ABSTRACT
Soybeans (Glycine max) (V3 stage) were sprayed once with nanoparticles (NPs) of AgO, B, CeO, CuO, MnO, MoO3, SiO, TiO, or ZnO and exposed to Fusarium virguliforme, the cause of sudden death syndrome. Up to 80% root rot was observed in greenhouse experiments. However, NP CuO, B, MoO3, or ZnO reduced the root rot severity by 17-25%. Infected roots and shoots had significant changes in B, Mg, P, S, Si, and Zn, but NP treatment restored levels to that of the healthy control. For example, the increased root Mg and Mn contents induced by disease were reversed by NP B and Mn amendments. In vitro assays found that the NPs did not inhibit the pathogen. This, along with the restoration of altered nutrient levels in the plant tissue, suggests that modulated plant nutrition increased disease defense. Treatment of seedlings with nanoscale micronutrients may be a new tool in promoting soybean health.
Subject(s)
Fungicides, Industrial/pharmacology , Glycine max/drug effects , Metal Nanoparticles/analysis , Metals/pharmacology , Oxides/pharmacology , Plant Diseases/prevention & control , Fungicides, Industrial/chemistry , Fusarium/drug effects , Fusarium/physiology , Metals/chemistry , Oxides/chemistry , Plant Diseases/microbiology , Glycine max/physiologyABSTRACT
Stem bleeding disease (resinosis) of coconut palm is caused by Thielaviopsis paradoxa and is very important in the state of Sergipe, Brazil. Understanding the epidemiological behavior of the disease is essential for establishing more efficient control strategies. Thus, we characterized the temporal progression and spatial distribution of stem bleeding in a commercial orchard under conditions of natural infection in the area of Neopolis, Sergipe. Three plots with 729 plants each were selected and evaluated every two months for stem bleeding incidence. In the temporal analysis, the monomolecular model gave the best fit to data on disease incidence, as it accurately showed the temporal dynamics of the disease during the experiment period. The spatial pattern of stem bleeding varied over time, with initial infections presenting random pattern and then evolving to aggregate pattern during evaluations. This indicates that the disease may have originated from the pathogen survival structures, followed by auto infections caused by dissemination from plant to plant, either by humans, by contact between roots, or by the vector Rhynchophorus palmarum.
