Phytophthora cinnamomi : Population Densities in Forest Soils

Population densities of Phytophthora cinnamomi, associated disease and environmental factors were studied concurrently during a 2-year period in three different forest ecosystems. Pathogen populations showed seasonal variation, low values being obtained for winter months associated with soil temperatures less than 10°C. Populations increased with warmer temperatures for spring and summer, but declined during dry periods in late summer or early autumn when the soil water potential was lower than -9 bars, although at that period soil temperatures were favourable. High populations were recorded in autumn, then declined with decrease in soil temperatures during winter. Correlation coefficients indicated a highly significant relationship between pathogen populations and soil temperatures from autumn to early summer, and between soil moisture and pathogen population for summer and autumn, in the Brisbane Ranges independently of site. The same pattern was evident in wetter forests at Narbethong and savannah woodlands at Wilson's Promontory, although results were not significant. Disease was evident wherever the pathogen occurred among susceptible hosts. The savannah woodland, the dry shrubby sclerophyll forest and the wetter sclerophyll forest all contained susceptible dominants; consequently disease was associated with changes in the forest community such as early death of the understorey, later die-back and death of the trees, and an increase in sedges and in bare ground. Symptoms and deaths increased with time from invasion. The severity of disease and its rate of extension, apart from spread by free water, were associated with environmental factors such as shallow soil, poor drainage and low soil water-holding capacity. These were characteristic of the Brisbane Ranges, where destruction of the forest community was severe and the rate of disease extension rapid. In the deep krasnozem at Narbethong and the deep sands of Wilson's Promontory, destruction was confined to the most susceptible hosts, disease extension was continuous but slow, and deaths occurred in a mosaic throughout the infected zone.