VIEW ARTICLE

Ecology and Epidemiology

Effect of Flooding on Development of Phytophthora Root Rot in Fraser Fir Seedlings. C. M. Kenerley, Former graduate research assistant, Department of Plant Pathology, North Carolina State University, Raleigh 27650; K. Papke(2), and R. I. Bruck(3). (2)Undergraduate honors student, Department of Forestry, North Carolina State University, Raleigh 27650; (3)Assistant professor, Departments of Plant Pathology and Forestry, North Carolina State University, Raleigh 27650. Phytopathology 74:401-404. Accepted for publication 28 September 1983. Copyright 1984 The American Phytopathological Society. DOI: 10.1094/Phyto-74-401.

The effect of flooding on root rot caused by Phytophthora cinnamomi in Fraser fir (Abies fraseri) seedlings was assessed. Soil infested with propagules of P. cinnamomi but without seedlings, and infested and uninfested soil into which 2-yr-old Fraser fir seedlings were transplanted, was continuously flooded for 0, 24, and 48 hr. Inoculum density of P. cinnamomi was quantified at 2, 9, and 23 days and seedling mortality was assessed 33 days after flooding. In treatments with infested soil and seedlings, inoculum density was greater (P = 0.01) with flooding than without flooding at days 9 and 23. Final seedling mortality and infection were also higher (P = 0.01) with the two flooding treatments (24 or 48 hr) compared to no flooding. Inoculum density was found to decline similarly among the treatments without the host regardless of the flooding period. A separate series of experiments demonstrated that significant increases in the production of secondary inoculum occurred within 3 days of flooding infested soil containing the host. The greatest rate of increase in secondary inoculum was recorded between days 5 and 7 following flooding. In experiments with zoospore suspensions used as inoculum, no difference in seedling infection was found between flooded or unflooded treatments at any inoculum level tested. Flooding (24 or 48 hr) appears to increase seedling infection and mortality by promoting production and dispersal of inoculum rather than predisposing the host.