Response surface models to predict potato tuber infection by Fusarium sambucinum from duration of wetness and temperature, and dry rot lesion expansion from storage time and temperature.

Dry rot (Fusarium sambucinum) of potatoes causes significant yield loss in storage and may also produce mycotoxins. Disease dynamics of dry rot development in potato tubers after harvest was studied and modeled. Potato tubers were surface sterilized, wounded, inoculated with a spore suspension of F. sambucinum and incubated in mist chambers placed in growth chambers at 4, 8, 12, 16 or 20 degrees C. After 0, 3, 6, 12, 24 and 48 h of incubation five tubers from each treatment were removed, dried and stored at 16 degrees C and 95% RH for 15 days. Inoculated tubers were also maintained in mist chambers for 24 h at 16 degrees C for the establishment of initial infections, dried, and stored at 4, 8, 12, or 16 degrees C for up to 90 days at 95% RH. At 15 days intervals, tubers were sliced, diameters and depths of diseased area measured, and data transformed to proportion of maximum volume diseased (PVD). The amount of infection was least at the lowest temperature tested and at the end of a 3-h wet period, but infection increased with an increase in wetness duration and temperature. At a storage temperature of 16 degrees C, lesions expanded rapidly reaching maxima in about 45 days of storage. A cubic regression model to predict infection potential from incubation temperature and duration of wetness explained 94.2% of the variation in PVD. A cubic regression model to predict lesion expansion potential as a function of storage temperature and duration explained 99.7% of the variation in PVD. These models could be used to manage potato dry rot, after validation under commercial conditions.