Abstract
In southern Ontario rootrot of sugar beets may be caused by Aphanomyces cochlioides Drechs., Pythium aphanidermatum (Edson) Fitz., Pythium ultimum Trow, or Rhizoctonia solani Kuehn. The distribution of these fungi was found to be limited to soil type rather than to locality, A. cochlioides thus being found in the clay soils and P. aphanidermatum only in the sand loam. They were not present in the subsoil and were most abundant in the top two or three inches of surface soil. A. cochlioides, which was found for the first time in Canada in 1946, causes the so-called blackroot of sugar beets, and is the most economically important pathogen encountered. Blackroot appears either as an early acute attack or a later chronic one, but the acute phase is of major importance and occurs in epiphytotics during seedling development, usually when the beet is from two to five weeks old. Weather records and experiments have shown that serious disease outbreaks only occur when moisture is abundant and soil temperature exceeds 60° F. Susceptibility is sharply correlated with the developmental rhythm of the seedling and ends when the cortex of the hypocotyl is sloughed off. A. cochlioides is homothallic, attacks the hypocotyl of the beet, and develops in the intercellular spaces of the cortex. It will not grow at relative humidities of less than 99% and this sensitivity to all but extremely high humidity is believed to limit its parasitic activity. Microbiological studies indicated that the number of organisms in the rhizosphere of diseased sugar beet roots is much larger than in that of healthy beet roots. Since parallel rhizosphere responses followed local artificial killing of roots, they are believed to be due in part at least to the utilization of necrotic tissues or substances released on their breakdown. Streptomycin, but not penicillin, was effective in controlling rootrot in greenhouse experiments. Control with Arasan is achieved in part through a direct fungicidal action, but the evidence suggests that it may be due to a shift in the microbiological balance of the soil flora unfavorable to the pathogen.
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