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First Report of Brown Rot on Apple Fruit Caused by in Pennsylvania
- K. A. Peter, V. L. Gaskins, B. Lehman, W. M. Jurick
- Plant disease 2015 v.99 no.8 pp. 1179
- Malus domestica, Monilinia fructicola, agar, apples, brown-rot fungi, color, conidia, ethanol, fruit growing, fungal diseases of plants, internal transcribed spacers, lesions (plant), microbial detection, monitoring, mycelium, orchards, pathogenicity, pathogens, pests, polymerase chain reaction, ribosomal DNA, sequence analysis, species identification, stone fruits, storage temperature, trees, Chile, Indiana, Mid-Atlantic region, Pennsylvania, Serbia, West Virginia
- Brown rot, caused by Monilinia fructicola (G. Wint.) Honey, is the most economically important stone fruit disease in North America (Chen et al. 2013). In the fruit growing Mid-Atlantic region, the fungus was reported to cause disease on apple in West Virginia in 1956 (Adams and Tamburo 1957). In September 2013, a ‘Jonamac’ apple was found with brown rot symptoms on a tree at harvest in a commercial orchard in Lancaster County, PA, which has a history of brown rot disease on stone fruit. Approximately 1% of the apple trees within walking distance of affected stone fruit had at least one apple on the tree with brown rot symptoms. Infected apples were most noticeable later in the season; the decayed tissue was soft and the entire fruit surface was covered with light colored mycelium in concentric rings with tufts of abundant grayish-brown conidia. A single spore isolate of the infecting fungus was cultured on potato dextrose agar (PDA) at 25°C to assess morphological characteristics and was identified to species. The fungus produced a grayish-colored colony with uneven margins and had a dark brown to black colored reverse. Conidia production was formed in branched and unbranched monilioid chains. Lemon shaped conidia were one celled, hyaline, and on average 15 × 10 μm (n = 50), which is consistent for M. fructicola (Chen et al. 2013). Growth rate was analyzed using 0.5 strength PDA, Richards defined, and V8 agar in triplicate petri plates and was 3.1 mm/d (±0.30), 3.0 mm/d (±0.17), and 6.4 mm/d (±0.03), respectively, which was repeated. Species identification was verified by obtaining mycelial genomic DNA, amplifying the internal transcribed spacer (ITS) rDNA with ITS4/ITS5 primers via conventional PCR, and sequencing the amplicon directly (White et al. 1990). MegaBLAST analysis revealed the 2× consensus amplicon sequence has the highest similarity (100% identical, 0.0 E value) with M. fructicola isolate DL172.04 (GenBank Accession No. DQ314728.1) and was 99% identical to M. fructicola isolates from Indiana (KJ541032.1), Serbia (JN176564.1), and Chile (JN001480.1). Pathogenicity was verified using 20 ‘Golden Delicious’ apples that were surface sanitized with soap and water, sprayed with 70% ethanol, and dried. Fruit were wounded with a sterile nail to a 3 mm depth at the equator and inoculated with water or 25 µl of a conidial suspension (104 spores/ml) of the isolate, and stored at 25°C for 5 days. Water-inoculated and uninoculated control fruit were symptomless, while pathogen-inoculated fruit had 100% decay incidence with mean lesion diameters of 36.1 mm (±0.39). Inoculated apples had soft, round lesions with even margins and light brown mycelium near the inoculation site. The fungus was reisolated from inoculated fruit and identified as M. fructicola. To our knowledge, this is the first report of M. fructicola causing brown rot on apple fruit in Pennsylvania. Although M. fructicola is a common pathogen in the United States, other Monilinia sp., such as M. fructigena and M. polystroma, are regulated pests. As a result, monitoring brown rot pathogens, especially infecting apple both pre and postharvest, could lead to early detection of these regulated pests if introduced.