The Biology and Control of Botrytis Bunch Rot

The critical timing of infections that cause Botrytis bunch rot (BBR) has long been a
focus of international debate: Some believe in the primacy of infections that occur at
bloom (which remain latent thereafter until the preharvest period, when they become
active and rot the berries), whereas others believe that post-veraison infections cause the
most damage. In this project, we have shown that latent infections can readily become
established when clusters are inoculated at bloom or during the early stages of berry
development, but that the vast majority of these infections fail to become active, i.e., they never cause disease. In contrast, berries become much more susceptible to BBR after
veraison, and inoculating just one or two berries per cluster at that time resulted in up to
50 to 60 additional diseased berries per cluster at harvest. Thus, severe disease losses
appear to result largely from secondary disease spread during the post-veraison period.
Nevertheless, bloom-time infections can serve the critical function of primary disease
foci (i.e., the sources of secondary spread) if they do become active before harvest.
Viewing bloom versus post-veraison infections as the primary and secondary phases of
disease development, respectively, largely resolves the dispute over their relative
importance, since it is the combination of the two that causes serious losses. High berry N
content, high relative humidity during the preharvest period, and high soil water content
after veraison were all shown to promote the activation of latent infections established at
bloom; thus, these factors can help initiate an epidemic preharvest. Tightly compressed
bunches were shown to dramatically facilitate post-veraison disease spread, and this
appears to be the primary factor responsible for the long-observed correlation between
cluster compactness and BBR severity. High berry N content also was shown to promote
secondary spread under conditions of otherwise light to moderate disease pressure.
Fungicide programs contributed to disease management by reducing both the initial
establishment of primary infections (sprays at bloom) and their spread upon activation
(sprays at bunch closure, veraison, and/or preharvest); the relative importance of specific
spray timings depended on the particular year of the trial and weather events during these
periods. When applied at veraison, the fungicide, cyprodinil (Vangard), showed some
ability to eradicate latent infections that had been established at bloom, whereas
fenhexamid (Elevate), iprodione (Rovral), and boscalid (Endura) did not. Following
applications at bloom and bunch closure, Vangard also appeared to provide significantly
greater residual protection within the berries at veraison than did the other tested