaining brown rot samples were identified as M. laxa and M. fructigena. The positive samples were confirmed by the M. fructicola PCR protocols of Hughes et al. (4), following the EPPO diagnostic protocol (1). Eight amplicons obtained with the PCR protocol of Hughes et al. (4) were sequenced, compared with each other, and blasted to the NCBI database. These amplicons were identical to each other and had a 100% match to 16 M. fructicola isolates originating from several countries including the United States, New Zealand, Japan, and China. The unicellular, hyaline, lemon-shaped conidia of three isolates grown at 22°C on PDA averaged 14.4 ± 1.3 μm long and 8.8 ± 0.77 μm wide, therefore fitting the description for M. fructicola (1). Koch's postulates were fulfilled by reproducing brown rot symptoms on mature apricots inoculated with conidia. Six days after inoculation, typical brown rot symptoms appeared on inoculated fruits while control fruits remained healthy. Molecular tests performed with the protocol of Côté et al. (3) and Hughes et al. (4) confirmed the presence of M. fructicola on the inoculated fruits. In 2009, the presence M. fructicola in the orchard where the pathogen was detected in 2008 was verified. One hundred and thirty-seven apricots showing brown rot symptoms were collected and tested (3). M. fructicola was recovered from two samples, indicating the persistence of the pathogen in the orchard. To our knowledge, this is the first report of natural infection of M. fructicola in a Swiss orchard. References: (1) Anonymous. OEPP/EPPO Bull. 33:281, 2003. (2) E. Bosshard et al. Plant Dis. 90:1554, 2006. (3) M.-J. Côté et al. Plant Dis. 88:1219, 2004. (4) K. J. D. Hughes et al. OEPP/EPPO Bull. 30:507, 2000.
low, water-soaked areas on the underside of the leaf. Within two to three days, the spots become well defined, slightly sunken, and turn dark brown to black. All infected plant samples reacted positively with the ImmunoStrip test for Xanthomonas hortorum pv. pelargonii (Agdia). Isolations were made from leaf spots and discoloured vessels of the geranium plants on yeast dextrose calcium carbonate (YDC) agar. Twenty-one bacterial isolates from the diseased tissues formed yellowcoloured mucoid and convex colonies on King's medium B and YDC medium. All these isolates were characterized as non spore-forming, Gram negative, rod-shaped, motile, aerobic, oxidase-negative, catalasepositive and amylolytic-positive. Pathogenicity was confirmed by stab inoculation of healthy geranium cuttings with pure cultures of all the isolates (Nameth et al., 1999). Reference strain GSPB 1955 and sterile distilled water were used as positive and negative controls respectively. Characteristic brown lesions at the point of inoculation were observed within five to seven days on geranium cuttings for all tested isolates. Identification of the isolates was confirmed by DAS-ELISA and by polymerase chain reaction amplification with pathovar-specific primers. A 1AE2 kb fragment specific for X. hortorum pv. pelargonii (Manulis et al., 1994) was obtained, as well as a 197 bp DNA product with the primer pair XcpM1 ⁄ XcpM2 (Sulzinski et al., 1996). All of the test results were similar to those of the reference strain GSPB 1955. This is the first report of occurrence of bacterial blight disease caused by X. hortorum pv. pelargonii on geranium plants grown in commercial floriculture greenhouses in Turkey.
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