1 Department of Plant Pathology, North Carolina State University, Raleigh, NC 27695, USA; 2Department of Statistics, North Carolina State University, Raleigh, NC 27695, USA

Background and objectives
Diseases caused by soil-borne, oomyceteous pathogens in the genus Phytophthora are responsible for significant economic losses on important crops worldwide. Phytophthora species frequently develop virulent races, which can overcome single-gene resistance in host plants. These diseases continue to cause losses on many crops because management practices, including the use of genetic resistance, are not entirely effective. In addition, metalaxyl-insensitive populations of P. ;capsici were discovered in North Carolina pepper fields in 1997 and this had made management of Phytophthora blight more difficult as shown by the alarming increase in the occurrence of the disease. The pepper-P. ;capsici pathosystem is more complex than other Phytophthora pathosystems in that virtually every part of the plant can be infected. Pathogens of the genus Phytophthora can spread by several distinct mechanisms including: (1) movement from root to root down rows either by root growth to inoculum, inoculum movement to roots, or root-to-root contact; (2) inoculum spread in surface water; (3) splash dispersal from soil to leaves, stems, or fruit ; and (4) aerial dispersal from sporulating lesions on leaves, stems or fruit. The paucity of information on the spatial dynamics of inoculum dispersal of soil-borne pathogens and disease development has hindered our ability to develop sustainable management strategies for Phytophthora diseases.

Results and conclusions
In the first portion of our research we characterized the dynamics of spatial patterns of disease caused by naturally occurring inoculum of P. ;capsici in seven commercial pepper fields over time and identified the primary mechanisms of inoculum dispersal. The pathogen was dispersed primarily by movement from root to root down rows (mechanism 1) and by surface water (mechanism 2). Limited splash dispersal (3) was observed late in the epidemic and no aerial dispersal (mechanism 4) was observed. Disease severity displayed strong spatial dependence and a high degree of anisotrophy over time, indicating strong aggregated patterns of disease with distinct directional orientation [1].

We then modified the pathosystem by means of cultural and chemical management strategies to permit specific, inoculum dispersal mechanisms to operate in artificially infested pepper fields and determined their subsequent impact on specific spatial and temporal components of epidemic development. Dispersal of soil inoculum was suppressed and disease was only 2.5-43% with no-till wheat stubble from an autumn-sown cover crop. Final disease incidence was 71-72% and pathogen spread occurred within and across rows when all dispersal mechanisms were operative in plots with bare soil. Final disease was 42-78% with black plastic mulch when a sporulating pepper fruit placed on the surface served as the source of initial inoculum. The fungicide metalaxyl applied in the irrigation system did not suppress within-row spread of surface inoculum from a sporulating fruit on plastic but did limit across-row spread (final disease was 11.5-14%). Pathogen dispersal mechanisms were modified most dramatically by the no-till cropping system [2].

The effect of inoculum source type and a rye vetch cover crop on within-row spread of Phytophthora blight was subsequently investigated in noninfested plots or plots infested with either sporangia or oospores. Rows were covered with black plastic, stubble from a rye-vetch cover crop or left bare. Final disease incidence in bare soil plots was 100%, 69%, and 10% in rows infested with sporangia, oospores, or noninfested soil, respectively. In contrast, final disease incidence in rye-vetch plots was 11%, 12% and 3%, and in black plastic covered plots was 7%, 20%, and 18% in rows infested with sporangia, oospores, or noninfested, respectively. Above-ground symptoms were severest in bare soil plots amended with sporangia, demonstrating significant within-row spread of this inoculum source.

1. Larkin, RP, Gumpertz, M L, Ristaino, JB, 1995. Phytopathology 84, 191-203.
2. Ristaino, J B, Parra, G, Campbell, CL, 1997. Phytopathology 87, 242-249.