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.

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Seed transmission of Pantoea stewartii was evaluated by assays of more than 76,000 plants in greenhouse and field grow-out trials. Fourteen P. stewartii-infected seed lots were obtained from two dent corn inbreds and two sweet corn cultivars that were inoculated with either a rifampicin and nalidixic acid-resistant strain (rif-9A) or a wild-type strain (SS104) of P. stewartii. Four additional seed lots were collected from naturally infected inbreds. Percentages of infected kernels ranged from 0.8 to 72%, as determined by agar plating or by individual-kernel enzyme-linked immunosorbent assay (ELISA). Plants grown from this seed were assayed by a stem-printing technique that consisted of cutting and pressing a cross-section of each stem onto agar media. Prints were examined for development of P. stewartii colonies after 24 and 48 h. The transmission rate from seed produced on the inoculated plants was 0.066% (28 of 42,206 plants), based on all seedlings assayed. Transmission was estimated to be 0.14% from infected kernels. The transmission rate from seed produced on naturally infected plants was 0.0029% (1 of 34,924 plants), based on all seedlings, and 0.022% from infected kernels. Seed transmission occurred significantly less often (P = 0.034) from seed produced on naturally infected plants than from seed produced on inoculated plants, probably due to greater kernel damage caused by ear shank inoculation. The rarity of seed transmission of P. stewartii from heavily infected seed lots that would ordinarily be rejected due to poor germination suggests that the likelihood of seed transmission from good quality commercial seed corn is virtually nonexistent.

In established rapeseed-growing districts, ascospores discharged from crop residues were shown to be the major source of infection for black leg disease. Infection from seed was of relatively minor importance. The potential amount of ascospore inoculum on crop residues was related to severity of the disease in the original field. Rainfall of more than 1.0 mm was required for large ascospore discharges, but smaller ones occurred in light rain or dew. Discharge from the same crop residues increased greatly between April and May, remained at a high level until August, and then gradually declined until by January very few spores were discharged. In April, discharge resumed and the same cycle was repeated. The amount of crop residue surviving in fields from the previous year declined by 90% during the growing season. No relationship was apparent between the amount of rainfall during the period when infection occurred and the disease severity in crops sown at different times. Stem canker development was less severe in plants grown at 8° than in those grown at 12° and 15°C.

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