M. Temsah, L. Hanna, A.T. Saad
doi: 10.4454/jpp.v92i2.184
The development of the bacterial knot of oleander, caused by the Pseudomonas savastanoi, was studied at different intervals after inoculation to examine anatomical changes in inoculated twig tissues, the movement of bacteria within host tissues, and the formation of defense reactions of the host plant. Pseudomonas savastanoi invades stem tissues of oleander by moving from the inoculation wound into intercellular spaces of parenchyma tissues and systemically further away through the laticifers. Bacterial invasion of oleander tissues causes degradation of primary cell walls of parenchyma cells and laticifers and formation of bacterial cavities followed by hypertrophic and hyperplasic activities. Hyperplasic activities lead to the formation of meristematic cell masses, with differentiation of vascular bundles, which contributes to the development of the knot. The host develops observable microscopic anatomical defense reactions at the different stages of host invasion. Lignin deposits form on the primary cell walls of parenchyma cells and laticifers around bacterial cavities to limit the movement of the pathogen. Tyloses form in the secondary xylem vessels, blocking them and preventing further movement of the bacteria within the vessels. Finally, the formation of impermeable periderm around bacterial cavities, neoformed tissues, xylem elements, and at the surface of the knot, leads to its final decline.