Wildfire disease of tobacco.

Pseudomonas tabaci (Wolf and Foster) Stevens, produces an exotoxin, detectable as a bacteriumfree, chlorotic halo, surrounding the necrotic focus of infection in the leaf of a susceptible host at the site of inoculation (Braun, 1955). Garber and Heggestad (1958) reported that species of Nicotiana and varieties of Nicotiana tabacum differed in their susceptibility, ranging from highly susceptible to resistant, when leaves of plants grown in the greenhouse were inoculated with washed suspensions of this pathogen. Included in this series of host were three varieties or breeding lines of N. tabacum having wildfire resistance determined by a dominant gene transferred by hybridization from Nicotiana longiflora (Clayton, 1947; Heggestad and Clayton, 1955). Relatively few cases of disease resistance in plants have been explained on the basis of a specific compound or compounds present in resistant hosts and absent in susceptible ones (Holton, 1959). In the absence of the humoral and cellular defense mechanisms commonly found in animals, it is reasonable to assume that plants resort to local biochemical or physiological mechanisms, once the pathogen has effected entry into the host. Garber (1960) has proposed a theory of pathogenicity which considered numerous mechanisms leading to resistance. An investigation of the nature of resistance to wildfire disease of tobacco was undertaken on the assumption that the pathogen may be responsible for altering its microenvironment in the tobacco leaf at the site of inoculation.