Sclerotinia sclerotiorum is an economically important fungal pathogen of broadacre cropping worldwide. Significant yield loss occurs in canola following the establishment of S. sclerotiorum on the primary raceme. As S. sclerotiorum grows along the canola raceme it necrotises host tissue, effectively restricting the ability of the plant to translocate nutrients. Observations made during routine stem infection assays led us to test the hypothesis that the virulence of S. sclerotiorum on canola is enhanced on mature racemes. We conducted a time of sowing (TOS) experiment by sowing seed of cultivar Charlton in a randomized block design at 7 day intervals over a three week period (n = 10 plants per TOS). Plants were propagated in 5 L pots of UWA mix (Richgro), in a temperature controlled glasshouse under natural light, with a controlled watering schedule. The developmental stage of each raceme was documented, by measuring primary raceme height (mm) every 7 days and recording the onset of flowering. All racemes were inoculated with S. sclerotiorum strain CU11.19 at the 6th node below the oldest floral branch at 18, 17, 16 and 15 weeks after sowing (WAS). The node width (mm) was recorded and weekly lesion length measurements (mm) were conducted for 4 weeks. Lesions that established on mature racemes (18 WAS) were significantly larger than lesions on the most immature racemes (15 WAS) (Tukey’s HSD P < 0.05). Following natural raceme desiccation, total sclerotia were extracted and weighed. Mature racemes (18 WAS) developed 16 fold more sclerotia than younger racemes (P < 0.001). Together these data suggest that older, mature racemes are more easily overcome by S. sclerotiorum, resulting in a greater mass of sclerotial development. We hypothesize that changes in the source-sink relationship within the plant may contribute to the differences observed.