Janet Caprile

Laboratory survival of Drosophila suzukii under simulated winter conditions of the Pacific Northwest and seasonal field trapping in five primary regions of small and stone fruit production in the United States.

BACKGROUND Drosophila suzukii was first found in Oregon in August 2009. The threat of this pest to regional small and stone fruit production industries led to investigations on its overwintering capabilities in fruit-growing regions in the Pacific Northwest. Knowledge of its cold tolerance will help in the development of computer models to forecast seasonal population growth and decline. RESULTS Of 1500 adults or pupae, 22 (1.4%) individuals survived the 84 day experimental chilling period. Most (86%) of the survivors were subjected to 10 °C temperature treatments. Survival decreased significantly at lower temperature treatments. Freezing temporarily increased the mortality rate but did not significantly affect overall mortality over the trial period. Flies that emerged from pupae are estimated to survive for up to 103-105 days at 10 °C and for shorter periods at lower temperatures. Field trapping in five fruit production areas has demonstrated overwintering survival in California and Oregon, but lower survival is predicted in Eastern Washington and Michigan. CONCLUSION The experiments reported here indicate that long-term survival of D. suzukii is unlikely at temperatures below 10 °C. Field data from five climatic regions indicated extended low initial D. suzukii field presence in 2010 in all regions except California, where field presence was recorded earlier.

Population dynamics and ecology of Drosophila suzukii in Central California

Drosophila suzukii is a serious pest of several fruit crop systems in California’s Central Valley, which is one of the world’s major fruit-growing regions. This study followed D. suzukii seasonal population dynamics in multiple cropping and riparian systems in four cherry-producing counties of the Valley. Apple cider vinegar baited traps were used to monitor D. suzukii adults weekly, from April 2013 to July 2014, in 28 fields. Results show peak captures in the spring and fall seasons. In cherry orchards, adult trap counts were the highest near harvest (June) and declined thereafter, as fly populations moved to other crop (e.g., citrus) or non-crop habitats. The number of captured adults was positively related between pairs of sampled sites based on their proximity but was negatively related to differences in fruit ripening periods between different crops, suggesting that fly populations moved among crop and/or non-crop habitats during the year or had varying population dynamics on different crops and in different seasons. Mature egg load per female was higher during the fruiting season but lower during the winter season, with the majority of winter-captured females not containing mature eggs. This survey also reports for the first time the presence of trapped D. suzukii adults bearing melanized and encapsulated parasitoids in North America, non-target captures of larval drosophilid parasitoids in the traps, as well as the occurrence of larvae in the ovaries of adult female D. suzukii.

First report of Calosphaeria pulchella associated with branch dieback of sweet cherry trees in California

California is the second largest sweet cherry producer in the United States with approximately 10,800 ha and an average annual crop value of approximately

Calosphaeria Canker of Sweet Cherry Caused by Calosphaeria pulchella in California and South Australia

150 million. Perennial canker diseases constitute major threats to the cherry industry productivity by reducing tree health, longevity, and yields. During the course of summer 2006, we observed severe limb and branch dieback of sweet cherry (Prunus avium L.) in San Joaquin, San Benito, Contra Costa, and Stanislaus counties of California. Isolation from diseased branches repeatedly yielded the fungus Calosphaeria pulchella (Pers.: Fr.) J. Schröt. (1,2). Cankers and vascular necroses had developed in tree limbs and branches, generally initiating from the heart wood and later spreading into the sapwood. External symptoms of disease may be unapparent throughout the early stages of infection, particularly in large diameter shoots. Older infections often appeared as wilted leaves. Branches and trunks affected with cankers from which C. pulchella was isolated also generally bore perithecia of C. pulchella beneath the periderm. Perithecia were nonstromatic and arranged in dense, circinate groups, with elongated necks converging radially and fissuring the periderm. Asci were unitunicate, clavate, and 45 to 55 × 5 to 5.5 μm. Ascospores were allantoid to suballantoid, hyaline, and 5 to 6 × 1 μm. Colonies on potato dextrose agar (PDA) were dark pink to red in their center with a white margin. Conidia were hyaline, allantoid to oblong-ellipsoidal, and (3-) 4 to 6 (-9) × 1.5 to 2 (-2.5) μm. Identification of C. pulchella isolates also was confirmed by sequence comparison in GenBank database using the internal transcribed spacer region (ITS1-5.8S-ITS2) of the rDNA. Sequences of California isolates shared 100% similarity with C. pulchella reference isolate CBS 115999 (EU367451) (2). ITS sequences of the California isolates used in this study were deposited into GenBank (Nos. HM237297 to HM237300). Pathogenicity of four isolates recovered from the margin of active cankers was determined by branch inoculations. In December 2006, 2- to 4-year-old twigs of P. avium cv. Bing were inoculated with a 5-mm cork borer to remove bark and by placing an agar plug from the growing margin of 8-day-old colonies directly into the fresh wound, mycelium side down. Ten branches per isolate were inoculated. Ten control shoots were inoculated with noncolonized agar plugs. Inoculations were covered with vaseline and wrapped with Parafilm to retain moisture. Branches were harvested in July 2007 and taken to the laboratory to be examined for canker development, and the extent of vascular discoloration in each branch was assessed. Isolations from the edge of discolored tissue were conducted to fulfill Kochs postulates. After 8 months, C. pulchella was reisolated from 100% of the inoculated branches. Length of vascular discoloration averaged 62.5 mm in branches inoculated with the four C. pulchella isolates and 16.5 mm in the control twigs. No fungi were reisolated from the slightly discolored tissue of the controls. To our knowledge, this study constitutes the first report of C. pulchella as a pathogen of sweet cherry trees in California. References: (1) M. E. Barr. Mycologia 77:549, 1985. (2) U. Damm et al. Persoonia 20:39, 2008.

Mass releases of Trichogramma wasps can reduce damage from codling moth.

California is the second largest sweet cherry producer in the United States with annual revenues up to

Organic apple production manual.

200 million. The South Australian cherry industry generates about 10% of Australias overall production with approximately 1,500 metric tons of cherries produced yearly. In California, perennial canker diseases and subsequent branch dieback are responsible for extensive damage throughout sweet cherry orchards, reducing annual yields and tree longevity. Surveys of cherry orchards and isolation work were conducted in California to identify the main canker-causing agents. Calosphaeria pulchella was the main fungus isolated from cankers, followed by Eutypa lata and Leucostoma persoonii, respectively. Preliminary surveys in cherry orchards in South Australia documented C. pulchella and L. persoonii in cankers. The pathogenicity of C. pulchella in sweet cherry was confirmed following field inoculations of 2- to 3-year-old branches. C. pulchella was able to infect healthy wood and produce cankers with as much virulence as E. lata or L. persoonii. Spore trapping studies were conducted in two sweet cherry orchards in California to investigate the seasonal abundance of C. pulchella spores. Experiments showed that rain and sprinkler irrigation were important factors for aerial dissemination. Finally, this study illustrates the symptoms and signs of the new disease Calosphaeria canker.