Effect of canopy cover,seeding depth,and soil moisture on emergence of Centaurea maculosa and C. diffusa*

The effects of canopy cover, seeding depth, and soil moisture on emergence of Centaurea maculosa Lam. and C. diffusa Lam. were studied. Canopy cover had no effect on ermergence rate (seedlings/day/100 seeds) of either species. Seeds of both species emerged faster when placed on the soil surface. Emergence rate decreased as seeding depth increased. Both species required more than 55% initial soil moisture to initiate emergence, with 65–70% being optimum. Percentage emergence followed exactly the same trend as emergence rate. C. maculosa had better emergence characteristics over a wider range of conditions than C. diffusa, possibly being some of the reasons for the former having a wider geographical distribution in the United States and Canada.     

The effects of ultraviolet-B (UV-B: 290–320 nm) radiation on blister blight disease of tea (Camellia sinensis)

Sunlight is known to reduce the incidence of blister blight disease of tea, caused by Exobasidium vexans . The effects of the ultraviolet-B (UV-B: 290–320 nm) component of solar radiation on the disease and the development of E. vexans were studied in the field in Sri Lanka using UV-screening filter materials held over a commercial crop. Exclusion of UV-B radiation by Polyester, which reduces fluxes in the UV-B region by approximately 75–85%, increased both the number of translucent spots (immature sites of infection) and number of sporulating blisters (mature sites of infection), but it had little or no effect on the sporulation of the pathogen. When basidiospores were artificially inoculated on leaves, and were exposed to full or filtered solar radiation, their survival and germination increased when UV-B wavelengths were removed; significant differences were found 62 h after inoculation. However, UV-B did not affect the extension of germ tubes. This study indicates that the UV-B component of solar radiation plays an important role in the natural regulation of blister blight disease in the field.     

A model of plant virus disease epidemics in asynchronously-planted cropping systems

A mathematical model was developed of the dynamics of a plant virus disease within a spatially-referenced lattice of fields of a host crop. The model can be applied to crops in continuous, contiguous cultivation such as tropical irrigated rice. Disease progress in each field of the host crop was assumed to be logistic and determined by incidence within the field itself as well as incidence in neighbouring fields, depending on the gradient of disease spread. The frequency distribution of planting dates (represented by the proportion of the total number of fields planted in successive months) was assumed to follow a normal distribution and the variance of planting date was used as a measure of cropping asynchrony. Analysis of the model revealed that disease incidence within the lattice (i.e. mean incidence over all fields) depended upon the infection efficiency, the slope of the dispersal gradient, and the variance in planting date. Disease endemicity depended mainly on planting date variance and disease persisted in the lattice if this variance exceeded a certain threshold. Above the threshold for persistence, the response of mean disease incidence to planting date variance was non-linear and the region of greatest sensitivity was closest to the threshold. Thus, disease systems that show moderate rather than high cropping asynchrony are more likely to be influenced by changes in the variance of planting date. Implications for the area-wide management of rice tungro virus disease are discussed.     

Evaluation of host and bacterial gene modulation during Lawsonia intracellularis infection in immunocompetent C57BL/6 mouse model

BackgroundProliferative enteritis caused by Lawsonia intracellularis undermines the economic stability of the swine industry worldwide. The development of cost-effective animal models to study the pathophysiology of the disease will help develop strategies to counter this bacterium.ObjectivesThis study focused on establishing a model of gastrointestinal (GI) infection of L. intracellularis in C57BL/6 mice to evaluate the disease progression and lesions of proliferative enteropathy (PE) in murine GI tissue.MethodsWe assessed the murine mucosal and cell-mediated immune responses generated in response to inoculation with L. intracellularis.ResultsThe mice developed characteristic lesions of the disease and shed L. intracellularis in the feces following oral inoculation with 5 × l0⁷ bacteria. An increase in L. intracellularis 16s rRNA and groEL copies in the intestine of infected mice indicated intestinal dissemination of the bacteria. The C57BL/6 mice appeared capable of modulating humoral and cell-mediated immune responses to L. intracellularis infection. Notably, the expression of genes for the vitamin B12 receptor and for secreted and membrane-bound mucins were downregulated in L. intracellularis -infected mice. Furthermore, L. intracellularis colonization of the mouse intestine was confirmed by the immunohistochemistry and western blot analyses.ConclusionsThis is the first study demonstrating the contributions of bacterial chaperonin and host nutrient genes to PE using an immunocompetent mouse model. This mouse infection model may serve as a platform from which to study L. intracellularis infection and develop potential vaccination and therapeutic strategies to treat PE.