Violet root rot of carrot, caused by Rhizoctonia crocorum (Pers.) DC, appears in Ontario in midsummer, and by the fall progresses to cause deep lesions in the fleshy root of the carrot. Isolation of the fungus from diseased carrot was successful only from mature infection bodies. Of all the media tried meat–malt agar supported the best growth of R. crocorum. While three types of hyphae were produced only those of the subiculum propagated the fungus, and only the subiculum and sclerotia were capable of initiating a parasitic attack on carrots. R. crocorum can infect any part of a carrot root, does not require a wound infection court, and can spread uniformly over the carrot regardless of where primary infection occurs. Although the development of the carrot, the growth of R. crocorum, and the incidence of infection reached a maximum within the pH range of from 5.5 to 6.5, both host and fungus tolerate, and infection occurs within, a much wider pH range. The cardinal temperatures for infection were 5°, 20°, and 30 °C., and there was a close correlation between the temperatures for best growth of the fungus and the host and that for maximum infection. Infection did not occur until the plants were eight weeks old, after which the disease spread until the carrots matured. Initial penetration occurred by hyphal tips forcing their way between the cells of the periderm. Both intercellular and intracellular hyphae were formed abundantly but they did not become established beyond the cambium. Infection bodies began in cells of the periderm where intracellular hyphae accumulated in masses prior to breaking through the outer layer of periderm cells. Two types of histological response to infection were observed: In one a cork layer, formed beneath the infection bodies, resulted in the development of shallow lesions, whereas in the other the infected tissues were broken down and deep lesions were formed in the carrot.