1Research Institute of Organic Agriculture, CH-5070 Frick, Switzerland; 2 Institute for Applied Plant Biology, CH-4124 Schönenbuch, Switzerland

Background and objectives
Brown rot, caused by Monilinia laxa Honey, has become an important pathogen of sweet cherry (Prunus avium L.) in Switzerland. The occurrence of blossom blight is influenced by inoculum density and climatic conditions. However, prediction of disease occurrence in the field is difficult because effects such as the climatic conditions during the susceptible phenological stage of the host, or the inoculum density, are difficult to distinguish. The aim of this study was to determine tolerance thresholds of blossom blight and to analyse the influence of climatic conditions, inoculum density, and phenological stage on blossom blight incidence of sweet cherry in Swiss orchards.

Materials and methods
Field observations were conducted in 1991 and 1992 in six commercial orchards in Switzerland. The trees received no fungicide treatments. The climatic conditions (temperature, r.h., precipitation, wetness duration) were monitored by means of a data-logger. Six trees of P> ;avium L. cv. Star were chosen in each site and observed twice per week from bud burst until harvest. The individual blossoms of 96 spurs per site were assigned to phenological stages and to the stages of the symptoms of M. ;laxa. A bouquet spur was considered infected if exudates of gum were visible. Within a distance of 1.5 ;m of the observed branches, mummified fruit and blighted spurs with infected blossoms of the previous year were assessed as sources of primary inoculum.

The confidence intervals of the infection dates were determined a posteriori for each site, based on the symptoms of the diseased blossoms, and the temperatures during the incubation period. This infection interval was standardized to a 'physiological wetness duration' based on methods described in a previous study [1].

Results and conclusions
Blossom blight caused by M. ;laxa was present in all sites. The disease incidence between the sites varied from 2.4% infected blossoms per spur to up to 64.7%. The method used to determine a posteriori the 95% confidence interval of the infection date allowed the determination of susceptible phenophases and the analysis of the environmental factors conducive to blossom blight. Blossoms in full bloom were predominant during the confidence interval, indicating that most blossoms were infected in full bloom. In general, severity of disease increased with higher density of inoculum sources and longer physiological wetness duration. The amount of inoculum sources within a distance of 1.5 ;m accounted for most of the differences between the individual infection rates. All confidence intervals calculated included rain events and periods of wetness, suggesting that precipitation is an important factor for inoculum production and dispersal, or for the infection process. The carrying capacity (maximum rate of ripe fruit per initial blossom) was 0.32 if losses due to pests were excluded. Although blossom blight linearly reduced fruit onset, only disease severities above 40% caused fruit onset below the carrying capacity. However, spur blight incidence increased sharply if blossom blight was greater than 20% and the following climatic conditions were conducive to spur infection. Therefore, a tolerance threshold of 20% of infected blossoms, dependent on both crop loss due to blossom blight and potential destruction of spurs, is suggested for cv. Star.

In conclusion, blossom blight increased with longer physiological wetness duration and higher number of inoculum sources within a distance of 1.5 ;m. At densities below one source of inoculum, the tolerance threshold of 20% blighted blossoms was not exceeded, regardless of the climatic conditions during the susceptible period. Climatic parameters alone were insufficient for prediction of severity of disease, whereas the determination of the density of inoculum sources within trees was found to be appropriate to assess the risk of incidenceof blossom blight .

1. L Tamm, Minder Chr E, Flückiger W, 1994. Phytopathology 85, 401-408.