The relative importance of several infection pathways (silks, stalks, and seed) leading to kernel infection of maize hybrids by Fusarium moniliforme was investigated in field experiments in 1993 and 1994. Systemic movement of specific fungal strains within plants was detected by using vegetative compatibility as a marker. Transmission of F. moniliforme from inoculated seed to stalks and developing kernels was detected in two of three field experiments; the seed-inoculated strain was detected in kernels on approximately 10% of ears. The percentage of kernels infected with the seed-inoculated strain ranged from 0 to 70%, with a mean of 0 to 2.5% (0 to 8.3% of F. moniliforme-infected kernels). Other pathways to kernel infection were more effective than seed transmission and systemic infection. F. moniliforme strains inoculated into the crowns and stalks of plants were found throughout the stalks and in up to 95% of the kernels in individual plants. Infection through the silks was clearly the most effective pathway to kernel infection. This was the only inoculation method that significantly increased overall incidence of F. moniliforme infection in kernels; the silk-inoculated strain infected up to 100% of the kernels in individual ears, with a treatment mean as high as 83.7% of kernels. When plants were silk-inoculated, the percentage of kernels infected by other F. moniliforme strains from the seed or stalk was reduced, apparently due to competition among strains. This study provides evidence that systemic development of F. moniliforme from maize seed and stalk infections can contribute to kernel infection, but silk infection is a more important pathway for this fungus to reach the kernels.

Hydathodes of tomato leaves served as extremely efficient infection courts for the bacterial canker pathogen, Clavibacter michiganensis subsp. michiganensis. Chlorotic lesions developed at the tips of leaflet lobes about 2 weeks after inoculation of guttation droplets. Lesions expanded along the leaflet margins and became necrotic. Movement of C. michiganensis subsp. michiganensis from the inoculated leaflet into the rachis was slow and erratic. Histological observations revealed that pathogen populations first developed within large intercellular spaces lying beneath the stomata, which serve as water pores in tomato hydathodes. Bacteria were first observed within vessels of the large marginal fimbriate veins 7 days after inoculation. By 14 days after inoculation, large populations could be seen within the vessels; and by 21 days after inoculation, tissue collapse was widespread and masses of bacteria could be seen in the intercellular spaces and within necrotic cells.

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Two greenhouse and two field experiments were conducted in 1994 and 1995 to quantify the incidence of maize kernel infection resulting from systemic infection of maize plants by Fusarium moniliforme. Seeds were infected by two methods: (i) spray-inoculation of maize silks during seed development (field-infected), and (ii) soak-inoculation of mature seeds in a spore suspension (laboratory-infected). Plants were grown from infected seeds and assayed for systemic infection by the seed-inoculated strain, determined by vegetative compatibility of recovered isolates with the original strain. The seed-inoculated strain was recovered from stalks and kernels of plants grown from both types of infected seed. Mature plants grown from field-infected seeds had a higher percentage of their kernels infected with the seed-inoculated strain compared with plants from laboratory-infected seed. Mean incidence of infection by the seed-inoculated strain was 9.9 to 29.4% of all kernels (33.0 to 55.9% of F. moniliforme-infected kernels) in the plants grown from field-infected seed. Some plants from infected seed were subsequently silk-inoculated, and the silk-inoculated strain was recovered from a much higher percentage of kernels (26.5 to 37.5% of all kernels or 77.9 to 78.4% of F. moniliforme-infected kernels) than was the seed-inoculated strain; furthermore, silk inoculation significantly reduced incidence of kernel infection by the seed-inoculated strain. Seed infection by F. moniliforme resulted in systemic infection of plants and kernels. However, local infection (via silks) was a more important pathway to kernels than was systemic infection, and strains infecting the silks competed successfully against those entering the kernels through systemic development.

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