Occurrence ofBotrytis cinereaand Subsequent Disease Expression at Different Positions on Leaves and Bunches of Grape

Abstract

The occurrence of Botrytis cinerea and subsequent disease expression at different positions on leaves and bunches of grape was determined from 1996 to 2000. Different techniques were used to detect viable inoculum on material obtained from table (cvs. Barlinka and Dauphine) and wine grape (cv. Merlot) vineyards. Isolations were made from berry skins on Kerssies' B. cinerea selective medium or on water agar medium supplemented with paraquat. Leaves and parts of bunches bearing three to seven berries on a short rachis section were used untreated or treated with paraquat, or were frozen for 1 h at -12°C. Paraquat and freezing were used to terminate host resistance and to promote the development of the pathogen from the tissues. The material was used untreated to detect the pathogen on the surface, or were surface-sterilized to detect mycelia (latent infection) in the tissue. B. cinerea occurred in a consistent pattern in leaves and bunches in all vineyards. Based on the combined data for tissues exposed and unexposed to paraquat, B. cinerea occurred predominantly in bunches and was mostly associated with the bases of the berry and the pedicel. Overall, approximately 30% of the berries yielded B. cinerea at these positions. The next prominent positions occupied were leaf blades, rachises, and laterals, of which approximately 20% yielded B. cinerea. The pathogen occupied the petioles less often (10%), and the berry cheek infrequently (5%). The stylar end of the berries, on the other hand, was virtually free (0.02%) of the pathogen. Disease expression in bunches displayed the pattern showed by the inoculum ecology, and symptoms consistently developed first at the berry-pedicel attachment zone. The isolation studies showed that the pathogen seldom occurred on the surface or in the skin tissue near the base, cheek, or stylar end of berries. Latent infections in the berry base were also few at véraison and harvest. Collectively, the findings indicate that conidia dispersed in early season in bunches, and residing superficially at the berry-pedicel attachment zone, are a major factor in B. cinerea bunch rot.

Effect of Y-trellis and vertical shoot positioning training systems on downy mildew and botrytis bunch rot of grape in highlands of southern Brazil

“…Infections by B. cinerea early in the season may remain dormant (latent infections) while berries are green, but under favorable conditions, may resume growth and cause bunch rot as the grapes approach veraison. In this situation, the disease can spread rapidly from berry to berry within clusters and among clusters (Holz et al, 2003;Keller et al, 2003;Wilcox, 2007). Harvest occurred March 15, 2013, and April 2, 2014, meaning that disease evaluations for 2013-2014 were carried out a total of 40 days longer than in 2012-2013.…”

Gray mold caused by Botrytis cinerea limits grape production in Chile

“…Symptoms start at the berry base as a reddish-brown discoloration and progresses toward the stylar end of the grape berry. This appears to be the most frequent B. cinerea infection pathway during blooming (Holz et al, 2003;Keller et al, 2003b;Pezet and Pont, 1986;Viret et al, 2004;Zoffoli et al, 2009). b. Stylar end infection through the stigmata at bloom. Symptoms appear at the stylar end of mature berries.…”

“…Berry symptoms commonly appear as reddish-brown discoloration that starts at the pedicel end and progresses toward the stylar end (Holz et al, 2003). Small (approximately 0.5 mm in diameter), round, reddish-brown necrotic spots often appear on the berry cheek after rainfall near harvest time, and reddish-brown decay at the stylar end has been observed in Chilean vineyards (Zoffoli et al, 2009).…”

“…The highest conidial concentrations occur on warm humid days after rain (Diaz, et al, 1998;Leyronas and Nicot, 2013;Mundy et al, 2012;Rodríguez-Rajo et al, 2002Stepalska, and Wolek, 2005). The conidia are produced in multiple and very diverse substrates (Coertze and Holz, 1999;Corbaz, 1972;Holz et al, 2003;Nair and Nadtotchei, 1987;Williamson et al, 2007).…”

“…Current knowledge indicates that a complex enzymatic process, rather than the pressure caused by hyphae penetration, is primarily responsible for active penetration (Tenberge, 2004). Passive (indirect) penetration can occur through natural openings (stomata and lenticels) and wounds (Holz et al, 2003;Kars and van Kan, 2004).…”